COMMENTARY

HIV/AIDS: March 15, 2004

John Bartlett, MD

Disclosures

March 15, 2004

In This Article

Other HIV/AIDS Studies

Etiology of Clinical Proctitis Among Men Who Have Sex With Men.

Klausner JD, Kohn R, Kent C. Etiology of clinical proctitis among men who have sex with men. Clin Infect Dis. 2004;38:300-302. This is a retrospective review of clinical proctitis in gay men seen at a sexually transmitted diseases clinic in San Francisco, California. The review included men with rectal symptoms of pain, itching, tenesmus, rectal bleeding, or discharge who underwent clinical evaluation, including anoscopy with diagnostic tests for Chlamydia trachomatis, Neisseria gonorrhoeae, herpes simplex virus (HSV), and syphilis. The results show relatively high rates of gonorrhea, chlamydia, and HSV. No pathogen was found in 46 of the 101 patients studied. These results are summarized in Table 5 .

Comment: There were multiple studies of the newly recognized "gay bowel syndrome" in the late 1970s and early 1980s. However, subsequent attention and study has been sparse, in part attributed to reduced frequency thought to reflect changing practices by gay men in response to the HIV epidemic. This study clearly indicates that it is still an issue, since the cases were studied in 2001-2002. Also, the etiology is about the same as previously, although HSV is newly recognized as an important component. This finding not only affects management but also has HIV prevention implications. The authors note that two thirds of the participants were HIV negative and that proctitis increases the risk of HIV by up to 9-fold.[3,4]

Papagno L, Spina CA, Marchant A, et al. Immune activation and CD8(+) T-cell differentiation towards senescence in HIV-1 infection. PLoS Biol. 2004;2:E20. The authors studied 2 groups of patients. One group was studied during acute HIV infection followed through resolution and subsequently when there was virologic control with antiretroviral drugs. The second group was a cross-sectional study of untreated patients in 3 categories: acute infection, chronic nonprogressors (CD4+ cell count > 500 cells/mcL with no treatment for 10 years), and patients with a negative CD4+ cell slope. The laboratory methods used CD4+ cells, CD8+ cells, and CD38+ cells with techniques to determine activation level and differentiation state. Their results showed that acute HIV produces massive activation of CD8+ cells that resulted in highly differentiated CD8+ cells directed at multiple antigens, including Epstein-Barr virus and cytomegalovirus, as well as HIV. The differentiation of CD8+ cells and CD4+ cells eventuate in a "scathe of replicative senescence." The authors conclude that chronic stimulation from HIV produces T-cell exhaustion and this accounts for disease progression.

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