Molecular interactions between human herpesviruses and the human immunodeficiency virus type 1
TL;DRAbstract
Human immunodeficiency virus type 1 (HIV-1) is the etiologic agent that causes acquired immunodeficiency syndrome (AIDS). HIV-1 infected individuals frequently are infected with other viruses, including herpesviruses. Lymphocytic cells infected with both HIV-1 and human herpesvirus 6 (HHV-6), can enhance cytopathic effects caused by viral infection. Previously, several HHV-6 genes have been identified that enhance transcription of HIV-1. Since HIV-1 is capable of trans-activating herpesviruses, a reciprocal interaction between the two viruses is possible. Interactions between HIV-1 and HHV-6 were analyzed in lymphocytes. Dually infected cells show an increased HHV-6 viral titer, an increase in HHV-6 RNA, and an increase in HHV-6 protein synthesis. Similarly, T-cells transfected with the entire HIV proviral genome, or the HIV-1 trans-activator gene, tat, displayed an increase in HHV-6 viral production. The bi-directional interactions between HHV-6 and HIV-1 may accelerate depletion of C
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Human immunodeficiency virus type 1 (HIV-1) is the etiologic agent that causes acquired immunodeficiency syndrome (AIDS). HIV-1 infected individuals frequently are infected with other viruses, including herpesviruses. Lymphocytic cells infected with both HIV-1 and human herpesvirus 6 (HHV-6), can enhance cytopathic effects caused by viral infection. Previously, several HHV-6 genes have been identified that enhance transcription of HIV-1. Since HIV-1 is capable of trans-activating herpesviruses, a reciprocal interaction between the two viruses is possible. Interactions between HIV-1 and HHV-6 were analyzed in lymphocytes. Dually infected cells show an increased HHV-6 viral titer, an increase in HHV-6 RNA, and an increase in HHV-6 protein synthesis. Similarly, T-cells transfected with the entire HIV proviral genome, or the HIV-1 trans-activator gene, tat, displayed an increase in HHV-6 viral production. The bi-directional interactions between HHV-6 and HIV-1 may accelerate depletion of C
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