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Pathogenesis of Human Immunodeficiency Virus Type-1 (HIV-1)-Associated Dementia: Role of Voltage-Gated Potassium

James P Keblesh, Benjamin C Reiner, Jianuo Liu

    Retrovirology : Research and Treatment
    |July 24, 2010
    PubMed

    Insights

    Voltage-gated potassium (K(v)) channels are implicated in HIV-1-associated dementia (HAD). Altered K(v) channel activity in brain cells contributes to cognitive deficits, suggesting new therapeutic targets.

    Area of Science:

    • Neuroscience
    • Immunology
    • Virology

    Background:

    • HIV-1-associated dementia (HAD) causes cognitive and behavioral issues in HIV-infected individuals.
    • Despite HAART, HAD persists due to antiretroviral drug limitations and growing HIV-1 resistance.
    • HAD pathogenesis involves infected mononuclear phagocytes releasing neurotoxic products.

    Purpose of the Study:

    • To investigate the role of voltage-gated potassium (K(v)) channels in HAD pathogenesis.
    • To explore K(v) channels as potential therapeutic targets for HAD and related neurodegenerative disorders.

    Main Methods:

    • Literature review of studies on HAD, HIV-1 infection, and K(v) channels.
    • Analysis of how cellular and viral products in HAD affect K(v) channel activity.
    • Examination of the link between K(v) channel dysfunction and cognitive deficits.

    Main Results:

    • Alterations in cellular and viral products associated with HAD impact K(v) channel function.
    • Dysfunctional K(v) channels in mononuclear phagocytes and neurons contribute to neuronal injury.
    • K(v) channel dysfunction correlates with observed cognitive deficits in HAD.

    Conclusions:

    • Voltage-gated potassium (K(v)) channels are critically involved in the development of HAD.
    • Targeting K(v) channels presents a promising new therapeutic strategy for HAD.
    • K(v) channels may also be targets for other inflammatory neurodegenerative diseases.

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