Antibody to herpes simplex virus type 2 as a marker of sexual risk behavior in rural Tanzania.
ABSTRACT A serosurvey was conducted in a random sample of 259 women and 231 men in 12 rural communities in Mwanza Region, Tanzania, using a type-specific ELISA for Herpes simplex virus type 2 (HSV-2) infection. Seroprevalence rose steeply with age to approximately 75% in women >=25 years old and 60% in men >=30. After adjusting for age and residence, HSV-2 prevalence was higher in women who were married, in a polygamous marriage, Treponema pallidum hemagglutination assay (TPHA)-positive, had more lifetime sex partners, or who had not traveled. Prevalence was higher in men who were married, had lived elsewhere, had more lifetime partners, had used condoms, or were TPHA-positive. HSV-2 infection was significantly associated with recent history of genital ulcer. The association between HSV-2 infection and lifetime sex partners was strongest in those <25 years old in both sexes. This association supports the use of HSV-2 serology as a marker of risk behavior in this population, particularly among young people.
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ABSTRACT: HIV prevalence is decreasing in much of sub-Saharan Africa (SSA), but the drivers of the decline are subject to much dispute. Using mathematical modeling as a tool for hypothesis generation, we demonstrate how the hypothesis that the drop in prevalence reflects declines in sexual risk behavior is self-consistent. We characterize these potential declines in terms of their scale, duration, and timing, and theorize on how small changes in sexual behavior at the individual-level could have driven large declines in HIV prevalence.Epidemics 09/2014; 8:9–17. · 2.38 Impact Factor
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ABSTRACT: The HSV-1 ICP34.5 protein strongly influences neurovirulence and regulates several cellular antiviral responses. Despite the clinical importance of HSV-2, relatively little is known about its ICP34.5 ortholog. We have found that HSV-2 produces up to four distinct forms of ICP34.5 in infected cells: full-length protein, one shorter form sharing the N-terminus, and two shorter forms sharing the C-terminus. These forms appeared with similar kinetics and accumulated in cells over much of the replication cycle. We confirmed that the N-terminal form is translated from the primary unspliced transcript to a stop codon within the intron unique to HSV-2 γ34.5. We found that the N-terminal form was produced in a variety of cell types, and by 9 of 10 clinical isolates. ICP27 influenced but was not required for expression of the N-terminal form. Western blot and reverse transcription PCR indicated the C-terminal forms did not contain the N-terminus, and were not products of alternative splicing or internal transcript initiation. Expression plasmids encoding methionine at amino acids 56 and 70 generated products which co-migrated in SDS-PAGE with the C1 and C2 forms, respectively, and mutation of these sites abolished C1 and C2. Using a recombinant HSV-2 encoding HA-tagged ICP34.5, we demonstrated that the C-terminal forms were also produced during infection of many human and mouse cell types, but were not detectable in mouse primary neurons. The protein diversity generated from the HSV-2 γ34.5 open reading frame implies additional layers of cellular regulation through potential independent activities associated with the various forms of ICP34.5.Journal of Virology 07/2014; · 4.65 Impact Factor