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HSV-2 Coinfection Seems to Slow Early CD4 Drop With HIV
  2nd International Workshop on HIV Transmission
August 26-28, 2007
Washington, DC
Mark Mascolini
Although infection with herpes simplex virus type 2 (HSV-2) raises the risk of HIV infection [1], carrying HSV-2 appeared to slow early CD4 drops with HIV, according to results of a 186-person study in Sao Paulo [2]. Researchers from San Francisco and Sao Paulo concede that the surprising finding "poses a striking paradox, and its public health implications are not immediately clear."
The study involved 186 antiretroviral-naive people whose HIV seroconversion date lay within the previous 170 days. Jason Barbour (University of California, San Francisco) and coworkers monitored these people until they left the cohort or started antiretrovirals when their CD4 count fell below 350 (according to Brazilian guidelines). No one took the antiherpes drug valacyclovir. HIV-1 subtypes B, F, and B/F predominate in Brazil.
Upon entering the cohort, participants had a median age of 30.8 years (interquartile range [IQR] 24.7 to 36.3 years), a median viral load of 4.3 log copies/mL (about 20,000 copies), and a median CD4 count of 535 (IQR 409 to 698). The cohort included 168 men (92%) and 18 women. At the time of HIV diagnosis, 101 people (54%) had a positive test for HSV-2 and 45 (39%) were positive for anti-hepatitis B virus (HBV) core antibody.
People with and without HSV-2 coinfection did not differ in age, gender, race, or CCR5 delta32 genotype. Nor did they differ in CD8-cell count or T-cell activation state, or in HIV load over time--a result confirming a finding in a California cohort [3] but contradicting results from a study in rural Uganda [4]. Through 24 months of follow-up, CD4 counts drifted downward in people without HSV-2 but remained stable in those with HSV-2.
CD4 tallies were 57 cells lower for every 10-fold higher viral load, a highly significant correlation (P < 0.0001). After statistical adjustment for viral load impact, coinfected people sustained CD4 counts an average 69 cells higher over 24 months of follow-up than people without HSV-2 (P = 0.04).
HSV-2 coinfection correlated positively with HBV core antigen serostatus (P = 0.02). After statistical adjustment for HBV and HIV load, people with HSV-2 had an average of 89 more CD4 cells than people without HSV-2. That difference fell just shy of statistical significance (P = 0.07), perhaps because of the small size of the study. Barbour suggested that the impact of HSV-2 on CD4 count appears to be independent of HBV status or HIV load.
Becoming infected with HSV-2 after HIV diagnosis did not sustain CD4 counts.
Barbour and colleagues called for follow-up studies to search for biologic mechanisms that may explain this baffling result, to rule out potential confounders (such as HBV coinfection), and to assess potential links between CD4 count and HSV-2 status in adults without HIV infection.
1. Brown JM, Wald A, Hubbard A, et al. Incident and prevalent herpes simplex virus type 2 infection increases risk of HIV acquisition among women in Uganda and Zimbabwe. AIDS. 2007;21:1515-1523.
2. Barbour JD, Sauer MM, Sharp ER, et al. Higher CD4+ T cell counts among HIV-1/HSV-2 co-infected adults in early HIV-1 infection. 2nd International Workshop on HIV Transmission. August 26-28, 2007. Washington, DC. Abstract 6.
3. Cachay ER, Frost SD, Richman DD, et al. Herpes simplex virus type 2 infection does not influence viral dynamics during early HIV-1 infection. Clin Infect Dis. 2007;95:1270-1277.
4. Duffus WA, Mermin J, Bunnell R, et al. Chronic herpes simplex virus type-2 infection and HIV viral load. Int J STD AIDS. 2005;16:733-735.
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