PubMed · 11364561
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J S James. 1997-08-15. Consensus letter: Peter Duesberg.. https://pubmed.ncbi.nlm.nih.gov/11364561/
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Highly active antiretroviral therapy (HAART) curtails human immunodeficiency virus type 1 (HIV-1) replication in lymphatic tissues and partially reverses the pathological damage associated with infection, but the genes that mediate these pathological and reparative processes remain largely unknown. To identify these genes, we used microarrays to profile gene expression in serial lymph node biopsy specimens obtained before and after treatment. We discovered approximately 200 treatment-responsive genes, many of them known mediators and moderators of immune activation and defenses, particularly innate defense genes, which, surprisingly, were expressed at all stages of HIV-1 infection. Most of the rest of the treatment-responsive genes we categorized as mediators of trafficking, reformation of active follicles, and tissue repair. We propose a model in which nearly counterbalanced functions of mediators and moderators of immune activation and defenses account for the slow dynamics of HIV-1 infection before treatment. This model suggests that there could be a role for anti-inflammatory agents, alone or in combination with HAART, in treating HIV-1 infection by tipping this balance to mitigate pathology.
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Although HIV-1/AIDS emerged late in the last century, more than 42 million individuals have been infected and 25 million have died worldwide, making AIDS, like malaria, a strong selective force for disease-associated genetic factors. Many of the genes that mediate immune response or that are co-opted by HIV-1 for completion of its lifecycle show differences in allele frequencies, as a result of drift, migration or selection. Here we show that the majority of AIDS candidate genes and AIDS restriction genes show significant differences in allele frequencies, possibly the result of historic selective pressures. These genes are undergoing present day natural selection in populations with high AIDS prevalence.