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Updated: Mar 15, 2026
Dissecting Host-virus Interaction in Lytic Replication of a Model Herpesvirus
Published on: October 7, 2011
Manipulation of the host cell membrane by human γ-herpesviruses EBV and KSHV for pathogenesis
Fang Wei1, Qing Zhu2, Ling Ding2
1Sheng Yushou Center of Cell Biology and Immunology, School of Life Sciences and Biotechnology, Shanghai Jiao Tong University, Shanghai, 200240, China.
Abstract:
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.
Insights
Human oncogenic herpesviruses Epstein-Barr virus (EBV) and Kaposi's sarcoma-associated herpesvirus (KSHV) manipulate host cell membranes. They use viral proteins to evade immune responses, promoting viral replication and tumorigenesis.
Area of Science:
- Virology
- Cell Biology
- Immunology
Background:
- The cell membrane is crucial for cellular functions like communication and metabolism.
- Intracellular pathogens, particularly oncogenic herpesviruses like EBV and KSHV, manipulate host cell membranes.
- These viruses exploit membrane composition to evade immune surveillance and enhance replication.
Purpose of the Study:
- To review and highlight recent findings on how EBV and KSHV manipulate host cell membrane signals.
- To understand the mechanisms by which these viruses remodel cell membranes.
- To elucidate how membrane manipulation aids in immune evasion and viral infection.
Main Methods:
- Review of existing literature on EBV and KSHV interactions with host cell membranes.
- Analysis of viral proteins (receptors, ligands) encoded by EBV and KSHV.
- Examination of viral life cycle phases and their associated membrane manipulation strategies.
Main Results:
- EBV and KSHV encode similar membrane-associated proteins, including receptors and ligands.
- These viral proteins are expressed at different stages of the viral life cycle.
- Membrane remodeling by EBV and KSHV facilitates evasion of host antiviral immunity.
Conclusions:
- EBV and KSHV utilize host cell membrane manipulation as a key strategy for survival and replication.
- Understanding these viral-induced membrane changes is critical for developing antiviral therapies.
- Targeting viral manipulation of cell membrane signals may offer new avenues for cancer treatment.
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