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  AIDS 2010
18th International AIDS Conference (IAC)
July 18-23 2010
Vienna, Austria
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Gays With Well-Controlled HIV Not Protected From Lymphogranuloma Venereum
  XVIII International AIDS Conference, July 18-23, 2010, Vienna
Mark Mascolini
Challenging a hypothesis about development of lymphogranuloma venereum (LGV) in HIV-infected gay men, researchers in Great Britain found that a lower CD4 count and a higher viral load do not predispose men to this often painful sexually transmitted infection [1]. The investigators suggested instead that high-risk sex and sex networks may be primary LGV risk factors in gays.
LGV appears as a genital ulcer accompanied by inguinal (groin) lymph node enlargement. Over the past decade physicians who care for gay men in Europe and North America began noticing outbreaks of the disease, which usually appears in gays as severe proctitis with constitutional symptoms. Some LGV experts hypothesized that gay men with HIV may be particularly susceptible to LGV because of immune suppression.
To test that hypothesis, London clinicians and public health workers devised a case-control study comparing "cases" of HIV-infected men with confirmed LGV and two types of "controls"--gay men without confirmed LGV but with LGV symptoms (symptomatic controls) and gay men without LGV and with no LGV symptoms (asymptomatic controls).
The 154 HIV-infected men studied included 66 LGV "cases," 53 symptomatic controls, and 35 asymptomatic controls. The investigators interviewed the men about their sexual history and requested CD4 counts and viral loads recorded in the men in the months before their LGV diagnosis or inclusion in this study. A CD4 count within the preceding 3 months was available for 77% of LGV cases, 62% of symptomatic controls, and 71% of asymptomatic controls. A viral load within the past 3 months was available for 73% of LGV cases, 57% of symptomatic controls, and 74% of asymptomatic controls.
The cases and two control groups all had a median age around 40 and a statistically equivalent median duration of HIV infection: 4.7 years in cases, 5.5 years in symptomatic controls, and 7.1 years in asymptomatic controls (P = 0.137 versus cases). About 70% of each group were receiving antiretroviral therapy.
Median CD4 count reported within the past 3 months was statistically equivalent for cases (530), symptomatic controls (470), and asymptomatic controls (470). Overall median viral load for all three groups lay below 40 copies. Median viral loads of men not taking antiretrovirals also proved statistically equivalent in 19 cases (23,374.5 copies), 14 symptomatic controls (13,000 copies), and 11 asymptomatic controls (15,676 copies) (P = 0.548).
Most cases and controls had stable CD4 counts over recent months, men taking antiretrovirals had maintained undetectable loads, and viral loads in untreated men did not differ between cases and either group of controls. The investigators cautioned that they did not have complete CD4 and viral load records on these men, so they may have missed transient dips in CD4 count or spikes in viral load. They suggested that "engagement in higher risk sexual behaviors and networks may account for the disproportionate numbers of HIV-positive [gay men] diagnosed with LGV."
1. French P, Sullivan A, White J, et al. Baseline absolute CD4 counts and viral loads in HIV positive individuals with lymphogranuloma venereum: the results of a multi-centre case control study in the UK, LGV-net. XVIII International AIDS Conference. July 18-23, 2010. Vienna. Abstract MOPE198.