Herpes simplex virus type-1 can reactivate transcription of latent human immunodeficiency virus.
The human immunodeficiency virus, HIV (formerly T-cell lymphotropic virus type III, HTLV-III or lymphadenopathy-associated virus, LAV) is the primary cause of AIDS (acquired immune deficiency syndrome). Patients with AIDS have profound immunosuppression as a result of almost complete absence of the OKT4+ cell population and are predisposed to a number of opportunistic infections as well as to certain malignant diseases such as Kaposi's sarcoma and B-cell tumours. The majority of the opportunistic infections observed in AIDS patients are from the herpesvirus group and these are frequently the cause of death in AIDS patients. We have therefore investigated the effect of herpes virus infection on the expression of HIV and we provide evidence that herpes simplex virus type I (HSV-I) can reactivate transcription of latent HIV. In OKT4+ human T-cells HIV replicates to high virus titres, resulting in high level expression of viral RNA. This high level of expression has been attributed to virus-associated trans-acting factors that increase gene expression, directed by the HIV long terminal repeats (LTR), post-transcriptionally. In our studies we have tested whether transcription directed by the LTR of HIV is stimulated by HSV-I.
D000911:Antibodies, Monoclonal; D004279:DNA, Viral / Q000032:analysis; D004591:Electrophoresis, Polyacrylamide Gel; D005786:Gene Expression Regulation; D006678:HIV / Q000235:genetics*; D006801:Humans; D012367:RNA, Viral / Q000378:metabolism; D012091:Repetitive Sequences, Nucleic Acid; D018139:Simplexvirus / Q000235:genetics*; D014158:Transcription, Genetic
D000911:Antibodies, Monoclonal; D004279:DNA, Viral; D012367:RNA, Viral