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The cell membrane regulates many physiological processes including cellular communication,homing and metabolism. It is therefore not surprising that the composition of the host cell membrane is manipulated by intracellular pathogens. Among these, the human oncogenic herpesviruses Epstein–Barr virus(EBV) and Kaposi’s sarcoma-associated herpesvirus(KSHV)exploit the host cell membrane to avoid immune surveillance and promote viral replication.Accumulating evidence has shown that both EBV and KSHV directly encode several similar membrane-associated proteins, including receptors and receptor-specific ligands(cytokines and chemokines), to increase virus fitness in spite of host antiviral immune responses. These proteins are expressed individually at different phases of the EBV/KSHV life cycle and employ various mechanisms to manipulate the host cell membrane. In recent decades, much effort has been made to address how these membrane-based signals contribute to viral tumorigenesis. In this review, we summarize and highlight the recent understanding of how EBV and KSHV similarly manipulate host cell membrane signals, particularly how remodeling of the cell membrane allows EBV and KSHV to avoid host antiviral immune responses and favors their latent and lytic infection.
The cell membrane regulates many physiological processes including cellular communication, homing and metabolism. It is therefore not not surprising that the composition of the host cell membrane is manipulated by intracellular pathogens. Among these, the human oncogenic herpesviruses Epstein- Barr virus (EBV) and Kaposi’s A colonum of evidence that has both both EBV and KSHV directly encode several similar membrane-associated proteins, including receptors and receptor-specific ligands (cytokines and chemokines ), to increase virus fitness in spite of host antiviral immune responses. These proteins are expressed individually at different phases of the EBV / KSHV life cycle and employ various mechanisms to manipulate the host cell membrane. In recent decades, much effort has been made to address how these membrane-based signals contribute to viral tumorigenesis. In this review, we summarize and highlight the recent understanding of how EBV and KSHV species manipulate host cell membrane signals, particularly how remodeling of the cell membrane allows EBV and KSHV to avoid host antiviral immune responses and favors their latent and lytic infections.