Current perspectives on the molecular pathogenesis of virus-induced cancers in human immunodeficiency virus infection and acquired immunodeficiency syndrome.
A distinct group of cancers particularly threaten human immunodeficiency virus (HIV)-infected people. Most HIV/acquired immunodeficiency syndrome (AIDS)-associated cancers have a substantial component of viral etiology. Epstein-Barr virus (EBV), Kaposi's sarcoma-associated herpesvirus (HHV8), human papillomavirus (HPV), and HIV have been implicated in the etiology of cancers in AIDS. The molecular mechanisms by which HPV, EBV, HHV8, and HIV persist and cause cancer are summarized. The viral etiology of AIDS-associated cancers is important because pharmacologic and immunologic strategies to prevent or attack persistent or latent virus infection and cell growth transformation may be useful in preventing and treating these cancers. Effective immune attack on latent and persistent virus infection will require enhanced cellular immune responses. Such responses may be achievable through active immunization or by in vitro expansion of viral and host specific cytotoxic and helper T lymphocytes. Enhanced knowledge of clinically applied T-cell immunology may also be useful in preventing and treating HIV infection and other opportunistic infections in HIV-infected people.
Department of Microbiology, Molecular Genetics, and Medicine, Harvard University, Boston, MA, USA. Ekieff@rics.bwh.harvard.edu
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D000163:Acquired Immunodeficiency Syndrome / Q000150:complications* / Q000276:immunology / Q000821:virology; D000818:Animals; D015658:HIV Infections / Q000150:complications* / Q000276:immunology / Q000821:virology; D006801:Humans; D009369:Neoplasms / Q000150:complications* / Q000276:immunology / Q000821:virology*