Antimicrobial polypeptides are key Anti-HIV-1 effector molecules of cervicovaginal host defense

Authors

    Authors

    A. M. Cole;A. L. Cole

    Comments

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    Abbreviated Journal Title

    Am. J. Reprod. Immunol.

    Keywords

    AIDS; defensin; innate immunity; mucosa; retrocyclin; vagina; HUMAN-IMMUNODEFICIENCY-VIRUS; LEUKOCYTE PROTEASE INHIBITOR; RHESUS-MACAQUE LEUKOCYTES; HUMAN AIRWAY EPITHELIA; REPLICATION IN-VITRO; ANTI-HIV ACTIVITY; BACTERIAL VAGINOSIS; DENDRITIC CELLS; BETA-DEFENSINS; PORE FORMATION; Immunology; Reproductive Biology

    Abstract

    Mucosal surfaces of the cervix and vagina are portals for heterosexual transmission of human immunodeficiency virus type 1 (HIV-1) and, therefore, play a fundamental role in the pathogenesis of primary infection. Cationic antimicrobial polypeptides including defensins are the principal effector molecules of mucosal innate immunity against microbes and viruses such as HIV. In cervicovaginal secretions, antimicrobial polypeptides constitute the majority of the intrinsic anti-HIV-1 activity, synergism between cationic polypeptides is complex, and full anti-HIV-1 activity involves the complete complement of cationic polypeptides. Periods in which cationic antimicrobial polypeptide expression is reduced are likely associated with increased susceptibility to HIV-1 infection. This review provides an overview of the role of cationic antimicrobial polypeptides in innate cervicovaginal anti-HIV-1 host defense, and discusses how hormones and bacterial infections can regulate their expression. Emphasis is placed on the theta-defensin (retrocyclin) class of anti-HIV-1 peptides and their potential for development as topical microbicides to prevent HIV-1 transmission.

    Journal Title

    American Journal of Reproductive Immunology

    Volume

    59

    Issue/Number

    1

    Publication Date

    1-1-2008

    Document Type

    Article

    Language

    English

    First Page

    27

    Last Page

    34

    WOS Identifier

    WOS:000251626700003

    ISSN

    1046-7408

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