Psychosocial predictors of sexual risk taking were investigated in a community sample of 502 HIV-positive and HIV-negative African American men enrolled in the African American Health Project. Poisson regression analyses were used to estimate the relative contributions of psychosocial risk and protective factors in predicting sexual risk as measured by a sexual risk behavior index. HIV-negative men, men who have sex with men and women (MSM/W), and men who have sex with men (MSM) engaged in more high-risk sexual behaviors than heterosexuals and HIV-positive men, but men who were HIV-positive carried a heavier burden of psychosocial risk factors. High psychological distress, being HIV-negative, older age, low socioeconomic status (SES), and being an MSM/W were the best predictors of sexual risk. HIV serostatus and sexual orientation differences were obtained, with high psychological distress being the most consistent predictor regardless of serostatus or sexual orientation. Results confirm previous findings of riskier sexual lifestyle among MSM/W, men with low SES, and men who are experiencing significant psychological distress.

Central nervous system opportunistic infections (CNS-OI) are a significant cause of morbidity and mortality in AIDS. While current interventions are increasingly successful in treating CNS-OI, little information exists regarding long-term behavioral outcomes among survivors. In this exploratory study we examined neurocognitive data among three groups of adults with different AIDS-related CNS-OI: 15 with past cryptococcal meningitis (CM), 8 with toxoplasmosis encephalitis (TE), and 8 with progressive multifocal leukoencephalopathy (PML). A group of 61 individuals with AIDS, but without CNS-OI, was used as a comparison group. A battery of standardized neuropsychological tests assessing a variety of cognitive domains was administered upon entry. Results indicate that individuals with a history of CNS-OI were most impaired on measures of cognitive and psychomotor speed relative to the HIV+ comparison group. Among the CNS-OI groups, individuals with history of TE had the most severe and varied deficits. The results are discussed in relation to what is known about the neuropathological consequences of the various CNS-OIs. While this is the first systematic group study of residual CNS-OI effects on neurocognitive function, future studies employing more participants, perhaps focusing on specific CNS-OIs, will further characterize the long-term outcomes in AIDS-related CNS-OI. KeywordsOpportunistic infection; AIDS; Neuropsychological functioning; Toxoplasmosis encephalitis; Progressive multifocal leukoencephalopathy; Cryptococcal meningitis Address correspondence to Andrew Levine, National Neurological AIDS Bank, 11645 Wilshire Blvd., Suite 770, Los Angeles, 90025, CA, USA (ajlevine@mednet.ucla.edu). NIH Public Access NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author ManuscriptSince its introduction in 1996, highly active antiretroviral therapy (HAART) has, when used in combination with adjunctive and prophylactic antibiotic therapy, dramatically decreased the incidence of central nervous system opportunistic infections (CNS-OI) and has improved the longevity of people with AIDS (Collier et al., 1999;Neuenburg et al., 2002; San-Andreas et al., 2003). HAART has also contributed to improved survival among those AIDS patients who develop a CNS-OI (Kirk et al., 2002). These conditions, which at one time typically resulted in death, can now be treated. Further, while HIV infection itself may lead to neuropathological changes, the CNS-OIs common among AIDS patients often result in more severe structural brain lesions. Currently, little information exists regarding the long-term cognitive and functional outcomes in individuals who survive AIDS-related CNS-OIs. For example, do most survivors of AIDS-related CNS-OI recover to such a degree that they can return to work or independent living? Examination of the changes in survivors' neuropsychological abilities is necessary to understand the benefits and limitations of current treatments, to identify obstacles in returning affected individuals to independence...

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Charcot–Marie–Tooth (CMT) type 1 disease is the most common human hereditary demyelinating neuropathy. Mutations in pmp22 cause about 70% of all CMT1. Trembler-J (TrJ/+) mice are an animal model of CMT1E, having the same spontaneous pmp22 mutation that is found in humans. We compared the behavior profile of TrJ/+ and +/+ (wild-type) in open-field and elevated-plus-maze anxiety tests. In these tests, TrJ/+ showed an exclusive head shake movement, a lower frequency of rearing, but a greater frequency of grooming. In elevated-plus-maze, TrJ/+ defecate more frequently, performed fewer total entries, and have fewer entries to closed arms. These hippocampus-associated behaviors in TrJ/+ are consistent with increased anxiety levels. The expression of pmp22 and soluble PMP22 were evaluated in E17-hippocampal neurons and adult hippocampus by in situ hybridization and successive immunohistochemistry. Likewise, the expression of pmp22 was confirmed by RT-qPCR in the entire isolated hippocampi of both genotypes. Moreover, the presence of aggregated PMP22 was evidenced in unmasked granular hippocampal adult neurons and shows genotypic differences. We showed for the first time a behavior profile trait associated with anxiety and a differential expression of pmp22/PMP22 in hippocampal neurons of TrJ/+ and +/+ mice, demonstrating the involvement at the central level in an animal model of peripheral neuropathy (CMT1E).

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