Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0021051 (immunodeficiency)
 71,517 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Recent studies indicate that human immunodeficiency virus type 1 (HIV) gene expression can be dramatically enhanced by certain heterologous viral and chemical agents, implicating these as potential reactivating agents of latent virus infection. A common denominator shared by these agents is their ability to cause stress responses in cells. In an effort to determine whether stress responses affect HIV gene expression, we examined the effects of ultraviolet light (UV) and mitomycin C, on HIV gene expression as well as on viral growth and development. We demonstrate that these agents enhance HIV gene expression up to 150-fold. These levels are similar to those obtained by the tat gene product, the HIV trans-activating factor responsible for enhancing viral gene expression. The increase in gene expression after UV irradiation appears to require transcription but not de novo protein synthesis, and correlates with an accumulation of stable mRNA. Most importantly, UV irradiation of human T-cells prior to viral infection significantly shortens the viral growth cycle. Apparently, UV-induced cellular stress is highly conducive for viral replication and growth. We further demonstrate that even direct sunlight can activate HIV gene expression. These results demonstrate that DNA damaging agents, and perhaps other agents which elicit SOS-like stress responses in mammalian cells, can activate HIV expression thereby enhancing viral replication and development.
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PMID:Activation of human immunodeficiency virus type 1 by DNA damage in human cells. 312 61

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.
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PMID:Current perspectives on the molecular pathogenesis of virus-induced cancers in human immunodeficiency virus infection and acquired immunodeficiency syndrome. 970 95