Chapter 15

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

Paul Shapshak

Paul Shapshak

Division of Infectious Diseases and International Medicine, Tampa General Hospital, Departments of Internal Medicine and Psychiatry-Behavioral Medicine, USF Health, Tampa, FL, 33606

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Alireza Minagar

Alireza Minagar

Departments of Neurology and Anesthesiology, Louisiana State University Health Sciences Center, Shreveport, LA, 71301

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Pandjassarame Kangueane

Pandjassarame Kangueane

Biomedical Informatics, 17A Irulan Sundai Annes, Pondicherry, 607402 India

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Simon Frost

Simon Frost

Antiviral Research Center, Department of Pathology, University of California San Diego, San Diego, CA, 92103

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Sergei L. Kosakovsky Pond

Sergei L. Kosakovsky Pond

Antiviral Research Center, Department of Pathology, University of California San Diego, San Diego, CA, 92103

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Selene Zarate

Selene Zarate

Department of Genetics, Independent University of Mexico City, City, San Lorenzo 290 Col. Del Valle, 03100 México, D.F, México

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Elyse Singer

Elyse Singer

Department of Neurology, UCLA David Geffen School of Medicine, Los Angeles, CA, 90024

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Deborah Commins

Deborah Commins

Department of Pathology (Neuropathology), University of Southern California Keck School of Medicine, Los Angeles, CA, 90089

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Anne De Groot

Anne De Groot

EpiVax, Inc. and Biomedical Center, Brown University School of Medicine, Providence, RI, 02912

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Miguel Quinones-Mateu

Miguel Quinones-Mateu

Life Sciences Division, Diagnostic Hybrids, Athens, OH, 45701

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Ernest Terwilliger

Ernest Terwilliger

Harvard Institute of Medicine, Boston, MA, 02115

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First published: 01 October 2008

Summary

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.

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