Reactivity on tests for HIV in sub-Saharan Africa not explained by sexual or vertical transmission.

Recently, researchers from Emory University in Atlanta and from Albert Einstein College of Medicine in New York City, after a comprehensive review concluded: “An expanding body of evidence challenges the conventional hypothesis that sexual transmission is responsible for more than 90% of adult HIV infections in Africa. Differences in epidemic trajectories across Africa do not correspond to differences in sexual behavior. Studies among African couples find low rates of heterosexual transmission, as in developed countries. Many studies report HIV infections in African adults with no sexual exposure to HIV and in children with HIV-negative mothers. Unexplained high rates of HIV incidence have been observed in African women during antenatal and postpartum periods” (138).

Researchers state: “By the end of the 1980s, a consensus emerged among AIDS experts dealing with Africa that over 90% of adult HIV infections in sub-Saharan Africa were acquired through heterosexual contact and less than 2% through unsafe injections [139-142]. Unfortunately, this consensus was achieved without research to address confound between sexual and medical exposures” (138).

The very similar frequency of AIDS in both genders in Africa has been blamed by HIV/AIDS researchers and institutions on sexual promiscuity. However, in one model “Anderson and colleagues assumed a mean rate of annual partner change of 3.5 [143]. In contrast, surveys in 12 African countries show unweighted averages of 74% of men and 91% of women aged 15-49 years with no non-regular sex partners in the past year, and only 3.7% of men and 0.7% of women with more than four non-regular partners [144]” (138).

Empiric data show that promiscuity is, rather, a matter in developed countries: “A survey in Denmark found that 19% of adults aged 18-59 years reported more than one sex partner in the past year [145]; a survey in France found 17% of men and 7.9% of women aged 18-44 years reported more than one sex partner in the past year [146]; and a survey in the UK found that 17% of men and 8.4% of women aged 16-44 years reported more than one sex partner in the past year [147]” (138). Despite this, the frequency of AIDS in developed countries is about 11 men to 1 woman.

“A Zambian study that sequenced viruses to determine epidemiological linkage reported at least 13% of sequences in newly infected persons were not related to their partner’s HIV[148]” (138).

“A study in Zimbabwe in the 1990s found 2.1% HIV prevalence among 933 women with no sexual experience [149]. In a 1988 study of discordant couples in Rwanda, 15 of 25 HIV-positive women with HIV-negative partners reported only one lifetime sex partner [150]. In a 1990 study of teenagers in Uganda, 6.9% of women with no sex partners in the last five years were HIV-positive vs 23% for those with one or more partners; for men, 1% with no partners in the last five years were HIV-positive vs 2.5% of those reporting partners [151]. Among young adults 15-24 years old in Tanzania, a 1995 study found HIV prevalence of 5.6% among men and 3.6% among women who did not report any lifetime sexual activity vs 4.8% and 12% for men and women reporting one or more sexual partners [152]. In a 1999 study in South Africa, 6.8% of women and 1.2% of men 14-24 years old reported never having sex were HIV positive; however, a validation study found some under-reporting of sexual activity [153]. In a case-control study in Uganda, in two of seven cases with only one lifetime sexual partner, the partner was HIV-negative, three were HIV-positive, and two others not tested [154]” (138).

About a fifth of HIV-positive children in Africa have HIV-negative mothers: “A study in Kinshasha in 1985 found 39% (16 of 44) of HIV-positive inpatient and outpatient children 1-24 months old to have HIV-negative mothers; only five of 16 had been transfused [155]. A study in Rwanda in 1984-86 found 20% (15 of 76) of children 1-48 months old with AIDS or AIDS related complex had HIV-negative mothers; only 15 children had been transfused [156]. In a later report from Rwanda, 7.3% (54 of 704) of mothers of children with AIDS were HIV-negative; transfusions were identified as a risk factor for 22 of the 54 children [157]. Of 26 children less than 15 years old admitted to Uganda Cancer institute with Kaposi’s sarcoma during 1989-94 for which the mother was tested for HIV, 19% (5 of 26) had HIV-negative mothers [158]. A study in Burkina Faso in 1989-90 found 23% (11 0f 48) of HIV-positive children to have HIV-negative mothers [159]. In a 1994 report from Cote d’Ivoire, De Cock and colleagues report that 21% (3 of 14) of children with HIV-1 had mothers without HIV-1, and one of two with HIV-2 had a mother without HIV-2 [160]” (138).

“HIV incidence during antenatal and/or post-partum periods exceeded what could be expected solely from sexual transmission” (138,161-171). “In one of the seven studies of antenatal and post-partum women [171], 30 of 634 women had HIV positive partners; three of these 30 women seroconverted in a year” (138,171). “HIV prevalence in African men is generally lower than in women, and many infected men are partnered with infected women. In eight studies of African couples with HIV in one or both partners [150,172-178], the average percent of women with HIV was more than double the percent without HIV who had HIV-positive partners” (138). The high prevalence of HIV reactivity in women during antenatal or post-partum periods “suggests that something more than simply heterosexual transmission is involved” (138). “Whatever happens during one or two pregnancies and post-partum periods – whether iatrogenic or sexual or something else – may largely account for observed high levels of HIV among low risk women in at least some African communities” (138).

“The recognition that significant proportions of HIV in African adults and children cannot be explained on the basis of current knowledge about sexual and vertical transmission” allowed the researchers from Emory University and Albert Einstein College of Medicine to postulate a hypothesis of “iatrogenic transmission” through medical instruments such as syringes and injections (138).

At this point it is important to remember that there are several publications seriously criticizing the accuracy of tests currently used to diagnose HIV infection (179-184).

Long ago, HIV researchers were aware of the lack of specificity of the HIV antibody tests, especially in countries in Africa where “reactivity may be affected when subjects have dad recurrent malaria and other parasitic diseases [perhaps because of autoantibodies involving antigens in the lymphocyte cell line used to grow the virua] [185] or previous pregnancies [perhaps because of antibodies to DR4 or other HLA types] [186-188]” (189). The US researcher insisted that: “Since the reliability of ELISA test for the measurement of HTLV-III/LAV antibody in Africa sera has been questioned, the extent of this problem remains uncertain” (189). Speaking about the seroepidemiology in Central African countries, a British immunologist states: “It now appears that some of the results obtained were false positives” (190).

Mann also knew that tests for HIV often wrongly identify antibodies to HIV in blood samples (191). “False positives can also occur, if, for example, the frozen blood has thawed and then been refrozen. To make the situation even more complex, many Africans probably have relatively high levels of antibodies, proteins that signal the body’s attempt to fight disease, in their blood, as a result of having other infections, such as malaria. These numerous antibodies tend to bond to one another and cause blood samples to become sticky, which may lead to false positive results” (191).

“Results in serological surveys for antibodies against HIV in Africa were initially distorted by a high false-positive rate” (192).

It is amazing to note that public health officials also know that “serologic studies of HIV in Africa have been inconsistent because of problems in interpretation of the results from ELISA and Western blot tests of banked specimens, particularly from malaria endemic areas, and the validity of these data has been questioned” (193).

Currently, pharmaceutical companies that make and commercialize the kits for HIV tests acknowledge the inaccuracy of these tests. Accordingly, the inserts that come with the kits typically state the following: “Elisa testing alone cannot be used to diagnose AIDS, even if the recommended investigation of reactive specimens suggests a high probability that the antibody to HIV-1 is present” (194). The insert for one of the kits for administering the Western blot warns: “Do not use this kit as the sole basis of diagnosis of HIV-1 infection” (195). The insert that comes with a popular kit to run viral load warns: “The amplicor HIV-1 monitor test, version 1.5, is not intended to be used as a screening test for blood or blood products for HIV or as a diagnostic test to confirm the presence of HIV infection” (196). Abbott goes even farther when it warns: “At present there is no recognized standard for establishing the presence or absence of antibodies to HIV-1 and HIV-2 in human blood” (194).

There are abundant scientific publications explaining that there are more than 70 different documented conditions that can cause the antibody tests to react positive without an HIV infection (179-184). Some of the conditions that cause false positives on HIV tests are: past or present infection with a variety of bacteria, parasites, viruses, and fungi including tuberculosis, malaria, leishmaniasis, influenza, common cold, leprosy and history of sexually transmitted diseases; the presence of polyspecific antibodies, hypergammaglobulinemias, the presence of autoantibodies against a variety of cells and tissues, vaccination, and the administration of gamma globulins or immunoglobulins; the presence of autoimmune diseases like erythematous lupus, sclerodermia, dermatomyositis and rheumatoid arthriris; the existence of pregnancy and multiparity; a history of rectal insemination; addiction to recreational drugs; several kidney diseases, renal failure and hemodialysis; a history of organ transplantation; presence of a variety of tumors and cancer chemotherapy; many liver diseases including alcoholic liver disease; hemophilia, blood transfusions and administration of coagulation factor; even the simple condition of aging, to mention just a few of the conditions (182-184). Interestingly, most of these conditions are common to the African scenario.

The above considerations permit the proposition that reacting positively on tests for HIV is caused by multiple, repeated, and chronic exposure to chemical, physical, biological, mental, and nutritional stressor agents (184). One of the first consequences of poverty is malnutrition, making individuals susceptible to infectious and parasitic diseases, which in turn stimulate the production of polyspecific antibodies, many of which are being detected by HIV tests.

Many are attempting to explain that the current morbidity and mortality of African communities are a consequence of HIV infections. However, it is possible that reacting positively on the so-called tests for HIV in Africa is a result of chronic exposure to poverty and its consequences, such as malnutrition, infections, and parasites (184).