Herpesviruses and retroviruses are distinct taxonomically, yet have the potential for multiple bidirectional interactions. In vitro, these interactions have largely been studied in terms of herpesvirus up-regulation of HIV genome expression and/or transmissibility. This can be demonstrated in vitro through experiments showing transactivation, CD4 up-regulation, Fc receptor induction, pseudotype formation, cytokine production, and antigen presentation. In addition, once HIV has induced immunosuppression several herpesviruses can reactivate, and so cause disease in their own right. The in-vivo correlates of these phenomena are difficult to study in humans but evidence is reviewed to support the concept that herpesviruses may be activating HIV, so that potential clinical benefit could be obtained through the use of antiviral drugs active against herpesviruses. Whether the clinical benefits seen in particular trials could be ascribed to inhibition of herpesvirus disease, or to herpesvirus infection driving HIV pathogenesis, remains a controversial area.
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P. D. Griffiths (1996) studied this question.
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