Chapter 15 : The Role of Viral Genetic Variability in HIV-Associated Neurocognitive Disorder

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This chapter talks about the neuro-AIDS epidemic. Recent decreases in the heterogeneity of HIV sequences for many strains that have occurred in several places in the world including Southeast Asia are described, and their possible association with human behaviors such as drug abuse is considered. Genetic variability and sequence heterogeneity are key features of HIV. Its enzyme, reverse transcriptase (RT), exhibits the ability to jump between nucleic acid strands during replication, resulting in recombination of different types of HIV that infect the same cell. The basic risks for HIV infection are no mystery. Sexual activity, drug abuse (injection), transfusion, needle-sticks, and transplacental transmission are primary risks. It has been hypothesized that there are long-term viral reservoirs of HIV-1. These can exist in the context of T-cell latency as well as highly active antiretroviral therapy (HAART). HIV-associated neurocognitive disorders (HAND) recognized a spectrum of neurocognitive impairments ranging from asymptomatic neurocognitive impairment to HIV-1- associated mild neurocognitive disorder to full-blown HAD. HIV viral isolates and strains with different sequences appear to be important for the pathogenesis of brain disease in neuro-AIDS, and early studies identified HIV-1 isolates related to neuro-AIDS. Genetic recombination is a highly significant and effective mechanism associated with this genetic hypervariability that protects HIV-1 from immunity and eventually leads to profound immunosuppression and demise of AIDS patients.

Citation: Shapshak P, Minagar A, Kangueane P, Frost S, Kosakovsky Pond S, Zarate S, Singer E, Commins D, Groot A, Quinones-Mateu M, Terwilliger E. 2009. The Role of Viral Genetic Variability in HIV-Associated Neurocognitive Disorder, p 201-218. In Goodkin K, Shapshak P, Verma A (ed), The Spectrum of Neuro-AIDS Disorders. ASM Press, Washington, DC. doi: 10.1128/9781555815691.ch15
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Maximum likelihood phylogenetic trees for env sequences from different brain regions. MG94 x TrN93 codon model was used to infer the trees, scaled on the expected number of nucleotide substitutions per site per unit time. Bootstrap support values for clade-separating branches were obtained via 1,000 neighbor-joining bootstrap trees.

Citation: Shapshak P, Minagar A, Kangueane P, Frost S, Kosakovsky Pond S, Zarate S, Singer E, Commins D, Groot A, Quinones-Mateu M, Terwilliger E. 2009. The Role of Viral Genetic Variability in HIV-Associated Neurocognitive Disorder, p 201-218. In Goodkin K, Shapshak P, Verma A (ed), The Spectrum of Neuro-AIDS Disorders. ASM Press, Washington, DC. doi: 10.1128/9781555815691.ch15
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Distance-based tests for viral population division

Citation: Shapshak P, Minagar A, Kangueane P, Frost S, Kosakovsky Pond S, Zarate S, Singer E, Commins D, Groot A, Quinones-Mateu M, Terwilliger E. 2009. The Role of Viral Genetic Variability in HIV-Associated Neurocognitive Disorder, p 201-218. In Goodkin K, Shapshak P, Verma A (ed), The Spectrum of Neuro-AIDS Disorders. ASM Press, Washington, DC. doi: 10.1128/9781555815691.ch15
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Selective pressure on sequences by brain region

Citation: Shapshak P, Minagar A, Kangueane P, Frost S, Kosakovsky Pond S, Zarate S, Singer E, Commins D, Groot A, Quinones-Mateu M, Terwilliger E. 2009. The Role of Viral Genetic Variability in HIV-Associated Neurocognitive Disorder, p 201-218. In Goodkin K, Shapshak P, Verma A (ed), The Spectrum of Neuro-AIDS Disorders. ASM Press, Washington, DC. doi: 10.1128/9781555815691.ch15

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