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Updated: Jun 18, 2026

Identifying Dysregulated Genes Induced by Kaposi's Sarcoma-associated Herpesvirus (KSHV)
Published on: September 14, 2010
Early events in Kaposi's sarcoma-associated herpesvirus infection of target cells
1H.M. Bligh Cancer Research Laboratories, Dept. of Microbiology and Immunology, Chicago Medical School, Rosalind Franklin University of Medicine and Science, North Chicago, Illinois 60064, USA. bala.chandran@rosalindfranklin.edu
Abstract:
Kaposi's sarcoma-associated herpesvirus (KSHV), the most recently identified member of the herpesvirus family, infects a variety of target cells in vitro and in vivo. This minireview surveys current information on the early events of KSHV infection, including virus-receptor interactions, involved envelope glycoproteins, mode of entry, intracellular trafficking, and initial viral and host gene expression programs. We describe data supporting the hypothesis that KSHV manipulates preexisting host cell signaling pathways to allow successful infection. The various signaling events triggered by infection, and their potential roles in the different stages of infection and disease pathogenesis, are summarized.
Insights
Kaposi's sarcoma-associated herpesvirus (KSHV) infection involves early cellular events, including how the virus enters cells and influences host gene expression. KSHV manipulates host cell signaling pathways for successful infection and pathogenesis.
Area of Science:
- Virology
- Cell Biology
- Immunology
Background:
- Kaposi's sarcoma-associated herpesvirus (KSHV) is a significant human pathogen.
- Understanding KSHV's early infection mechanisms is crucial for developing antiviral strategies.
Purpose of the Study:
- To review current knowledge on the early stages of KSHV infection.
- To elucidate the role of host cell signaling pathways in KSHV pathogenesis.
Main Methods:
- Literature review of studies on KSHV infection.
- Analysis of virus-receptor interactions and entry mechanisms.
- Examination of viral and host gene expression during early infection.
Main Results:
- KSHV utilizes specific envelope glycoproteins for cell entry.
- Intracellular trafficking pathways are essential for KSHV infection.
- KSHV actively manipulates host cell signaling pathways to facilitate infection.
Conclusions:
- Early KSHV infection is a complex process involving intricate virus-host interactions.
- Host cell signaling manipulation is a key strategy for KSHV pathogenesis.
- Further research into these early events can inform therapeutic interventions.
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