Experimental oral polio vaccines and acquired immune deficiency syndrome

The simian immunodeficiency virus (SIV) of the common chimpanzee is widely acknowledged as the direct ancestor of HIV-1. There is increasing historical evidence that during the late 1950s, kidneys were routinely excised from central African chimpanzees by scientists who were collaborating with the polio vaccine research of Dr Hilary Koprowski, and sent - inter alia - to vaccine-making laboratories in the USA and Africa, and to unspecified destinations in Belgium. While there is no direct evidence that cells from these kidneys were used as a substrate for growing Dr Koprowski's oral polio vaccines, there is a startling coincidence between places in Africa where his CHAT vaccine was fed, and the first appearances in the world of HIV-1 group M and group-M-related AIDS. Because of the enormous implications of the hypothesis that AIDS may be an unintended iatrogenic (physician-caused) disease, it is almost inevitable that this theory will engender heated opposition from many of those in the scientific establishment, and those with vested interests.     

Pulmonary Mycobacterium tuberculosis in acquired immune deficiency syndrome.

A case of pulmonary infection with Mycobacterium tuberculosis in a patient with the acquired immune deficiency syndrome (AIDS) was studied. Diagnosis of AIDS was confirmed by the finding of pulmonary M tuberculosis with oral and oesophageal candidiasis accompanied by characteristic immunological changes with evidence of infection with human T cell lymphotropic virus III. Treatment of this patient was complicated by an unusual drug interaction between rifampicin and ketoconazole, leading to subtherapeutic serum concentrations and poor clinical response to treatment. Intravenous treatment was more effective than oral treatment. This drug interaction should be studied in greater detail as ketoconazole and rifampicin may be used together to treat patients with candidiasis and infection with M tuberculosis.     

DNA image cytometry in acquired immune deficiency syndrome (AIDS)

In nine cases with the acquired immune deficiency syndrome (AIDS), including four stage I cases, three stage II cases and two stage III cases, DNA image cytometry was performed on Feulgen-stained lymph node imprint smears. Diploidy was found in three cases, tetraploidy in three cases and octoploidy in two cases. Aneuploid DNA distribution patterns were not seen. The lymphoid cells showed an enormously increased proliferation rate. Two cases in stage I revealed characteristic intranuclear DNA inclusions in lymphoid cells. These results indicate that DNA image cytometry may be useful as an adjunct to surgical pathology in certain cases to assist in the differential diagnosis between AIDS and benign conditions of the lymphoid system as well as between AIDS and malignant lymphomas, which usually have aneuploid DNA patterns.     

The burden of proof and the origin of acquired immune deficiency syndrome

There is a distinct difference in the way that different theories about the origin of acquired immune deficiency syndrome have been treated, with the widely supported cut-hunter theory given relatively little scrutiny, while the oral polio vaccine theory has been subject to intense criticism. This difference in treatment cannot be explained as application of the scientific method. A better explanation is that the burden of proof is put on all contenders to the cut-hunter theory, giving it an unfair advantage, especially given that this assignment of the burden of proof appears to reflect non-scientific factors.     

Alterations in the gut microbiota of patients with acquired immune deficiency syndrome

Acquired immune deficiency syndrome (AIDS), caused by infection with human immunodeficiency virus (HIV), is associated with gastrointestinal disease, systemic immune activation and changes in the gut microbiota. Here, we aim to investigate the gut microbiota patterns of HIV‐infected individuals and HIV‐uninfected individuals in populations from South China. We enrolled 33 patients with HIV (14 participants treated with highly active antiretroviral therapy [HAART] for more than 3 months; the remaining 19 individuals had not received treatment) and 35 healthy controls (HC) for a cross‐sectional comparison of gut microbiota using stool samples. Gut microbial communities were profiled by sequencing the bacterial 16S rRNA genes. Dysbiosis was more common among patients with AIDS compared with healthy individuals. Dysbiosis was characterized by decreased α‐diversity, low mean counts of Bacteroidetes, Faecalibacterium, Prevotella, Bacteroides vulgatus, Dialister and Roseburia inulnivorans, and high mean counts of Proteobacteria, Enterococcus, Streptococcus, Lactobacillus, Lachnociostridium, Ruminococcus gnavus and Streptococcus vestibularis. Increased abundance of Bacilli was observed in homosexual patients. Proteobacteria were higher among heterosexual patients with HIV infections. Tenericutes were higher among patients with history of intravenous drug abuse. Restoration of gut microbiota diversity and a significant increase in abundance of Faecalibacterium, Blautia and Bacteroides were found in patients receiving HAART compared to those who did not receive. HIV infection‐associated dysbiosis is characterized by decreased levels of α‐diversity and Bacteroidetes, increased levels of Proteobacteria and the alterations of gut microbiota correlate with the route of HIV transmission. The imbalanced faecal microbiota of HIV infection is partially restored after therapy.     

HLA-associated susceptibility to acquired immune deficiency syndrome in HIV-1-seropositive subjects

No difference in HLA-A, B or DR gene frequencies could be observed between 172 control subjects and 180 HIV-1-seropositive subjects of European ancestry diagnosed through the systematic screening of blood donations. In contrast, progression to acquired immune deficiency syndrome (AIDS; 21 patients) or CD4 lymphocyte loss equal or more than 20% over a 6-month period (37 subjects) was found to be associated with the B8DR3 haplotype (relative risk = 10.64, p less than 0.003, and 2.23, p less than 0.092, respectively). Other independently significant associations assessed through the multivariate Cox proportional-hazards model were B16, BW21 and B35 alleles as factors of bad prognosis. Conversely, A11 and DR4 alleles were factors favouring longer survival.