[Molecular dialogue between human retroviruses and host cells]

Abstract

Several exogenous retroviruses are etiologic agents of severe human diseases. Retrovirus replication depends on a plethora of highly specific interactions with the host cell resulting in the subversion of multiple cellular signal transduction pathways. Understanding the molecular cross-talk that regulates the relationship between the virus and the host cell is currently the objective of many researchers and should contribute to gain insight into puzzling features of the physiopathology of retrovirus infections. A large body of recent data indicates that retroviruses utilize a variety of unrelated cell surface receptors to initiate infection and modulate the homeostasis of the target cell following receptors binding. As an example, I discuss here the tremendous capacity of HIV-1 envelope glycoproteins to modulate kinases activation and nuclear translocation of transcription factors following binding to surface receptors CD4 and CXCR4. Viral envelope glycoproteins interaction with CD4 controls cell activation and proliferation required for virus production whereas interaction with CXCR4 favors apoptosis thereby decreasing the host immune response.