The effect of childhood trauma, ApoE genotype and HIV-1 viral protein R variants on change in cognitive performance.

OBJECTIVE: Gene-environment interactions contribute to the development of HIV-associated neurocognitive disorders. We examined whether childhood trauma, apolipoprotein E isoforms and viral protein R (Vpr) variants were associated with change in cognitive performance. Seventy-three seropositive women completed neuropsychological assessments at baseline and 1-year follow-up. We conducted genetic analyses using DNA obtained from blood and calculated risk scores based on Vpr amino acid 37, 41 and 55 variants that were previously associated with cognitive performance. RESULTS: Global cognitive scores declined significantly over the 1-year study period (p = 0.029). A reduction in global cognitive scores was associated with childhood trauma experience (p = 0.039).

Short Communication: A Quantitative System for Monitoring Blood-Circulating Viral Protein R of Human Immunodeficiency Virus-1 Detected a Possible Link with Pathogenic Indices.

We developed a detergent-free enzyme-linked immunosorbent assay (ELISA) for HIV-1 viral protein R (Vpr), an accessory protein of human immunodeficiency virus type-1 (HIV), and detected soluble Vpr in ∼22% of HIV patients who were receiving combination antiretroviral therapy and were free of plasma HIV RNA. Notably, the levels of CD8-positive cell count, soluble intercellular adhesion molecule-1 (sICAM-1), and C-C motif chemokine ligand 2 (CCL2), all of which are markers of chronic inflammation in HIV patients, were higher in Vpr-positive patients than in Vpr-negative patients. Because sICAM1 and CCL2 are associated with an increased risk of HIV-associated neurocognitive disorder, we propose that an established Vpr-ELISA would be useful for monitoring the risk of HIV complications during latent HIV infection.

Short communication: circulating plasma HIV-1 viral protein R in dual HIV-1/tuberculosis infection.

Circulating free HIV-1 viral protein R (Vpr) is found in up to one third of subjects with HIV-1 infection. Free Vpr presumably shares some of the immunopathogenic effects of cell-associated Vpr. Here we assessed Vpr in plasma and pleural fluid from HIV/tuberculosis (TB) dually infected subjects with pleural TB and from plasma of patients with pulmonary HIV/TB. Vpr was assessed by western blot analysis. In plasma from HIV/TB subjects with pulmonary TB free Vpr could be detected in 47%. Only one subject, among 26 tested, with HIV monoinfection showed plasma Vpr activity. The majority (87.5%) of patients with pleural HIV/TB demonstrated free Vpr reactivity in their plasma. However, no Vpr activity was found in autologous pleural fluid samples from pleural HIV/TB patients. Standard (s) Vpr reactivity was reduced markedly by the addition of sVpr to pleural fluid from HIV-uninfected subjects. A high incidence of plasma Vpr reactivity in HIV/TB patients implies heightened processing and release of this HIV-1 accessory protein during HIV/TB coinfection. The contribution of free Vpr to HIV-1 immunopathogenesis during HIV/TB needs to be studied.