Cytokine involvement in viral permissiveness and the progression of HIV disease.
Many viruses have evolved novel means of exploiting host defense mechanisms for their own survival. This exploitation may be best exemplified by the interrelationships between certain viruses and the host cytokine networks. Many viruses, including the human immunodeficiency virus type-1 (HIV-1), rely on the liberation and cellular action of host immune cytokines to expand their host cell range, to regulate their cellular expression, and to maintain their dormant state until the proper extracellular conditions arise. As again exemplified by HIV-1, viruses may also take an active role regulating cytokine expression and cell surface cytokine receptors. Because the viral life cycle, and in particular the HIV-1 life cycle, is so intertwined with cytokine regulatory networks, these networks represent potential points for therapeutic intervention. As our understanding of cellular cytokine pathways involved in viral infection and replication continues to expand, so too will our ability to design rational anti-viral therapies to alter multiple steps along the viral life cycle.
Butera
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Retrovirus Diseases Branch, Centers for Disease Control and Prevention, Atlanta, Georgia 30333.
D000163:Acquired Immunodeficiency Syndrome / Q000382:microbiology*; D016207:Cytokines / Q000494:pharmacology / Q000502:physiology*; D015497:HIV-1 / Q000472:pathogenicity*; D006801:Humans; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology / Q000502:physiology
D016207:Cytokines; D014409:Tumor Necrosis Factor-alpha