Vaccine Failure Is Setback in AIDS Fight

Test Subjects May Have Been Put at Extra Risk Of Contracting HIV

By David Brown
Washington Post Staff Writer
Friday, March 21, 2008; A01

The two-decade search for an AIDS vaccine is in crisis after two field tests of the most promising contender not only did not protect people from the virus but may actually have put them at increased risk of becoming infected.

The results of the trials, which enrolled volunteers on four continents, have spurred intense scientific inquiry and unprecedented soul-searching as researchers try to make sense of what happened and assess whether they should have seen it coming.

Both field tests were halted last September, and seven other trials of similarly designed AIDS vaccines have either been stopped or put off indefinitely. Some may be modified and others canceled outright.

Numerous experts are questioning both the scientific premises and the overall strategy of the nearly $500 million in AIDS vaccine research funded annually by the U.S. government.

“This is on the same level of catastrophe as the Challenger disaster” that destroyed a NASA space shuttle, said Robert Gallo, co-discoverer of the human immunodeficiency virus (HIV), which causes AIDS, and head of the Institute for Human Virology in Baltimore.

The recently closed studies, STEP and Phambili, used the same vaccine — made from a common respiratory virus called adenovirus type 5 that had been crippled and then loaded with fragments of HIV. Both studies were halted when it became clear the STEP study was futile and possibly harmful.

The results of the Phambili vaccine trial, which was conducted in South Africa, were revealed last month and only worsened the gloom. Although the number of new HIV infections in that study was far smaller than in STEP — and too few to draw firm conclusions from — those results, too, hinted at a trend toward harm among vaccine recipients.

Many researchers are questioning the scientific premises on which all those studies were based and are wondering, along with AIDS activists, what effect this near-worst-case scenario might have on tests of future vaccines.

The working hypothesis for what went wrong is that the vaccine somehow primed the immune system to be more susceptible to HIV infection — a scenario neither foreseen nor suggested by previous studies.

The National Institutes of Health, which funded the STEP and Phambili trials, is convening a meeting next week to reassess its AIDS vaccine program. But some respected scientists have already reached a verdict.

“None of the products currently in the pipeline has any reasonable chance of being effective in field trials,” Ronald C. Desrosiers, a molecular geneticist at Harvard University, declared last month at an AIDS conference in Boston. “We simply do not know at the present time how to design a vaccine that will be effective against HIV.”

He told a rapt audience that he has reluctantly concluded that the NIH has “lost its way in the vaccine arena” and that he thinks it should redirect its AIDS vaccine funds to basic research and away from human trials.

In this fiscal year, the NIH’s budget for AIDS vaccine research is $497 million. The STEP and Phambili trials were each expected to cost about $32 million. Pharmaceutical giant Merck & Co. has spent an undisclosed amount developing the vaccine and helping to manage the studies.

“We can’t afford to have any more trials like this,” said Mark Harrington, head of the activist Treatment Action Group and a longtime observer of AIDS research. “We have to stop and reassess and recommit to basic science, or people will begin to lose faith.”

At the moment, only two things are certain.

The first is that the vaccine, developed by Merck, could not have caused HIV infection because it contains only three proteins from HIV, not the entire virus. The second is that there are no obvious villains.

“I do not think that what happened in this trial is an example of scientists blindly rushing into dangerous things,” said John P. Moore, an AIDS virologist at Weill Cornell Medical College, who has criticized vaccine trials he considered futile. “In the general HIV-research community, I didn’t know anyone who said this was going to happen.”

Both trials recruited people who were at high risk of HIV infection through sexual activity. The STEP subjects included many male homosexuals; the Phambili volunteers were male and female heterosexuals. Half the people in each trial were randomly assigned to get three shots of vaccine, and half to get three shots of a harmless liquid containing no adenovirus or HIV proteins.

Each trial was to have 3,000 participants. STEP had finished enrolling subjects in North and South America, the Caribbean and Australia. Phambili (which means “moving forward” in the Xhosa language of South Africa) had signed up 801 by the time it was shut down.

While scientists hoped the Merck vaccine might prevent some infections, its chief purpose was to stimulate “cell-mediated” immunity to produce a less severe illness. Specifically, the vaccine was expected to lower the “viral load” of HIV in the bloodstream, which in turn would both prolong survival and lessen the chance the person would infect others.

Many experts are questioning the wisdom of that strategy, even if it had worked perfectly. Urging millions of people to take an AIDS vaccine that probably would not protect them from the virus, they say, would be a hard and confusing task, even in places where the epidemic still rages.

For the moment, that is an academic question. The vaccine failed to achieve any of its goals.

In both studies, people who got vaccine were more likely — not less — to become infected, with trends suggesting roughly a twofold risk. In the STEP study, which has many more cases to evaluate, nearly all that added risk was in people who had high levels of antibodies to adenovirus type 5 before they got their first shot — evidence they had been previously infected with that strain. Uncircumcised men in that group had the highest risk.

So how could this have happened?

The leading theory is that activation of the immune system, a cascade of events that occurs naturally when a person is infected with a virus or bacterium or gets a vaccine against one of them, in some way increased the risk of HIV infection.

Activation causes cells called CD4 T-lymphocytes (among many other things) to proliferate. CD4 cells are the targets of choice for HIV. In their activated state, they are coated with molecules called CCR5 co-receptors, which HIV needs to attach itself to a cell.

The hypothesis is that people who received the vaccine had greater-than-normal activation and consequently produced more and fatter cellular targets for HIV. That then increased their chances of becoming infected should they encounter the virus in unprotected intercourse.

Two things undercut this idea.

People have been suffering immune-activating infections and getting vaccines for years, and there has never been evidence that those events increased a person’s risk of acquiring HIV. These vaccine trials would be odd places to first notice such a thing. Furthermore, people in the STEP study who got the vaccine did not have more activated CD4 cells than people who got placebo — something that Merck vaccine executive Mark B. Feinberg called “kind of an interesting and unexplained observation.”

“There is something very, very peculiar” going on in the vaccine trials, said Anthony S. Fauci, head of the National Institute of Allergy and Infectious Diseases, which sponsored them.

The multiple surprises have reminded researchers how much they still do not know about HIV’s biology. It has also focused attention on questions they never asked.

For example, none of the monkey experiments with the Merck vaccine subjected animals to the kind of sexual exposure that people in the trial had — namely, repeated encounters with low doses of HIV, with no single exposure being especially high-risk.

Why not?

The researchers did not have any reason to believe the vaccine might be harmful (although they acknowledged it might not be effective), and in any case such a study would have required quite a large number of monkeys, which are expensive to acquire and maintain for research.

Instead, researchers vaccinated a relatively small number of monkeys with the Merck vaccine and then injected them with the monkey equivalent of HIV in a manner that guaranteed they would become infected. Those animals did much better over the long run than infected but unvaccinated ones.

That was once enough to move a vaccine into human trials. But it probably never will be again.


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Mortality in HIV-infected Ugandan adults receiving antiretroviral treatment and survival of their HIV-uninfected children: a prospective cohort study


Antiretroviral therapy (ART) is increasingly available in Africa, but physicians and clinical services are few. We therefore assessed the effect of a home-based ART programme in Uganda on mortality, hospital admissions, and orphanhood in people with HIV-1 and their household members.


In 2001, we enrolled and followed up 466 HIV-infected adults and 1481 HIV-uninfected household members in a prospective cohort study. After 5 months, we provided daily co-trimoxazole (160 mg trimethoprim and 800 mg sulfamethoxazole) prophylaxis to HIV-infected participants. Between May, 2003, and December, 2005, we followed up 138 infected adults who were eligible and 907 new HIV-infected participants and their HIV-negative household members in a study of ART (mainly stavudine, lamivudine, and nevirapine). Households were visited every week by lay providers, and no clinic visits were scheduled after enrolment. We compared rates of death, hospitalisation, and orphanhood during different study periods and calculated the number needed to treat to prevent an outcome.


233 (17%) of 1373 participants with HIV and 40 (1%) of 4601 HIV-uninfected household members died. During the first 16 weeks of ART and co-trimoxazole, mortality in HIV-infected participants was 55% lower than that during co-trimoxazole alone (14 vs 16 deaths per 100 person-years; adjusted hazard ratio 0·45, 95% CI 0·27–0·74, p=0·0018), and after 16 weeks, was reduced by 92% (3 vs 16 deaths per 100 person-years; 0·08, 0·06–0·13, p<0·0001). Compared with no intervention, ART and co-trimoxazole were associated with a 95% reduction in mortality in HIV-infected participants (5 vs 27 deaths per 100 person-years; 0·05, 0·03–0·08, p<0·0001), 81% reduction in mortality in their uninfected children younger than 10 years (0·2 vs 1·2 deaths per 100 person-years; 0·19, 0·06–0·59, p=0·004), and a 93% estimated reduction in orphanhood (0·9 vs 12·8 per 100 person-years of adults treated; 0·07, 0·04–0·13, p<0·0001).


Expansion of access to ART and co-trimoxazole prophylaxis could substantially reduce mortality and orphanhood among adults with HIV and their families living in resource-poor settings.

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Antiretroviral therapy (ART) is the most effective clinical intervention for reduction of mortality in people with HIV-1 infection. It is increasingly available in the developing countries where 90% of HIV-infected people live, including 63% in Africa.1 However, despite substantial efforts, most HIV-infected people in Africa who would benefit from ART do not have access to it.1 Availability in many areas is constrained by the high cost of medication,2–4 inadequate numbers of trained health-care providers,5,6 poorly equipped clinics,7 and distance to health centres.8,9 Effective ART programmes require high adherence to medication,10 attention to potential drug toxicity, and continuing diagnosis and treatment of opportunistic infections. Ideally, programmes in Africa would provide these services with limited use of physicians and minimum transportation requirements.5 Use of trained lay providers to deliver ART to HIV-infected people at their homes, collect standard health information, and refer patients for selected symptoms could potentially avoid adherence problems stemming from inadequate transportation to clinics and could reduce crowding at health centres.

Although several studies provide information about survival and changes in immunological and virological markers during ART in patients in Africa,11 an assessment of ART effectiveness requires a comparison group and a carefully followed up cohort because randomised trials would be unethical.12,13 Data for effectiveness of highly active antiretroviral therapy (HAART) from developed countries are few because contemporaneous comparison groups were taking dual treatment at the time HAART became available. In Africa, initial introduction of ART has usually been as HAART. Insight into the effectiveness of HAART in Africa could enable improved decision making by individuals, governments, and donor agencies.

We analysed data from two prospective cohort studies in rural Uganda—the first of co-trimoxazole prophylaxis and the second of HAART. The main purpose of the randomised HAART study was to evaluate three different treatment monitoring strategies. Data aggregated across monitoring groups were used to assess the effect of a home-based ART programme on mortality, hospital admissions, and orphanhood in people with HIV and their families. We assessed the effect of adding HAART to co-trimoxazole prophylaxis and the effect of HAART and co-trimoxazole compared with the time before either intervention.

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Participants and study design

HIV-infected participants (18 years or older) at the Tororo Branch of The AIDS Support Organisation (TASO), including those from Tororo, Busia, and Mbale districts in Uganda were enrolled. In study period 1, initiated in April, 2001, we followed up participants with home visits for a median of 5 months (figure 1). In study period 2, all participants with HIV without previous adverse reactions to sulfonamides were provided daily co-trimoxazole (160 mg of trimethoprim and 800 mg of sulfamethoxazole) prophylaxis and followed up for a median of 1·5 years (IQR 1·3–1·5). In study period 3, begun in May, 2003, we provided ART to all clinically or immunologically eligible participants from periods 1 and 2 and to newly enrolled participants—ie, additional HIV-infected clients from the same TASO Center and catchment area to reach a total sample size of 1045—and followed them up until December, 2005. After a median of 126 (IQR 84–432) days of follow-up on ART, all households were provided with two insecticide-treated bednets. Study methods for this sequential cohort were described elsewhere.14

Figure 1. Study profile

HIV-infected adults and HIV-uninfected household members enrolled and followed up in Tororo and Busia Districts, Uganda, 2001–05. ART=antiretroviral therapy.

The studies were approved by the science and ethics committee of the Uganda Virus Research Institute, the Uganda National Council of Science and Technology, and the institutional review board of Centers for Disease Control and Prevention (Atlanta, GA, USA). HIV-infected participants provided written informed consent. HIV testing and counselling and study enrolment were offered to all household members after they gave consent. CD4-cell count enumeration was done at baseline for HIV-infected participants. A household was defined as people who shared a hearth and slept in the same house or cluster of houses for at least 5 days per week for 3 or more months before baseline.

Households were visited every week by paid study staff who resupplied medicine and administered a standardised questionnaire about drug adherence, hospital admissions, potential symptoms of drug toxicity, or death of a household member in the preceding 7 days. Pill counts were done at the study clinic by a pharmacist. Any participant, including household members, who requested medical care was seen free of charge by a study physician. If admitted during the study, the admission fee and a daily stipend for food were provided. If a participant died during the study, a verbal post mortem with family members was done and medical records were examined.

Additional informed consent was obtained for repeat CD4-cell count testing at the start of period 3. All participants with a CD4-cell count of less than 250 cells per μL or severe HIV disease (defined as WHO stage 3 or 4 disease or a history of recurrent herpes zoster), were offered enrolment in a study that provided ART. Pulmonary tuberculosis alone was not an inclusion criterion because in Africa it is common in HIV-infected people without immune compromise. Our main aim in this part of the study was to assess different ART monitoring strategies; HIV-infected participants were randomly assigned to one of three groups: group one, clinical monitoring, quarterly CD4-cell counts, and measurement of viral loads; group 2, clinical monitoring and quarterly CD4-cell counts; and group 3, clinical monitoring alone. Sample size was decided on the basis of these comparisons. Data from comparison of these groups will be analysed at the end of 3 years of follow-up; only aggregate data are presented here.

Routine clinic visits were not made after enrolment, but HIV-infected participants were encouraged to come to the clinic or hospital if they were ill. HIV-infected participants were taken to the clinic for assessment during period 3 if they had specifically defined symptoms or severe illness during the home visit. Blood samples were taken every 3 months at home and transported to the laboratory for CD4 cell and viral load testing.

The first-line treatment regimen consisted of stavudine, lamivudine, and either nevirapine or efavirenz. For participants who developed evidence of ART treatment failure or toxicity, available agents included didanosine, zidovudine, tenofovir, and lopinavir or ritonavir. Drugs were delivered every week in prepacked pill boxes. Participants taking ART continued taking daily co-trimoxazole unless they had severe toxicity, irrespective of CD4-cell count.


Plasma samples were screened for HIV infection by two enzyme-linked immunoassays (EIA) in parallel (Recombigen HIV-1/HIV-2, Trinity Biotech, Dublin, Ireland; and Murex HIV.1.2.0, Abbot Diagnostics, Chicago, IL, USA). Specimens concordantly positive or negative received no further testing. Specimens with discordant results were retested by the same algorithm and if they were still discordant by western blot (LAV Blot, Biorad, Richmond, CA, USA). Dried blood spots obtained on filter paper from household members of participants were screened by EIA (Vironostika HIV, BioMerieux, Durham, NC, USA) and reactive specimens were confirmed by western blot. CD4-cell counts were measured by FACSCalibur, FACScan, or FACSCount flow cytometers (Becton-Dickinson, San Carlos, CA, USA) following standard protocols. HIV viral loads were measured by Cobas Amplicor (version 1.5, Roche, NJ, USA). The lower limit of the viral load assay was 400 copies per mL.

Statistical analysis

Data were entered by use of Epi Info (Centers for Disease Control and Prevention, Atlanta, GA, USA) and analysed with SAS (9·0, Cary, NC, USA). We compared groups by χ2, Wilcoxon rank sum, Wald’s, and Student’s t tests. We compared morbidity and mortality during ART and co-trimoxazole prophylaxis (period 3) with both co-trimoxazole alone (period 2) and without either medication (period 1). The point of origin for participants in every study period was the time at which they started the respective intervention. To adjust for differences between study period in immune status of participants, analyses were adjusted for the last CD4-cell count value before every period because the interventions could themselves affect CD4-cell count—eg, ART improved immune function. Few data were missing; when data for a variable were not present we inserted a missing category indicator.

A multivariable Cox regression model was developed to control for confounding variables. For analyses of rate of hospital admissions in HIV-infected participants, we used a Poisson regression model with a log-link function after adjusting for age and CD4-cell count as continuous variables, and sex and 3-month seasonal periods as categorical variables. We used generalised estimating equation methods with an exchangeable correlation structure for analysis of repeated measures in the same individuals.15 For analysis of orphanhood prevented, we included children for whom only one HIV-infected parent was alive and calculated time to parental death after adjusting for age and CD4-cell count. We calculated the number of HIV-infected participants needed to treat (NNT) with ART and co-trimoxazole to prevent an outcome16—eg, death or hospital admission, only for associations that were significant in a multivariate analysis. Multivariate results are presented unless otherwise specified.

Role of the funding source

Funding was provided by the US President’s Emergency Plan for AIDS Relief and Centers for Disease Control. Centers for Disease Control staff were involved in the study design, collection, analysis, interpretation of data, and writing of the report. The corresponding author had access to all data and made the decision to submit for publication.

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Figure 1 shows the study profile. Age and median CD4-cell count differed across study periods (table 1). Age and sex were similar for participants who newly enrolled during period 3 and those who had also participated in period 2 (data not shown); however, median CD4-cell count for newly enrolled participants in period 3 was lower (122 cells per μL vs 143 cells per μL, p=0·02). Median follow-up before co-trimoxazole was 154 (IQR 147–161) days, during co-trimoxazole was 532 (488–542) days, and during ART and co-trimoxazole was 749 (699–812) days.

Table 1. Baseline characteristics of participants before every intervention period

The median number of HIV-uninfected household members was three, the median age was 11 (IQR 6–16) years; 51% were female. Demographic characteristics of family members in different periods (data not shown) did not differ. Infants born to participants during the study were included in follow-up.

233 (17%) of 1373 participants with HIV and 40 (1%) of 4601 HIV-uninfected household members died. For the analysis of ART and co-trimoxazole compared with co-trimoxazole alone, an interaction between time on ART and the effect of ART on mortality was noted. Because of this finding, we used time-dependent covariates in the model to analyse data for the ART period separately for the first 16 weeks and after 16 weeks of follow-up (table 2). Compared with co-trimoxazole alone, mortality in HIV-infected participants during ART and co-trimoxazole was reduced by 55% during the first 16 weeks of treatment, and was 92% less after 16 weeks. Mortality during ART and co-trimoxazole was 95% less than that during no treatment.

Table 2. Mortality in HIV-infected adults during co-trimoxazole prophylaxis and antiretroviral therapy (ART) in Tororo and Busia Districts, Uganda, 2001–05

The benefits of ART improved over time; for the first 16 weeks of ART and co-trimoxazole compared with co-trimoxazole alone, 1 life-year was saved for every 14 people treated annually, and for later than 16 weeks of treatment 1 life-year was saved for every eight people treated annually. Compared with no intervention, only 4 people would need to be treated with ART and co-trimoxazole annually per life-year saved. A similar relative reduction in mortality for ART and co-trimoxazole was seen across all CD4-cell count strata; however, the NNT per life-year gained varied by the CD4-cell count at which treatment was initiated—eg, two people treated per life-year gained for those with a CD4-cell count less than 50 cells per μL, and 18 for people with a CD4-cell count greater than 200 cells per μL (table 2).

After adjustment for CD4-cell count, age, and interventions, mortality in men was higher than in women (hazard ratio [HR] 1·4, 95% CI 1·07–1·90, p=0·017). Verbal autopsies were available for 227 (97%) of 233 HIV-infected adults. 224 (99%) deaths were medically related and three (1%) were caused by injury.

Mortality in HIV-negative children aged less than 10 years was reduced by 77% (0·2 vs 1·0 deaths per 100 person-years; HR 0·23, 95% CI 0·09–0·57, p=0·001) when HIV-positive people were taking ART and co-trimoxazole compared with co-trimoxazole alone, and 81% less (0·2 vs 1·2 deaths per 100 person-years; 0·19, 0·06–0·59, p=0·004) compared with before co-trimoxazole. An interaction was noted between age and the effect of ART and co-trimoxazole on mortality of HIV-uninfected children; an association was seen only in children under 10 years old.

Of 17 HIV-negative children less than 10 years old who died; eight were aged less than 1 year, six were 1–4 years, and three were 5–9 years. Five children died after the death of a HIV-positive adult in the household and 12 died before an adult’s death. During the 28 days before death, none of the children were diagnosed with malaria. No interaction of bednets on the effect of ART and co-trimoxazole on mortality was noted in HIV-negative children.

Many children were at high risk of orphanhood. At baseline, information about HIV status of all living parents was known for 2556 children aged under 18 years in households. For 2126 (83%) of these children, all living parents had HIV. 1935 (91%) had only one parent in the household and that parent had HIV, and 191 (9%) had two HIV-infected parents. Compared with no intervention, ART and co-trimoxazole prophylaxis was associated with a 78% reduction in the number of orphans during the first 16 weeks of treatment (5·3 vs 12·8 per 100 person-years of adults treated; HR 0·22, 95% CI 0·13–0·30, p<0·0001), and with a 93% reduction after 16 weeks of treatment (0·9 vs 12·8 per 100 person-years of adults treated; 0·07, 0·04–0·13, p<0·0001).

1676 hospital admissions were recorded in HIV-infected participants. The frequency of admissions was 43% less during ART and co-trimoxazole than for co-trimoxazole alone, and 64% less compared with no intervention (table 3).

Table 3. Hospital admissions in HIV-infected adults during co-trimoxazole prophylaxis and antiretroviral therapy (ART) in Tororo and Busia Districts, Uganda, 2001–05

All 1045 participants were started on non-nucleoside reverse transcriptase inhibitor-containing regimens: stavudine, lamivudine, and nevirapine or efavirenz. During follow-up, 41 (4%) of 1045 people were changed to a protease inhibitor-containing regimen. Adherence to ART was excellent. As published previously,17 the medication possession ratio, a measure that incorporated pill count data and any lapses in pill delivery as a result of participants being on a drug holiday or being away from home, was greater than 95% for 89–97% of quarterly assessments.

CD4-cell counts increased during ART and co-trimoxazole prophylaxis (101 cells per μL increase per year, 95% CI 94–108 cells per μL) and decreased during co-trimoxazole alone (82 cells per μL decrease per year, 64–100 cells per μL; adjusted mean pairwise difference 127 cells per μL, 106–149, p<0·0001). Viral loads were available from all participants in the study of ART and 35% of those who survived throughout the co-trimoxazole study. Viral load decreased during ART (1·3 log10 copies per mL per year, 1·2–1·4) and was stable during co-trimoxazole prophylaxis alone (0·1 log10 copies per mL per year, 0·1–0·2; adjusted mean pairwise difference 1·2 log10 copies per mL, 1·1–1·4, p<0·0001). Baseline median viral load was 216000 (IQR 72000–536000) copies per mL; at 3 months after starting ART and thereafter, median viral load was less than the lower limit of detection. 889 (91%) of 972 participants had a viral load of less than 400 copies per mL at 3 months, 885 (96%) of 921 at 6 months, and 794 (96%) of 826 at 24 months (figure 2).

Figure 2. CD4-cell count and viral load changes in HIV-infected adults taking co-trimoxazole prophylaxis and antiretroviral therapy (ART) in Tororo and Busia Districts, Uganda, 2001–05

(A) Change in CD4 cell-count. (B) Proportion with undetectable viral load (less than 400 copies per mL).

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A home-based ART and co-trimoxazole programme was associated with a greater than 90% reduction in mortality in adults with HIV living in rural Uganda. These results were achieved even though no routine clinic visits were scheduled after initial enrolment, and home visits were provided by trained lay providers. Provision of ART to adults was also associated with a large reduction in mortality in their HIV-negative children, and with substantial reductions in the rate of orphanhood.

The overall effect of ART on mortality in this study was similar to or better than that seen in facility-based studies in Europe,12 Haiti,18 and Africa.11,13,19–23 These results were obtained in a challenging environment for both participants and the health-care system because mean per person expenditures were US$0·25 per day, 76% of participants did not have any post-primary education,17 and most houses did not have access to electricity or running water.

ART reduced mortality in HIV-infected adults even as an addition to an already-effective basic-care programme that included other interventions, such as co-trimoxazole prophylaxis and a home-based safe water system.24 Participants adhered well to ART, and treatment failure was rare. These findings, together with frequent monitoring and adherence support by home visitors, might have resulted in especially beneficial outcomes.25 Good adherence to drug regimens is essential for ART, and in this cohort less than 95% adherence was previously associated with the worst virological outcomes.17 Recommended second-line regimens in Africa include protease inhibitors that are more expensive than first-line drugs; incorporation of efforts to maintain excellent adherence might be useful to extend the effect of the initial regimen and also to reduce costs. We noted higher mortality in men than in women in our cohort. Sex differences in response to ART have been seen in some,26,27 but not all,12 studies and deserve further investigation. Compared with co-trimoxazole, the full effect of ART on mortality did not take place until 16 weeks after initiation of treatment. This lag might have occurred because ART takes time to restore immune function, whereas co-trimoxazole acts immediately as a prophylactic agent, or because ART has been associated with immune reconstitution inflammatory syndrome, especially during the first few months of treatment. Since mortality in participants was greatest during the first 16 weeks of treatment, strategies to reduce the rate of opportunistic infections and to rapidly treat illnesses that arise during this period need to be assessed.

One of the possible reasons for the small proportion of ART-eligible people taking ART in Africa is the insufficient numbers of physicians and other care providers throughout the continent—eg, in Uganda there are only about 2200 physicians, one per 12500 population.28 If provision of ART needed frequent routine visits to a physician, this could limit its widespread implementation. Additionally, poverty and restricted access to transportation reduce the ability of people to attend health-care facilities, and might limit patient retention.25 Because of these challenges, training lower cadres of health-care staff to monitor and provide other aspects of care has been proposed.29 In our study, the use of trained lay providers to monitor and refer patients reduced overall burden at the health centre and allowed senior health-care professionals to focus on diagnostic, preventive, and curative care. Limitation of the number of visits to facilities might also theoretically reduce the risk of nosocomial transmission of tuberculosis—a common infection in people with HIV in Africa.

The finding that mortality reductions and adherence rates were similar to those of facility-based studies is encouraging, but programmes with reduced follow-up outside a well-resourced clinical trial should be assessed. In June, 2007, of the 106000 people in Uganda taking ART, 15171 (14%) were receiving their drugs through home or community care—most through TASO home visits every 1 or 2 months.

We noted a reduction in mortality in HIV-negative children during the time that adults in the household were taking ART and co-trimoxazole compared with when they were taking co-trimoxazole alone. We saw a similar effect in HIV-negative children when we introduced co-trimoxazole prophylaxis.30 A possible explanation for the effect of these interventions is an association between parental and child mortality, which has been shown before for parents with31 and without32 HIV. In our cohort, death of a parent with HIV was associated with a three-fold increase in mortality in children under 10 years of age without HIV.30

The main limitation of our study was its observational design. Because ART has demonstrated efficacy against mortality in HIV-infected people, a study in people with advanced HIV disease should provide this intervention. Without a contemporary randomised control group, our results might have been confounded by survivor bias33 or seasonal variations, which might have overestimated the magnitude of intervention effects. To minimise these potential effects, we assessed CD4-cell counts at baseline and before every intervention, and adjusted for CD4-cell count, age, sex, and season in analyses. We might have overestimated the effect of ART on mortality if the clinical care provided to participants improved because of experience during the 5-year period, or because ART participants with severe illness during home visits could be taken to the study clinic for assessment. Last, home visits were made every week, albeit by lay workers, which limits generalisability.

In the 1990s, ART was shown to reduce morbidity and mortality from HIV/AIDS in developed countries. ART has been introduced into Africa and other resource-limited settings experiencing devastating HIV epidemics. For 83% of children in our study population, all living parents had HIV. Wide provision of ART and care in sub-Saharan Africa could have a profound effect on prevention of mortality in people with HIV, improve health and longevity of their children, and reduce the rate of orphanhood. Our findings support the efforts to bring ART to people with HIV throughout the world, irrespective of geographic or socioeconomic background.

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RB, DM, JRL, and JM were principal investigators and were involved in writing protocols and supervising study implementation. JM was the main author. WW coordinated the study involving ART and supervised implementation. PB developed, implemented, and coordinated data management, and JPE did the statistical analyses. RD supervised laboratory testing. JT assisted with interpretation of the findings and writing the report. AC helped to design and implement the study and ensured the protocol was applicable to TASO.

Conflict of interest statement

We declare that we have no conflict of interest.


We thank the staff of Tororo Hospital, staff and clients of TASO, US Embassy in Kampala, Global AIDS Program headquarters, and staff of Centers for Disease Control-Uganda, especially the informatics, clinical, laboratory, and administrative units of Centers for Disease Control-Tororo. The findings and conclusions in this report are those of the authors and do not necessarily represent the views of the Centers for Disease Control and Prevention.

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1WHO, UNAIDS. AIDS Epidemic Update. 2006: 
Available at:…

(accessed Nov 8, 2007)..

2Colebunders R, Kamya M, Semitala F, Castelnuovo B, Katabira E, McAdam K. Free Antiretrovirals must not be restricted only to treatment-naive patientsPLoS Med 2005; 2: e276. CrossRef

3Laurent C, Meilo H, Guiard-Schmid JB, et al. Antiretroviral therapy in public and private routine health care clinics in Cameroon: lessons from the Douala antiretroviral (DARVIR) initiativeClin Infect Dis 2005; 41: 108-111. CrossRef

4van Oosterhout JJ, Bodasing N, Kumwenda JJ, et al. Evaluation of antiretroviral therapy results in a resource-poor setting in Blantyre, MalawiTrop Med Int Health 2005; 10: 464-470. MEDLINE | CrossRef

5Miles K, Clutterbuck DJ, Seitio O, Sebego M, Riley A. Antiretroviral treatment roll-out in a resource-constrained setting: capitalizing on nursing resources in BotswanaBull World Health Organ 2007; 85: 555-560.

6Kober K, Van Damme W. Scaling up access to antiretroviral treatment in southern Africa: who will do the job?Lancet 2004; 364: 103-107. Abstract | Full Text | Full-Text PDF (473 KB) | CrossRef

7Pappas G, Aronovich D, Mukooyo E, Bunnell R, Kabatesi D, Mermin J. Access to basic HIV/AIDS related clinical services in Uganda: results of a nationally-representative health facility surveyAIDS Public Policy J 2006; 19: 75-85.

8Lwasa S. Planning for health infrastructure in Uganda: where is the need?
Available at: Geospatial Resource Portal:…

(accessed Nov 8, 2007)..

9Calmy A, Klement E, Teck R, Berman D, Pecoul B, Ferradini L. Simplifying and adapting antiretroviral treatment in resource-poor settings: a necessary step to scaling-upAIDS 2004; 18: 2353-2360. MEDLINE

10Bangsberg DR, Perry S, Charlebois D, et al. Non-adherence to highly active antiretroviral therapy predicts progression to AIDSAIDS 2001; 15: 1181-1183. MEDLINE | CrossRef

11Akileswaran C, Lurie MN, Flanigan TP, Mayer KH. Lessons learned from use of highly active antiretroviral therapy in AfricaClin Infect Dis 2005; 41: 376-385. CrossRef

12Sterne JA, Hernan MA, Ledergerber B, et al. Long-term effectiveness of potent antiretroviral therapy in preventing AIDS and death: a prospective cohort studyLancet 2005; 366: 378-384. Abstract | Full Text | Full-Text PDF (96 KB) | CrossRef

13Losina E, Yazdanpanah Y, Deuffic-Burban S, et al. The independent effect of highly active therapy on severe opportunistic disease incidence and mortality in HIV-infected adults in Côte d’IvoireAntivir Ther 2007; 12: 543-551.

14Mermin J, Ekwaru JP, Liechty CA, et al. Effect of co-trimoxazole prophylaxis, antiretroviral therapy, and insecticide-treated bednets on the frequency of malaria in HIV-1- infected adults in Uganda: a prospective cohort studyLancet 2006; 367: 1256-1261. Abstract | Full Text | Full-Text PDF (100 KB) | CrossRef

15Hardin J, Hilbe J. Generalized estimating equationsFlorida: Chapman and Hall/CRC, 2003:.

16Altman D, Andersen P. Calculating the number needed to treat for trials where the outcome is time to an eventBMJ 1999; 319: 1492-1495.

17Weidle PJ, Wamai N, Solberg P, et al. Adherence to antiretroviral therapy in a home-based AIDS care programme in rural UgandaLancet 2006; 368: 1587-1594. Abstract | Full Text | Full-Text PDF (107 KB) | CrossRef

18Severe P, Leger P, Charles M, et al. Antiretroviral therapy in a thousand patients with AIDS in HaitiN Engl J Med 2005; 353: 2325-2334. CrossRef

19Wools-Kaloustian K, Kimaiyo S, Diero L, et al. Viability and effectiveness of large-scale HIV treatment initiatives in sub-Saharan Africa: experience from western KenyaAIDS 2006; 20: 41-48. MEDLINE

20Badri M, Bekker LG, Orrell C, Pitt J, Cilliers F, Wood R. Initiating highly active antiretroviral therapy in sub-Saharan Africa: an assessment of the revised World Health Organization scaling-up guidelinesAIDS 2004; 18: 1159-1168. MEDLINE | CrossRef

21Stringer J, Zulu I, Levy J, et al. Rapid scale-up of antiretroviral therapy at primary care sites in Zambia: feasibility and early outcomesJAMA 2006; 296: 782-793. CrossRef

22Spacek L, Shihab HM, Kamya M, et al. Response to antiretroviral therapy in HIV-infected patients attending a public, urban clinic in Kampala, UgandaClin Infect Dis 2006; 42: 252-259. CrossRef

23Braitstein P, Brinkhof MW, Dabis F, et al. Mortality of HIV-1-infected patients in the first year of antiretorviral therapy: comparison between low-income and high-income countriesLancet 2006; 367: 817-824. Abstract | Full Text | Full-Text PDF (122 KB) | CrossRef

24Lule JR, Mermin J, Ekwaru JP, et al. Effect of home-based water chlorination and safe storage on diarrhea among persons with human immunodeficiency virus in UgandaAm J Trop Med Hyg 2005; 73: 926-933. MEDLINE

25Rosen S, Fox M, Gill CJ. Patient retention in antiretoviral therapy programs in sub-Saharan Africa: a systematic reviewPLoS Med 2007; 4: 1691-1700.

26Braga P, Cardoso M-R, Segurado A. Gender differences in survival in an HIV/AIDS cohort from Sao Paulo, BrazilAIDS Patient Care STDS 2007; 21: 321-328. MEDLINE | CrossRef

27Nicastri E, Angeletti C, Palmisana L, et al. Gender differences in clinical progression of HIV-1-infected individuals during long-term highly active antiretroviral therapyAIDS 2005; 19: 577-583. MEDLINE

28WHO. Working together for health: the World Health Report 2006
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29Samb B, Celleti F, Holloway J, Van Damme W, De Cock KM, Dybul M. Rapid expansion of the health workforce in response to the HIV epidemicNew Engl J Med 2007; 357: 2510-2514. CrossRef

30Mermin J, Lule J, Ekwaru JP, et al. Cotrimoxazole prophylaxis by HIV-infected persons in Uganda reduces morbidity and mortality among HIV-uninfected family membersAIDS 2005; 19: 1035-1042. MEDLINE

31Nduati R, Richardson BA, John G, et al. Effect of breastfeeding on mortality among HIV-1 infected women: a randomised trialLancet 2001; 357: 1651-1655. Abstract | Full Text | Full-Text PDF (84 KB) | MEDLINE | CrossRef

32El-Ghannam AR. The global problems of child malnutrition and mortality in different world regionsJ Health Soc Policy 2003; 16: 1-26. MEDLINE | CrossRef

33Walker S, Mulenga V, Ford D, et al. The impact of daily cotrimoxazole prophylaxis and antiretroviral therapy on mortality and hospital admissions in HIV-infected Zambian childrenClin Infect Dis 2007; 44: 1361-1367. CrossRef

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Affiliationsa. Centers for Disease Control and Prevention-Uganda, Global AIDS Program, National Center for HIV, Viral Hepatitis, Sexually Transmitted Disease, and Tuberculosis Prevention, Centers for Disease Control and Prevention, Entebbe, Uganda
b. Department of Medicine, Faculty of Medicine, University of British Columbia, Vancouver, BC, Canada
c. The AIDS Support Organisation, Kampala, Uganda
d. Centers for Disease Control and Prevention-Kenya, Coordinating Office for Global Health, Centers for Disease Control and Prevention, Nairobi, Kenya

Corresponding Author InformationCorrespondence to: Jonathan Mermin, Centers for Disease Control and Prevention-Kenya, Kenya Medical Research Institute, Mbagathi Road, Nairobi, Kenya

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Transmission of HIV-1 infection in sub-Saharan Africa and effect of elimination of unsafe injections

The Lancet 2004; 363:482-488


Public Health


Frequency of unsafe injections

Transmission efficiency via unsafe injections

Population attributable fractions (PAFs)

Age and sex patterns of infection

Sex as primary mode of HIV-1 transmission

South Africa




During the past year, a group has argued that unsafe injections are a major if not the main mode of HIV-1 transmission in sub-Saharan Africa. We review the main arguments used to question the epidemiological interpretations on the lead role of unsafe sex in HIV-1 transmission, and conclude there is no compelling evidence that unsafe injections are a predominant mode of HIV-1 transmission in sub-Saharan Africa. Conversely, though there is a clear need to eliminate all unsafe injections, epidemiological evidence indicates that sexual transmission continues to be by far the major mode of spread of HIV-1 in the region. Increased efforts are needed to reduce sexual transmission of HIV-1.

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In the 1980s, WHO1 estimated that unsafe injections and the use of other inadequately sterilised skin-piercing instruments caused 1·6% of HIV-1 infections in Africa. More recent estimates2 have put the proportion at 2·5% of all infections in sub-Saharan Africa. Gisselquist and colleagues3,4 argue, however, that unsafe injections are a major if not the main mode of transmission in the region, causing 20–40% of HIV-1 infections, and they question the orthodox epidemiological interpretations about the lead role of unsafe sex in transmission. There are few policy makers who would not agree that unsafe injections should be eliminated. However, the way in which Gisselquist and co-workers downplay the importance of sexual transmission could hinder efforts to control the sexual transmission of HIV-1 in sub-Saharan Africa. For example, the US Senate Committee on Health, Education, Labor, and Pensions has held hearings to establish whether HIV/AIDS funds should be devoted to programmes that target unsafe injections. Here, we review what we believe are Gisselquist and colleagues’ main arguments (table 1) to ascertain whether they provide convincing evidence against the prevailing view among epidemiologists that sexual intercourse is by far the most important route of transmission of HIV-1 in sub-Saharan Africa.

Table 1. Route of transmission of HIV-1: main arguments for and against unsafe injections

Frequency of unsafe injections

The number of injections administered for health reasons has been estimated at an average of 3·4 per person per year in low-income and middle-income countries.5 Of these, about 39% are given with unsafe injection equipment—ie, equipment that is reused without first being sterilised.6 Injections given with reused equipment are more common in the Middle East and south Asia than in sub-Saharan Africa, where the results of population-based surveys indicate that an estimated 2·1 injections are given per person per year, of which about 18% (approximate 95% CI 13–23) are given with reused equipment. This proportion is considerably less than the 50% of injections cited by Gisselquist and colleagues,7 and results in a mean of 0·4 potentially unsafe injections per person per year.6

Most injections in sub-Saharan Africa are given intramuscularly, and blood contamination of needles after use for intramuscular injection is infrequent. A threshold value of 0·0015 μL is thought by some to be the minimum amount needed to transmit HIV-1.8 The likelihood of encountering blood in syringes or needles that have been used for medically indicated intramuscular injection of HIV-1-infected patients in the USA has been estimated by PCR (with a mean limit of sensitivity of 0·09 μL to detect viral DNA from white blood cells) and enzyme immunoassay (with a mean limit of sensitivity of 0·00084 μL to detect antibodies to HIV-1).9 In one study,10 none of 184 syringes or needles tested positive for blood with the PCR assay, and only ten (5%) tested positive when the enzyme immunoassay was used. Furthermore, none of the needles or syringes was positive for HIV-1 DNA, as judged by an assay sensitive enough to detect proviral DNA with single-copy sensitivity. In a subsequent study10 of 80 needles or syringes tested with a nested PCR assay capable of detecting two infectious units of viral RNA, 66 of which had been used for intramuscular injection and 14 for subcutaneous injection, three (4%) were positive. However, the identification of HIV-1 RNA means only that the equipment is potentially infectious, since the assay does not identify whether the nucleic acid is from whole, or viable, virus. Moreover, findings of studies in health-care workers suggest that simple exposure to even viable virus, particularly in low concentrations, seldom results in transmission. A careful distinction should, therefore, be made between injections with needles and syringes that might not be sterile and those that are capable of transmitting HIV-1, with the latter being a fraction of the former.

Additionally, in health-care practice, procedures are commonly used that, though not guaranteeing the safety of the injection from HIV-1 contamination, will nevertheless further reduce the likelihood of contamination. Washing or, possibly, rinsing or soaking of syringes or needles will dilute any blood that might have contaminated the equipment. Experimentally, a single flush of a syringe or needle with water leads to an approximate 70% decrease in the proportion that contain sufficient HIV-1 to replicate in culture, while two flushes decrease that proportion by 95%.11 Furthermore, heating in water at 60–65°C will inactivate HIV-1 within seconds.12,13 Although the proportion of syringes or needles that are washed or heated is unknown, findings of several studies8,14–16 indicate that reused equipment is often sterilised or boiled. Storage of syringes or needles at room temperature also results in a decline in viral titre.17,18 Results of a survey15 of 16 rural health centres in Ethiopia showed that, although 12% of injections were given with reused equipment, the equipment had been boiled, steam-sterilised (although not always in accord with WHO standards), or heated with burning alcohol—HIV-1 RNA was not detected in any of 212 needles tested (approximate HIV-1 prevalence, 8·3%), with an assay capable of detecting 150 copies/mL.

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Transmission efficiency via unsafe injections

The best data on transmission efficiency via injections come from studies of health-care workers, among whom findings of longitudinal studies19 indicate an estimated risk of HIV-1 infection after direct percutaneous exposure of 0·3%. This summary estimate is an average of different risk estimates taken from studies of different exposure categories (0·2%—ie, one seroconversion in 497 exposures—if one uses only needlestick-puncture exposures).19,20

Gisselquist and colleagues use two arguments to arrive at their much higher estimated risk of transmission efficiency of 2·3%.7 A case-control study21 on occupational risk of HIV-1 infection identified several factors that increase the risk of infection, including deep injury, visible blood on the device, any procedure involving drawing blood from an artery or vein in the source patient, and terminal illness of the source patient. Gisselquist and colleagues used the proportion of cases and controls in the study that reported a deep injury to estimate the risk after a deep injury as 2·3%. They argued that this transmission risk is applicable to unsafe injections in health-care settings in Africa, but they neglected important factors in the study—namely, that 73% of exposures had venous or arterial blood as a source (compared with 31% of controls), that visible blood on needles was common, and that most patients probably had high viral loads. These factors, also with significant odds ratios, are unlikely to be present in typical African health-care settings, where intramuscular injections are most common, a cleaning procedure is likely before reuse of equipment, and source patients are less likely to have terminal illness—all these factors will lessen the calculated transmission efficiency of 2·3%. Furthermore, washing and heating of needles and syringes will greatly diminish even this lower transmission efficiency.

The second method Gisselquist and co-workers used for estimating the transmission probability relied on data from nosocomial outbreaks in Russia, Romania, and Libya.7 Even if one accepts their calculations and assumptions, unusual outbreaks are likely to have higher than usual transmission efficiency. The Russian outbreak was a result of a combination of intramuscular and intravenous (catheter and possibly transfusion) exposures;22 the Romanian outbreak involved the sequential, immediate use of large-bore needles in children; and there are few epidemiological data from the Libyan outbreak. To believe that their calculated risk of 2–7% can be generalised to the African setting is, therefore, erroneous.

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Population attributable fractions (PAFs)

Based on the findings of various studies, Gisselquist and colleagues4 calculate the PAFs (causal fractions) associated with injections and conclude that, “Many studies show 20%–40% of HIV infections in African adults associated with injections (though direction of causation is unknown)”. Furthermore, in analyses of data from the 1980s, Gisselquist and co-workers3 report that, “Overall, crude PAFs from general population studies through 1988 suggest that medical exposures were responsible for more African HIV than sexual exposures”.

The association of unsafe injections with prevalent HIV-1 infection has been examined in at least 19 cross-sectional studies. The results of most of these studies have shown an association between injections and HIV-1 infection, and relative risks are 1·16–2·96 (Seguy N, US Centers for Disease Control and Prevention, personal communication). In those studies that have adjusted for confounding, the adjusted relative risks were generally smaller than the unadjusted ones, indicating that other factors—in particular a history of sexually transmitted infections (STIs)—confound the association. Additionally, four published longitudinal studies23–26 have examined the association of incident HIV-1 infections with a history of injections. The results of two studies from Kinshasa, Democratic Republic of Congo,23 and Rakai, Uganda,24 noted no association between injections and risk of HIV-1 infection, whereas those of a third,25 from Rwanda, indicated no association after adjustment for other variables. The findings of the fourth study,26 from Masaka, Uganda, in which study participants were interviewed, on average, a year after seroconversion, showed a significant association in men but not women. Unpublished data from a longitudinal study in Mwanza Region, Tanzania, indicate a non-significant association between injections and HIV-1 seroconversion in men (p=0·08) and women (p=0·40) (Todd J, London School of Hygiene and Tropical Medicine, personal communication).

Potential reverse causality and residual confounding hamper the interpretation of these results on PAF. Because people with HIV-1 infection are more likely to be sick than those not infected, injections might have been given for the treatment of primary HIV-1 illness or complications of the infection. This notion is confirmed by data from a population-based study in Mwanza, where initially HIV-1-positive adults reported receiving nearly twice as many injections as HIV-1-negative people during 2 years of follow-up (Todd J, personal communication). Injections might also have been given for the treatment of STIs, which are a marker of unprotected sex and an important cofactor for HIV-1 transmission. STIs are, therefore, an important confounding factor that distorts the association between injections and HIV-1 infection. Not all studies have adjusted for STIs and, even if they have, STI episodes are imperfectly measured in retrospective observational studies.27 Even in longitudinal studies, reverse causality is a problem because the intervals between the last seronegative and first seropositive result are usually a year or more.

Furthermore, the PAF is calculated from the prevalence of the risk factor in the population and the relative risk associated with the risk factor. If measurement of the prevalence or the relative risk is inaccurate, the PAF will also be inaccurate. Data on sexual behaviour are notoriously imprecise and tend to be underestimates of true risk.28–30 For example, in one sub-Saharan Africa study,31 23 (2·3%) of 980 women aged 15–24 years who reported never having had sex were infected with HIV-1, but 15 (1·6%) of 958 of these same women were also pregnant. Underestimation of sexual exposure results in an underestimation of the relative risk of the association between risky sexual behaviour and HIV-1 infection and, thus, of the corresponding PAF. Data on the history of injections, on the other hand, are not affected by the same social desirability bias and should, therefore, be more accurate.

Finally, PAFs should be used with great care for epidemic infectious diseases. If they are taken to mean the proportion of infections in the population that occurs because of a risk factor, then the standard PAF calculations will give incorrect results. Infectious disease epidemics are dynamic, so that the proportion of infections in each risk group changes over time as the epidemic develops, and risk is a community effect, so that an increase in risk of infection for one individual increases the risk for all their subsequent contacts. The use of PAFs can be especially misleading for risk behaviour measured over a short time with respect to duration of infection. For example, the risk associated with sexual partners or injections over 1 year is not particularly informative of risk over a much longer period.

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Age and sex patterns of infection

One of the most consistent features of the HIV-1 epidemic in sub-Saharan Africa is its distribution by age and sex.31 We identified six population-based studies32–37 of the prevalence of HIV-1 infection in sub-Saharan Africa that included children. The findings of these studies showed that the prevalence of infection in children aged 5–14 years (an age-range in which they are less likely to have acquired the infection from their mother) was much lower than the prevalence in adolescents and adults aged 15 years or older (table 2, figure 1). If injections were a major mode of transmission, a much smaller discrepancy between HIV-1 prevalence in children and adults would be expected, since there is no evidence to suggest that children receive substantially fewer injections than adolescents and adults.

Table 2. Prevalence of HIV-1, according to age32–37
Figure 1. HIV prevalence by age and sex in Addis Ababa, Ethiopia, 199437

Even the low prevalence in the 5–14-year-old age group cannot be ascribed to unsafe injections because it includes some children infected by mother-to-child transmission, who have long survival times, or by transfusion. One study,36 in Masaka, Uganda, explored the modes of transmission in children. Of ten HIV-1-infected children aged 5–12 years, six had a mother who was infected or who had died from AIDS, one was probably infected through a blood transfusion, one possibly through unsafe injections, and in the remaining two the route of transmission remained unclear. Also, the findings of a study38 of mother-child pairs in Cote d’Ivoire showed that, of 20 infected children aged 15 months or older, 16 had an infected mother and the remainder had received a blood transfusion.

Results of longitudinal studies suggest that seroconversion in uninfected children is rare. In Uganda,39 for example, of 5451 HIV-1-negative infants aged 0–12 years followed-up for 8596 person-years, only one seroconversion occurred (0·12 seroconversions per 1000 person-years), and in Cote d’Ivoire,40 none of the children born to 266 persistently HIV-1-negative mothers seroconverted over a period of up to 48 months.

Another consistent feature of HIV-1 epidemics in Africa is the age and sex distribution in adolescents and adults. Female prevalence climbs during the teens and early twenties and peaks in the late twenties or early thirties, whereas male prevalence follows a similar pattern with a 5–10-year age delay (figure 1). The differences in prevalence between men and women in different age-groups cannot easily be explained by injections, unless wide variations in the frequency of injections by age and sex are assumed.

There are distinct patterns of injections by age and sex. However, they differ from patterns of HIV-1 infection. Several national demographic and health surveys undertaken in sub-Saharan Africa during 1999–2001 have included questions about number of injections in the past 3 months. Data from these surveys show that women receive more injections than men at all ages, with the difference being largest in the early twenties. Differences in the incidence of HIV-1 infection in women and men, however, are greatest at ages before those at which injection differences are large. Figure 2 shows the age patterns of the female-to-male ratio for HIV-1 incidence from two rural community cohort studies41,42 in Uganda and Tanzania, and the incidence of injections (from national demographic and health surveys in Uganda in 2000).43 Sexual transmission is the most likely explanation for the pronounced incidence of HIV-1 infection among women following the years of sexual debut. Thus, a more plausible explanation for the observed patterns is sexual transmission and sexual mixing between different age-groups—eg, young women have sex with older men who are more likely to be infected with HIV-1.

Figure 2. Female-male rate ratio of HIV-1 and injections received by age41–43

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Sex as primary mode of HIV-1 transmission

Figure 3 shows that infection with herpes simplex virus type 2 (HSV-2)—a common STI that often has no signs or symptoms (similar to HIV)—follows a similar pattern in sub-Saharan Africa to that of HIV-1 in the first 10–15 years after individuals reach the age of sexual maturity, lending further support to the notion that HIV-1 is frequently transmitted by sex.44,45 That sub-Saharan Africa has the highest rates of HSV-2 seroprevalence in the world,46 and that Africa has the highest burden of STIs in the world,47 lends biological validity to conclusions about both frequency of sexual transmission of HIV-1 and of risky sexual behaviour in sub-Saharan Africa.

Figure 3. Prevalence of infection with HIV-1 and HSV-2 by age and sex in two African regions44

HIV-1 is effectively transmitted by sex, as shown by high rates of infection among couples.48–50 Furthermore, concordant infections among couples, when examined in the context of a household, allow an examination of the contribution of sexual transmission to total numbers of infections. If injections were a frequent mode of transmission, infections clustered exclusively among adults in a household would be unexpected. Hira and colleagues48 studied 228 families in each of which one adult had HIV-1: of 150 men, 92 (61·3%) had infected wives; of 78 infected women, 57 (73·1%) had infected husbands; of 144 children aged younger than 5 years, 36 (25%) were infected and all had infected mothers; and of 120 children aged 5–10 years, three were infected (mother’s serostatus not reported). Unless there are huge disparities in injection practices between children and adults, only sexual transmission can explain the seroprevalence differences by age. The logical conclusion is that sexual transmission of HIV-1 is responsible for most infections not transmitted from mother to child.

Last, male circumcision has a consistent and significant protective effect against HIV-1 acquisition, with the findings of 21 of 27 studies showing a protective effect and an adjusted summary rate ratio of 0·42 (95% CI 0·34–0·54).51 Rates of HIV-1 in Africa are also inversely correlated with circumcision status.52,53 The findings of one longitudinal study50 showed a startling seroconversion rate of 16·7 per 100 person-years in 137 uncircumcised men compared with 0 of 50 circumcised men. In this study, acquisition of HIV-1 was not affected by an incident STI in the man, in particular, a genital ulcer or syphilis. This finding is important because, although an injection history was not reported, the seroconversions would not have occurred as a result of injections being given for treatment of an STI, as has been argued.3

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South Africa

South Africa provides an example of a country for which the hypothesis that unsafe injections are the primary mode of HIV-1 transmission does not stand. The South African HIV-1 epidemic has reached enormous proportions; prevalence among women attending sentinel surveillance antenatal care clinics reached 26·5% in 2002.54 However, South Africa has the most highly developed health-care system in sub-Saharan Africa and their blood-transfusion system is of developed-world standard.55 Unfortunately, there is no database of injection safety practices within South Africa. However, a year 2000 survey56 of 106 randomly-selected clinics in its neighbouring country, Zimbabwe, also hard-hit by the HIV-1 epidemic, showed safe injection practices in immunisation and, probably, other practice situations. Furthermore, our own personal communication with ten South African health-care authorities in March, 2003, indicated that all believed injection practices had been safe, with possible rare exceptions, since the HIV-1 epidemic began 10 years earlier.

The results of a national survey57 of South African children and adults, which indicated a prevalence rate of HIV-1 infection of 5·6% among 2–14 year-olds, were hence totally unexpected, and led to the charge by Brody and colleagues,58 in multiple writings, that the findings provided ignored evidence of iatrogenic transmission to hundreds of thousands of children. There are, however, questions about the exact validity of the survey findings—many were discussed by the report’s authors, but seemingly ignored by Brody and co-workers. There was, for instance, no increase in prevalence of infection in children by age (making iatrogenic infection an unlikely explanation, even considering deaths at early ages from infections acquired via mother-to-child transmission). Furthermore, the non-response rate in the survey was high because 29% of listed visiting points (mostly households) did not participate nor did 37% of eligible respondents in the remaining households, the test strategy may have been suboptimal, prevalence among children by race is the opposite of what other surveillance and death-registration data indicate, and the HIV-1 pattern by provinces in the survey was inconsistent with surveillance and previous research. Also, there is no evidence that AIDS is nearly as important a cause of mortality among children and teenagers as the survey numbers would suggest.59

Conversely, many sets of data point to unsafe sex as the cause of the epidemic in South Africa.60 For example, the findings of a 1998 survey61 in Carletonville—a community with considerable medical research capabilities and good quality medical care—indicated that the prevalence of HIV-1 among women was greater than 57%. Yet, of 118 children aged 13 and 14 years, none was seropositive. Sexual activity commenced at a later age than this, with a mean age of sexual debut of 15·9 years for men and 16·3 years for women. Consistent with these ages, the acquisition of HIV-1 in men and women began at age 15 years and escalated sharply, with men following women (figure 4). The curve mirrors that noted in a Zimbabwe community.62 Consistent with sexual transmission, acquisition of HIV-1 closely paralleled acquisition of HSV-2.45

Figure 4. HIV-1 infection rates by age and sex in Carletonville, South Africa61

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Reinterpretation of studies published by Gisselquist and colleagues provides no compelling evidence that unsafe injections are a dominant mode of HIV-1 transmission in sub-Saharan Africa. We agree, however, that unsafe injections are an unacceptable practice and that efforts should be increased to reduce exposure of patients to bloodborne infections in health-care settings. At the same time, improved data are needed to identify these risks. We believe that research should focus not just on the formal health-care system (both public and private), but also on the informal health-care system and possibly additional practices—eg, circumcision—where even fewer data are available. Meanwhile, epidemiological evidence indicates that sexual transmission continues to be the major mode of spread of HIV-1 in Africa.


G P Schmid, A Buvé, G P Garnett, G Calleja, R J Hayes, R Heimer, and JT Boerma conceived and designed the report. G P Schmid, A Buvé, PMugyenyi, R J Hayes, P D Ghys, R Heimer, and J T Boerma acquired the data; which was analysed and interpreted by G P Schmid, A Buvé, BGWilliams, R J Hayes, K M De Cock, J A Whitworth, S H Kapiga, CHankins, B Zaba, and J T Boerma. The article was drafted by GPSchmid, A Buvé, G P Garnett, J Calleja, P D Ghys, and J P Boerma, and revised by G P Schmid, A Buvé, P Mugyenyi, B G Williams, R J Hayes, KMDeCock, J A Whitworth, S H Kapiga, P D Ghys, C Hankins, B Zaba, RHeimer, and J T Boerma. G P Schmid and J A Whitworth provided the study materials, and G P Garnett and B G Williams the statistical advice.

Conflict of interest

None declared.

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We thank Maréa Magdalena Guraiib for her support, Judith Glynn and Nicole Seguy for assistance, Quarraisha Abdool Karim for thoughtful comments, and James Todd for permission to use unpublished information.

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24Wawer MJ, Sewankambo NK, Berkley S, et al. Incidence of HIV-1 infection in a rural region of UgandaBMJ 1994; 308: 171-173.

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31Gregson S, Nyamukapa CA, Garnett GP, et al. Sexual mixing patterns and sex-differentials in teenage exposure to HIV infection in rural ZimbabweLancet 2002; 359: 1896-1903. Abstract | Full Text | Full-Text PDF (149 KB) | MEDLINE | CrossRef

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39Mulder DW, Nunn A, Kamali A, Kengeya-Kayondo JF. Post-natal incidence of HIV-I infection among children in a rural Ugandan population: no evidence for transmission other than mother to childTrop Med Int Health 1996; 1: 81-85. MEDLINE

40Ekpini ER, Wiktor SZ, Satten GA, et al. Late postnatal mother-to-child transmission of HIV-1 in Abidjan, Cote d’IvoireLancet 1997; 349: 1054-1059. Abstract | Full Text | Full-Text PDF (56 KB) | MEDLINE | CrossRef

41Mbulaiteye SM, Mahe C, Whitworth JA, et al. Declining HIV-1 incidence and associated prevalence over 10 years in a rural population in south-west Uganda: a cohort studyLancet 2002; 360: 41-46. Abstract | Full Text | Full-Text PDF (102 KB) | MEDLINE | CrossRef

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48Hira SK, Nkowane BM, Kamanga J, et al. Epidemiology of human immunodeficiency virus in families in Lusaka, ZambiaJ Acquir Immune Defic Syndr 1990; 3: 83-86.

49Mann JM, Quinn TC, Francis H, et al. Prevalence of HTLV-III/LAV in household contacts of patients with confirmed AIDS and controls in Kinshasa, ZaireJAMA 1986; 256: 721-724. MEDLINE

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51Weiss HA, Quigley MA, Hayes RJ. Male circumcision and risk of HIV infection in sub-Saharan Africa: a systematic review and meta-analysisAIDS 2000; 14: 2361-2370. MEDLINE | CrossRef

52Bongaarts J, Reining P, Way P, Conant F. The relationship between male circumcision and HIV infection in African populationsAIDS 1989; 3: 373-377. MEDLINE

53Moses S, Bradley JE, Nagelkerke NJ, Ronald AR, Ndinya-Achola JO, Plummer FA. Geographical patterns of male circumcision practicesin Africa: association with HIV seroprevalenceInt J Epidemiol 1990; 19: 693-697. MEDLINE

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Affiliationsa. WHO, Geneva, Switzerland
b. Institute of Tropical Medicine, Antwerp, Belgium
c. Joint Clinical Research Centre, Kampala, Uganda
d. Imperial College, London, UK
e. London School of Hygiene and Tropical Medicine, London
f. Centers for Disease Control and Prevention, Atlanta, GA, USA
g. Harvard School of Public Health, Boston, MA
h. United Nations Joint Programme on AIDS (UNAIDS), Geneva
i. Yale School of Medicine, New Haven, CT

Corresponding Author InformationCorrespondence to: Dr George Schmid, Department of HIV/AIDS, WHO, 1211 Geneva 27, Switzerland

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Shocking: HIV, Contraception and Abortion and Africa – a Hidden Connection?

: January 28, 2008

By Ruben ObregonFor the past few days I’ve been reading “Population Control: Real Costs, Illusory Benefits,” a forthcoming book by Population Research Institute’s Steven Mosher.

What I found out in the section on AIDS in Africa stunned me.

In this chapter, Mosher details how the United States Agency for International Development (USAID) decided to integrate HIV/AIDS programs into existing family planning programs in Africa – with disastrous results.

Mosher attributes the reuse of dirty needles, including those used to inject Depo-Provera, for many of Africa’s HIV infections. He also suggests that Norplant implantation and abortion by manual vacuum aspirator (MVA) may also put African women at risk.

The problem is that in many areas, needles and MVAs cannot be properly disinfected prior to being used again. (You read that correctly – needles are reused!) Additionally, local blood supplies are unsafe, and are often used as a last resort – often resulting in only a delayed death.

Mosher points out that David Gisselquist, Stephen Potterat, and their research team found that “two thirds of HIV/AIDS in Africa results from injections with infected needles or other medical exposures to infected blood.”

In reviewing 22 separate studies in 2003, Gisselquist and Potterat found that:

• Injection was more associated with HIV than heterosexual sex.
• Most of those infected were in monogamous relationships
• Those who are more well off have higher rates of HIV, which is the opposite of typical STD patterns
• Clinic attendance was associated with HIV
• Infants also had high rates of non-mother to child transmission

They also found that sex related HIV cases only accounted for 25 to 35 percent of infections.

Mosher blames the situation on USAID’s AIDS/SRH (sexual and reproductive health) approach.

“The reason why the integrated AIDS/SRH approach hasn’t slowed the spread of HIV in Africa is because most HIV/AIDS cases on that continent are not the result of sexual contact at all. Rather they are the result of contact with HIV through dirty needles and other substandard, invasive medical procedures. More to the point, they are the result of the kinds things – Depo-Provera and other injections, Norplant insertions, IUD implantations, tubal ligations, and Manual Vacuum Aspirators (MVA) abortions – that are done to women at integrated AIDS/SRH clinics.”

Recently, efforts have been made to stop transmission by needle reuse, but it’s a bit too late for those who have already died or were infected.I find this information to be shocking, and I’m still wondering why we are funding family planning programs overseas to begin with? It seems like we have done more harm than anything.

For further reading:

Population Research Institute – Are Africans Promiscuous Unto Death?

WHO accused of huge HIV blunder

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Posted by Ruben at January 28, 2008 2:39 PM

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Biofuels: Africa’s new oil?

Biofuel: Africa’s new oil?

*Biodiesel can be produced from oil crops like rapeseed

Kimani Chege
5 December 2007
Source: SciDev.Net

Biofuel holds great promise for Africa but the research isn’t yet in place to reap the rewards, or analyse the pitfalls, reports Kimani Chege.

It is only ten o’clock in the morning and Kenyan taxi-van driver Richard Kamiri is already tired. Throughout the morning he has had to explain to his passengers the reason he has repeatedly hiked the fare. In just a week, crude oil prices have risen twice — with the people bearing the costs.

This scenario is increasingly common in energy-constrained Africa. Over-reliance on fossil fuels has long drained national budgets. Fuel prices are rising by the day and with little control over internationally determined prices, governments are seeking alternatives to meet the fuel needs of a rising urban population.

African governments are increasingly looking to biofuel as a viable way to do this.

Africa’s ‘oil fields’

According to Njeri Wamukonya, an energy expert with the UN Environment Programme, worldwide investment in bioenergy reached US$21 billion last year.

“Governments in developed and developing countries are putting in place bioenergy targets, with the main drivers being the energy security, climate change and development concerns,” says Wamukonya. The European Union, for example, has announced that it targets its member states to generate at least ten per cent of their energy from biofuels by 2020.

This increased demand for biofuel provides a market opportunity for the South, with its available natural resources. For instance, Brazil was producing 33 per cent of the world’s biofuel ethanol by the end of last year.

African countries are keen on transforming their expansive farmlands into the next ‘oil fields’.

The choices of crop are diverse — from corn to rapeseed and jatropha. Liquid biofuels include biodiesel derived from plant oils and bioethanol made from sugarcane, maize and other starchy crops. Global production of biofuels consists primarily of ethanol.

According to Cornelis van der Waal, an industry analyst with Frost & Sullivan — a South Africa-based consultation company providing advice on development policies — Africa has great biofuel potential due to its vast arable land and workforce.

He says, “Africa is by no means a current participant in the biofuels race compared to the rest of the world, but could potentially become the most important contributor to alternative fuels.”

“The question is not so much on whether Africa is ready for a biofuel revolution, but rather can Africa afford to miss the biofuels opportunity?”

Lagging behind in the biofuel race

A pan-African ministerial meeting held in March this year in Maputo, Mozambique marked a turning point. African ministers responsible for energy development in their countries announced a declaration committing to increased research in the development of renewable energy — notably biofuels. This has made many investors take a keen interest in the production of biofuels in Africa.

However, energy analysts say that investment in Africa has failed to take note of basic research needed. Despite well-established national agricultural research centres across Africa, there is little research to improve crops to yield more ethanol and biodiesel.

Van der Waal says that many African countries investigating biofuels, such as Kenya and Mozambique, do not currently have a large enough capacity for biofuels research.

He adds that biofuels research in Africa is inadequately funded, with most of it coming from governments and conducted in universities.

According to van der Waal, African countries should follow Brazil’s lead, where both the government and the private sector conduct research, sustaining an ethanol industry for more than 20 years. He says one of the continent’s strong points is its capacity to combine government and private research on biofuels, something it is not yet taking advantage of.

Current biofuels research also focuses too much on increased production efficiency rather than quality products, he says, adding that there are opportunities for many other biofuel products and applications besides ethanol and biodiesel. For instance, home-use fuel, such as paraffin, wood and coal, could be replaced by ethanol gel, made by mixing ethanol with a thickening agent and water. The gel fuel burns without smoke, and so does not cause respiratory problems associated with current fuels used in the home.

Catching up

Several African countries have biofuel research projects underway.

Nigeria, the world largest producer of cassava, is keen to use its major crop as an alternative to fossil fuel. The country currently uses a ten per cent blending standard of cassava ethanol with gasoline, though this is not compulsory.

Nigeria aims to produce cassava ethanol worth over US$150 million every year, once it establishes a suitable infrastructure. This includes construction of 15 ethanol plants with assistance from Brazil.

Nigeria aims to produce large
amounts of cassava ethanol
Credit: Flickr / My Little Photo

And in May, the government announced plans to establish a US$100 million ‘biofuel town’ near the capital, Lagos. This will create a 600 hectare settlement of 1,000 bioenergy experts — primarily from Nigeria, but also from other African countries and Brazil — who will work on novel technologies to improve bioenergy production.

Nigeria also aims to start importing Brazilian ethanol-powered vehicles by 2010.

This ambition is mirrored by Malawi. In October, the Ethanol Company of Malawi, a private fuel company, announced that it will import flex-fuel vehicles from Brazil to be used in a government-backed initiative to investigate the practicability of using ethanol-based fuels to power vehicles (see Malawi endorses ethanol-fuelled cars).

Malawi currently uses gasoline blended with ten per cent locally-made sugarcane ethanol. Through a public-private venture, the Malawi department of science and technology is implementing a research project to explore how local biofuels could alleviate the country’s energy needs. The highlight of research so far is the testing of a Mitsubishi Pajero car modified to run on ethanol in place of petrol for a distance of 1,000 kilometres.

The Brazilian influence is also apparent in neighbouring Mozambique, which shares a connection with Brazil as another former Portuguese colony. The southern African country has developed an effective biofuel sector based on sorghum and sugarcane, and the government has set aside over US$700 million for biofuel research, production and promotion.

Energy experts say Mozambique has potential to be a ‘biofuel superpower’. Van der Waal says the country has sufficient rainfall for extensive production of sugarcane, which is currently the most efficient crop for ethanol in terms of production cost, being much faster to process and producing more sugar (thanks to its water content) than maize or sorghum.

Scientists from the International Crops Research Institute for the Semi-Arid Tropics (ICRISAT) are developing sorghum varieties and hybrids that have higher amount of sugar-rich juice in their stalks for Mozambique.

ICRISAT is also working with a private Mozambican company, Rusni Distilleries Ltd, to establish a facility capable of producing 100,000 litres of sorghum ethanol a year. The venture has received a total investment of around US$30 million from Rusni, ICRISAT, and the Mozambique government, and, if successful, could boost the livelihood of 5,000 smallholder farmers through contract farming. ICRISAT and Rusni plan to collaborate with Petromoc, the national petroleum company of Mozambique to market the fuel.

Many African countries already
add ethanol to their gasoline
Credit: Flickr / sroemerm

Assessing the risk

Increased attention on biofuel research and development is, however, bringing a new debate to the continent. There is the worry that an increase in the use of food crops such as maize, cassava and sorghum is likely to increase the food price of most staple foods in Africa, notably corn.

“Price rise will depend on whether or not oil crops are planted on arable land that could otherwise be used for growing food crops, and whether water is diverted from food crops to irrigate the biofuel plantations,” says Jeremy Wakeford, a senior lecturer in economics at the University of Cape Town in South Africa.

The debate of crops for food versus crops for biofuels remains one of the major problems yet to be resolved in the sector. And it may affect Africa even if the continent does not enter the biofuels market.

Njeri Wamukoya says increasing biofuel development is likely to affect food aid. The United States for example, provides food aid from its surplus crops. “[But] if the surplus is used for [US] biofuels, will the United States supplement [food aid] with cash, and will the cost of food go up as a result?”

Wakeford says producing food for the population should be given priority, and suggests that new developments from research programmes will keep the biofuel sector going.

There is a need to diversify the sources and methods used to generate biofuel products, according to Mpoko Bokanga, director general of the African Agricultural Technology Foundation, which promotes technology transfer in Africa.

Addressing an African conference on biofuels in Addis Ababa, Ethiopia, in August, Bokanga said one possibility is to move from ethanol to butanol fuel production.

Butanol fuel can be manufactured from corn and molasses, has a high energy content and can be shipped through existing fuel pipelines. It is also safer to use than ethanol and gasoline, as it is less likely to evaporate into the surrounding air (which creates a fire risk). However, there has been little to no effort to promote butanol fuel because of historically low production yields compared to ethanol.

Bokanga also called for the establishment of ‘bioenergy scientific units’ in African countries conducting biofuels research, with experts available to advise governments on improving production efficiency.

The triple challenge facing Africa is achieving food security, energy security and sustainable development. Biofuels provides an opportunity to harness Africa’s vast biomass resources, but for that more research on better yielding crops, production methods, and use is needed. The journey has only just begun.

Related SciDev.Net articles:
UN head calls for more biofuels research
Biofuels: benefits and risks for developing countries

Related links:
International Crops Research Institute for the Semi-Arid Tropics

Photo Credit: Flickr/Neil’s Photo Album

Climate Change
Research and Development

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Stop AIDS Genocide By the Drug Cartel!

Call to the People and Governments of the World
Stop AIDS Genocide
By the Drug Cartel!

Matthias Rath, M.D.

Dr. Rath is the world-renowned scientist and physician who led the scientific breakthrough for the natural control of cardiovascular disease, cancer, immune deficiencies and other common health problems.

He identified the common cellular mechanisms behind the spread of cancer and viral diseases in the human body and natural ways to block them. His Research Institute of Cellular Medicine is a world leader in sciencebased, natural health approaches. His discoveries have been scientifically and clinically proven and published in leading scientific journals.

Dr. Rath was the first who identified the pharmaceutical ‘business with disease’ as the biggest obstacle for the control and eradication of today’s diseases and for effective and sustainable health care. Over the past years, his worldwide public health education campaigns, including the New York Times and other leading newspapers, have unmasked the pharmaceutical industry as an investment business dependent on the continuation and promotion of diseases. Dr. Rath and his Research Institute have also developed economic alternatives to the pharmaceutical ‘business with disease’.

“In contrast to the pharmaceutical industry, we offer our research findings and scientific expertise to the governments of the world free of charge for the benefit of their people.

We encourage governments and research institutions around the world to contact us immediately via our website in order to save millions of lives.”

Cape Town, May 2005

The HIV/AIDS epidemic has become one of the greatest threats to mankind ever. The African continent is hardest hit. According to the UN, 22 million Africans have already died from AIDS and every new day takes the lives of 6000 more African men, women and children.

This human tragedy has become a multi-billion dollar market for the pharmaceutical investment business – the drug cartel – in which the return on investment is based on the continuation of the AIDS epidemic. To maintain their global market with patented AIDS drugs, the pharmaceutical drug cartel promotes so-called anti-retroviral (ARV drugs) to combat immune deficiencies. These ARV drugs severely damage all cells in the body – including white blood cells – thereby not improving but rather worsening immune deficiencies and expanding the AIDS epidemic.

In February last year, the Vatican accused the ‘pharmaceutical cartel’ of committing genocide in Africa in the name of its multi-billion dollar profits with patented AIDS drugs.

The time has come to stop these crimes against humanity and to present to the people of Africa and the world the effective, safe and affordable solution to the AIDS epidemic. Progress in natural health now offers this opportunity.

Micronutrients Can Reverse the Course
In Khayelitsha, a township of Cape Town, South Africa, we conducted a clinical pilot study in HIVpositive patients with advanced AIDS who had never taken any ARV drugs. The goal of the study was to show that a combination of micronutrients can reverse the course of AIDS, even in its advanced stage.

This nutrient combination consisted of specific vitamins, amino acids, minerals and polyphenol extracts from green tea. The list of micronutrients in this program and details of the study are available on this Website.

Blood tests and clinical evaluations were performed at the start and after 4 weeks on the nutrient program. Already after the first month of this study, the clinical and blood test results were profound. Patients with the most severe stages of AIDS had the highest improvements of immune function. We decided to publish the key findings without delay for the benefit of all mankind.

In support of these findings, a July 2004 the New York Times had already reported about a study in pregnant women with AIDS in Tanzania, published in the July 1 issue of the New England Journal of Medicine. This 6-year study documented that multivitamins can delay the onset of AIDs by 50%.

No previously tested vitamins or ARV drugs have been able to show the reversal of clinical symptoms of AIDS as documented here. Moreover, in this study all known immune system markers – not only CD4 counts – significantly improved within the short period of only 4 weeks!

The scientific responsibility of these results is shared by Alexandra Niedzwiecki, Ph.D. (Dr. Rath Research Institute, USA), David Rasnick, Ph.D. (Dr. Rath Health Foundation, South Africa), Sam Mhlongo, M.D. (Head of Family Medicine, Medical University of Southern Africa, MEDUNSA, South Africa) and Matthias Rath, M.D.

AIDS-Related Skin Ulcer Reversed
Zola (20) is just one example for the clinical improvements seen in this study. Last year, when she experienced symptoms of weight loss, night sweating and coughing she consulted a clinic and was diagnosed with tuberculosis (TB) and tested HIV positive.

She was advised that after finishing her TB treatment, she should start taking antiretroviral (ARV) treatment but she objected because of the side-effects of ARV treatment. By that time she had developed symptoms of full-blown AIDS, including a deep neck ulcer that would not heal and eventually develop a severe infection (see picture A below). She also had pain in her legs and other parts of her body.

Soon after she started the nutrient program, the pains in her body stopped and she gained weight. The infected wound began to heal and after one month had almost completely disappeared (see picture B below).

South Africa Leads Global Health Liberation
from the Drug Cartel
Through the AIDS epidemic the drug cartel has turned South Africa and the African continent into a battleground to force its multi-billion dollar drug business upon the entire developing world. The people and the government of South Africa have taken on this fight by basing its health care system on effective and affordable natural health solutions. The scientific foundation for this health approach is documented in every textbook of biology and biochemistry: vitamins and other micronutrients are essential cofactors for optimum metabolism of millions of cells in our body – including the cells responsible for effective immune defense.

By doing so the South African government is tearing down the artificial wall built in the interest of the drug cartel between biological science and pharma-oriented medicine. Withholding life-saving information about effective natural health and keeping the people of the world ‘health illiterate’ has been the basis for the multibillion dollar global investment business with patented synthetic drugs. In this war between natural health and the ‘business with disease’ of the drug cartel there can be only one winner. The control of the AIDS epidemic through natural means, which is now in sight, will inevitably terminate the unscrupulous multi-billion dollar drug business with the AIDS epidemic. In this battle for its survival the drug cartel and its political stakeholders are currently mounting their ‘last offensive’ on Africa.

The control of the HIV/AIDS epidemic through vitamins and other micronutrients inevitably terminates the multi-billion dollar business with patented AIDS drugs. The natural control of the AIDS epidemic destroys not only the marketplace for the drug industry but its entire credibility. The drug cartel is being unmasked as an organization preventing natural, non-patentable health solutions in order to protect their global markets with dangerous, patented drugs and sacrificing the lives of people in genocidal proportions. The people and the government of South Africa are leading the global struggle for the liberation of human health from the drug cartel.

In this battle, no one can stay impartial. A victory for the people of Africa is a victory for the people of the world, liberating mankind from the yoke of the pharmaceutical cartel forever. Here is how you can help:

Further educate yourself on our web site and share this information with everyone you know!
Urge your government to stop abusing your tax money to promote the drug cartel’s business across Africa!
Demand the redistribution of funds to fight hunger and promote natural health solutions worldwide!
Send a message of support for the South African government to continue its leadership for health freedom!
Support South Africa in Its Struggle to Save Millions of Lives!
Send a message of support for the South African government to continue its leadership for health freedom!
Mail: Private Bag X1000, PRETORIA, 0001
Fax: (012) 323 8246

Mail: Private Bag X1000, CAPE TOWN, 8000
Fax: (021) 462 2838

The Dr. Rath Health Foundation is a non-profit organization dedicated to the promotion of natural health through research and education worldwide. This public health information has been made possible by contributions from thousands of people worldwide who have been helped by natural health. We are looking for people like You to join us in our mission to liberate human health from the drug cartel and achieve “Health for All by the Year 2020.”

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The Pharmaceutical Drug Cartel Launches World War III

The Pharmaceutical Drug Cartel
Launches World War III To Prevent
the Construction of a Healthy World

Never before in the history of mankind was a greater crime committed than the genocide organized by the pharmaceutical drug cartel in the interest of the multibillion-dollar investment business with disease. Hundreds of millions of people have died unnecessarily from AIDS, cancer, heart disease and other preventable diseases and the only reason that these epidemics are still haunting mankind is that they are the multibillion-dollar marketplace for the pharmaceutical drug cartel.

Never before in history was there a larger, more profitable and bloodier fraud than that perpetrated by the pharmaceutical drug cartel. Over almost a century it has built a global monopoly in health care based on fraud: the drug industry promises health to millions of people yet the entire industry depends on the continuation and expansion of diseases as the market places for their patented drugs.

Never before were the accomplices to this global drug-genocide more desperate about hiding this fraud and their crimes against humanity. They were never more anxious to prevent the collapse of this unscrupulous investment industry and the extinction of their fraud business with losses amounting to thousands of billions of dollars.

Never befor e were the financial groups behind the drug cartel, namely the Rockefeller and J.P. Morgan investment groups and their political puppets in the White House and 10 Downing Street, more worried that they will be held responsible in national and international courts for their crimes against humanity.

Never before were the profiteers of this global genocide and their political stakeholders in the US, UK and other countries forced to spend more money in order to prevent the imminent collapse of the global empire of the drug cartel.

Never before were the drug cartel and its stakeholders in medicine, the media and their storm troopers in the streets more eager to silence those who expose this global fraud and genocide. That is the background of the attacks against the Dr. Rath Health Foundation, against traditional medicine and against the government of South Africa.
Now, we, the people, must build a world without diseases!
All these actions by the drug cartel are not a sign of their strength but of their desperation. They are a reaction to a scientific breakthrough that will inevitably liberate mankind from the yoke of the drug cartel.

Now we, the people, have a chance to liberate ourselves from the deadly yoke of the drug cartel and replace it with a health care system based on effective, safe, non-patentable and affordable natural therapies.

Now we, the people, have a chance to build a world without diseases. This is possible by taking advantage of the scientific breakthrough in natural health which gives us all the chance to control the epidemics of AIDS, cancer, cardiovascular disease and other preventable disease.

Now we, the people, have a chance to implement the knowledge about the life-saving benefits of vitamins and other micronutrientsinto health care policies around the world, which will be the first step towards effective control of today’s most common diseases.

Now, the governments of the world have a chance too to implement these advances in natural health into public health policies as effective and affordable ways to improve the health of the people.

Today, the people of the world can accomplish the goal of building a world without diseases! The scientific understanding of the nature of today’s most common diseases and their natural remedies are available anywhere in the world. The eradication of today’s most common diseases is dependent on one factor only, how fast can we, the people of the world, spread this life-saving information worldwide.

The biggest obstacle to building a world without diseases is the pharmaceutical drug cartel which set out to block this information at all costs and at the risk of its own demise. It is for this reason that the drug cartel has broken cover and is fighting an open and all out war against the liberation of human health.

The Drug Cartel and Its Media Have Launched World War III to Try to Block the Realization of the Next Goal Uniting All Mankind: A World Without Disease
The year 2005 marks the 60th anniversary of the end of the Second World War and the victory over Nazi Germany. It also marks the beginning of the Third World War, a global misinformation war led by the multi-billion dollar pharmaceutical investment business with disease against all mankind.

The liberation of mankind from the yoke of the pharmaceutical cartel and the termination of the drug cartel genocide is a true world war affecting the life of each and every person on this planet, as well as the lives of generations to come.

For almost a century, the pharmaceutical investment business has led a silent war against the people of the world and built a global monopoly on drug-related health. It has gradually and silently infiltrated key parts of society including the media, medicine and politics. From this position of institutionalized power it has silently built its global monopoly based on patented drugs and has virtually outlawed all effective natural health approaches because they are not patentable. Hundreds of millions of people have paid the price of this global tyranny of the drug cartel with their lives.

But on May 6, 2005, the silence imposed by the drug cartel on its genocide was broken. The Dr. Rath Health Foundation published a “Call to the People and Governments of the World: Stop the AIDS Genocide of the Drug Cartel” in the New York Times, one of the world’s most influential newspapers. By announcing the advantage of natural means in controlling the AIDS epidemic, the Foundation uncovered the basis of the business with disease responsible for deaths in genocidal proportions. For the first time, the astonished world community learned that the drug cartel and its political stakeholders are leading a secret ‘War on Africa.’

This ‘War on Africa’ is, however, not limited to that continent. It is a war by the drug cartel against all mankind. Not surprisingly, this war is being led by the governments of the two largest drug export nations – the US and the UK – in order to subjugate the people of the world to its merciless grip. And not surprisingly either, the first target in this war is South Africa, a country that has become a world leader in health liberation by promoting natural health care solutions.

The drug cartel knows that its global survival is dependent on cementing its health monopoly in the developing world. The first battleground of the drug cartel’s strategy has become South Africa and the battle around the AIDS epidemic. The drug cartel’s first victory would be to force the South African government to abandon natural health solutions to fight AIDS and instead force it to distribute toxic AIDS drugs to millions of South Africans. Consequently, on May 8, two days after the New York Times publication, they mounted a frontal attack on the South African government.
We, the People of the World, Will Win this War in Order to Achieve Our Goal: A World Without Disease
The investment business with disease of the drug cartel has cost the lives of hundreds of millions of people, more than all the wars of mankind combined. If the people of the world do not act now, diseases like AIDS, cancer and cardiovascular disease which are killing four out of five people today, will continue for generations to come. Only if we, the people of the world, act now will we be able to liberate ourselves from the yoke of the drug cartel. The hidden World War III, the global war between the drug cartel and the people of the world, is well defined:

The purpose of World War III is the liberation of the people of the world from the unscrupulous yoke of the drug cartel and for the right to rid itself from Aids, cancer and other diseases.

The responsibility for World War III has been forced upon the people of the world by the drug cartel that has kept the health of the people of the world hostage for more than a century. The drug cartel has denied the people of the world the right to make their own health decisions and liberate themselves from today’s most common diseases.

The participants of World War III fall into two camps: on one side are the financial interests of a small group of investors behind the drug cartel – namely the Rockefeller and J.P. Morgan investment groups. On the other side are the health interests of the 6 billion people alive today and of all future generations to come. In this war there can be no compromise. If the drug cartel prevails, today’s common diseases will continue and hundreds of millions more people will pay the price with their lives. If the people prevail, the drug cartel’s investment business with disease will be terminated, opening up the way for the control and elimination of many of today’s common diseases.

What triggered World War III? The war of the drug cartel against the health of the people of the world has been going on silently for decades. But it was the unmasking of the genocide committed by the drug cartel in connection with the AIDS epidemic in Africa that has brought this war into the open. From the New York Times and other leading newspapers around the world, the information that the AIDS epidemic is an immune deficiency that can be controlled by vitamins and other natural means has reached the four corners of the world. This was the call to the people of the world to liberate themselves not only from the ‘business with AIDS’ but from the ‘business with disease’ in general.

The historic parallel of the beginning of World War III. It was on May 8, 2005, precisely the 60th anniversary of the end of the Second World War that the drug cartel launched its unprecedented attack on natural health and the South African government as the political leaders of this liberation of human health worldwide.

The differences between the previous World Wars and World War III. World War I and II were wars between rich countries fighting for the conquest of the world and its resources, including continued exploitation of the people and the natural resources of their colonies in the developing world. The key interest groups behind these wars were the petrochemical and pharmaceutical industries, which, amongst others, also financed the rise of Hitler in Nazi Germany. World War III is fundamentally different from the previous wars. It is a war between the health interests of the 6 billion people all over the world and the financial greed of a handful of drug cartel shareholders.

The decisive role of the developing world. The more than 4 billion people living in the developing world are the first victims of the drug cartel. The AIDS epidemic in Africa costs the lives of more than 6000 people every day, more than twice the number that died on September 11, 2001 in the World Trade Center. It is a scientific fact that the great majority of these lives could be saved by effective, safe and affordable natural means. Implementing this knowledge into health care policies in the developing world alone would save tens of millions of lives, billions in wasted health care costs and would decrease the dependency of the developing world upon the rich nations.

The role of South Africa. Together with a few other developing nations, South Africa has become a leader in the liberation of mankind from the business with disease. By taking up the fight against strangulating patents fees, the South African government has already taken the first step in the liberation of mankind from the yoke of the drug cartel. The second and even more important step is replacing a health care system based on mostly ineffective and toxic pharmaceutical drugs with a health care system based on effective safe and affordable natural health approaches.

The ‘weapons’ of World War III. World War I and II were fought with military force. In contrast, World War III is a war of information and education. On the one side are millions of people throughout the world whose role in this war is to learn and disseminate the factual, life-saving information about the benefits of vitamins and other natural health approaches for the control, prevention and eradication of diseases. On the other side are the forces of the drug cartel that – through its influence in the world media – has launched an information campaign of unprecedented proportions to discredit the scientific truth and to attack those who have become pioneers in spreading this breakthrough.

The possible escalation of World War III. It is not unlikely that, in their desperation and facing defeat during World War III, the drug cartel and its political stakeholders (primarily in the US and UK) will resort to the escalation of international crises – even starting a war against North Korea, Iran or any other country that lies in their interests. Such a terrible event would immediately draw world media attention away from the collapse of the drug cartel and allow the establishment of a dictatorship on behalf of corporate interests; the use of martial laws to protect the drug cartel’s global interests by military force; the abandonment of civil rights and the prosecution of those who fight for the liberation of natural health.

But even this last desperate step will not help the drug cartel to survive. Anticipating this escalation and by publicly talking about this threat we, the people of the world, will destroy the possibility for our opponent to resort to this last desperate move and to escalate WWIII into a military conflict.

The duration of WWIII. World War I and II lasted several years. The people of the world and their commitment to health will determine how long it will take to win World War III. The people of the world have to realize that we carry the strongest weapon in this war – the truth. The drug cartel can only continue its rule by brutally suppressing the facts about natural health and the global health liberation movement. And we have already had many victories in this war: the fact that the course of AIDS could be reversed by vitamins and essential nutrients – without the use of ARV drugs – is now known all over the world. The ingredients to fight the global AIDS epidemic are available to any government anywhere in the world, right now. Preventing the governments of Africa, South America and Asia from incorporating natural health approaches into their health care policies is no longer possible. The largest amount of bribery and even force can no longer stop the course of history and the liberation of mankind from the drug cartel. And this is just the beginning. The natural control of cancer and cardiovascular disease is also in sight.

Why WWIII will be the last world war. World War I and II were fought on behalf of economic interests promoting disease, death, exploitation and social injustice. World War III will not only liberate mankind from diseases, but also from the economic interests and profiteers that have subjected this planet for more than a century to their tyranny and in their insatiable corporate greed were the driving force behind the two previous World Wars. By exposing these economic interests to the world, we make sure that World War III will be the last world war mankind has to fight.

The winners of WWIII. The outcome of World War III is already clear. No economic or even military force can any longer prevent the liberation of mankind from diseases and from the business with disease. From now on all mankind is united by one goal: a world without diseases, a world of peace, health and social justice.

On this day, May 13, 2005, from Cape Town South Africa, we call upon the people of the world to join us in the largest liberation movement of all time: the liberation of human health.

We call upon you: Join us! The time to act is now!

Dr. Matthias Rath

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