PubMed · 8435023
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L J Schneiderman, N Jecker. 1993-02-22. Futility in practice.. https://pubmed.ncbi.nlm.nih.gov/8435023/
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To identify cancers that occur at higher rates in acquired immunodeficiency syndrome (AIDS) patients, the cancer experience of New York State (NYS) AIDS patients aged 15-69 years who were diagnosed between 1981 and 1994 was compared with that of the NYS general population. Sex and HIV risk group-specific standardized incidence ratios (SIRs), post-AIDS relative risks, and trends of relative risks were calculated to determine cancer risk. Among non-AIDS-related cancers, elevated SIRs were found for Hodgkin's disease (male, 8.0; female, 6.4; heterosexually infected males, 31.3); cancer of the rectum, rectosigmoid, and anus (male, 3.3; female, 3.0); trachea, bronchus, and lung (male, 3.3; female, 7.5); and brain and central nervous system (male, 3.1; female, 3.4; heterosexually infected females, 23.8) cancers. Moreover, significant trends of increasing relative risks from the pre-AIDS to the post-AIDS period were found for cancers of the rectum, rectosigmoid, and anus; trachea, bronchus, and lung; skin; and connective tissues (all sites, p < 0.05) among males. For AIDS-related cancers in women, invasive cervical cancer had an overall SIR of 9.1 (95% confidence interval: 6.9, 10.8) and a post-AIDS relative risk of 6.5 (95% confidence interval: 4.1, 9.7). This population-based registry linkage analysis evaluates cancer risk in AIDS patients by sex and risk factors and adds evidence that HIV-associated immunosuppression increases the risks of specific types of cancer.
CD8 T cells play an important role in protection and control of HIV-1 by direct cytolysis of infected cells and by suppression of viral replication by secreted factors. However, although HIV-1-infected individuals have a high frequency of HIV-1-specific CD8 T cells, viral reservoirs persist and progressive immunodeficiency generally ensues in the absence of continuous potent antiviral drugs. Freshly isolated HIV-specific CD8 T cells are often unable to lyse HIV-1-infected cells. Maturation into competent cytotoxic T lymphocytes may be blocked during the initial encounter with antigen because of defects in antigen presentation by interdigitating dendritic cells or HIV-infected macrophages. The molecular basis for impaired function is multifactorial, due to incomplete T-cell signaling and activation (in part related to CD3zeta and CD28 down-modulation), reduced perforin expression, and inefficient trafficking of HIV-specific CD8 T cells to lymphoid sites of infection. CD8 T-cell dysfunction can partially be corrected in vitro with short-term exposure to interleukin 2, suggesting that impaired HIV-specific CD4 T helper function may play a significant causal or exacerbating role. Functional defects are qualitatively different and more severe with advanced disease, when interferon gamma production also becomes compromised.