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Used acyclovir or valacyclovir during study follow-up.HSV-2 prevalenceOf the 2,499 participants, 1383 (55.3 ) tested negative for HSV-2 at baseline, 892 (35.7 ) tested positive, 223 (8.9 ) had indeterminate tests, and one test was not done. Of the 223 with indeterminate tests at baseline, 114 (51.1 ) tested positive for HSV-2 infection at some point during follow-up. Factors associated with testin
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Pectively, correspond to the type ii or iii microglial states described in the preceding paragraph. Further, the factors which cause polarization to M1 or M2, reinforce the maintenance of that phenotype in a cycle-like manner [8,9] (Figure 1). Increased M1 polarization is consistent with increased TNF-a observed in plasma and brain specimens in HAD and AD, and may play a role in the pathophysiolog
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E collected.Inside the in situ blood perfused models we haveE collected.Inside the in situ blood perfuse
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Ministered to HIV-infected young adults on highly active antiretroviral therapy (HAART).NIH-PA Author Manuscript NIH-PA Author Manuscript NIH-PA Author Manuscript2.2. Vaccine2. Materials and methodsThis was a prospective, multicenter trial carried out by the Pediatric AIDS Clinical Trials Group (PACTG) and the International Maternal, Pediatric, Adolescent, AIDS Clinical Trials (IMPAACT) network. T
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T among participants living in Peru (46.0 ), Brazil (37.8 ), and Ecuador (37.3 ), with lower prevalence among participants living in Thailand (6.4 ), South Africa (17.6 ), and the United States (27.1 ; P,0.001). Randomization group was not associated with HSV-2 prevalence at baseline (P = 0.44). In multivariable analysis, all factors remained significantly associated with HSV-2 prevalence with the
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Atinger H, Carpenter CB, et al. (2000) Protection of macaques against vaginal transmission of a pathogenic HIV-1/SIV chimeric virus by passive infusion of neutralizing antibodies. Nat Med 6: 207?10. 24. Bohnhorst J? Bj gan MB, Thoen JE, Natvig JB, Thompson KM (2001) Bm1Bm5 classification of peripheral blood B cells reveals circulating germinal center founder cells in healthy individuals and distur
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Molecules including major histocompatibility complex (MHC) II and CD40 [15]. Microglia expressing MHC II induce CD4+ T cells to generate IFN-g and TNF-a [16]. In the case of both HAD and AD, this response is considered harmful to the brain and in both diseases TNFa is elevated to neurotoxic levels while only in HAD is IFN-g is prominently elevated [14]. In HIV associated dementia (HAD; also known
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