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Dissecting Host-virus Interaction in Lytic Replication of a Model Herpesvirus
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HSV Replication: Triggering and Repressing STING Functionality.

Eric Krawczyk1, Chase Kangas1, Bin He1

  • 1Department of Microbiology and Immunology, College of Medicine, University of Illinois, Chicago, IL 60612, USA.

Viruses
|January 21, 2023
PubMed
Summary
This summary is machine-generated.

Herpes simplex virus (HSV) evades host immunity by neutralizing the STING pathway, a key antiviral defense. This review explores how HSV interacts with STING, impacting viral replication and disease.

Keywords:
STINGantiviral immunityherpes simplex virusinterferonpathogenesisviral replication

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Area of Science:

  • Immunology
  • Virology
  • Molecular Biology

Background:

  • Herpes simplex virus (HSV) establishes persistent infections through lytic and latent cycles.
  • Host immune responses, including the stimulator of interferon genes (STING) pathway, are crucial for controlling HSV.
  • STING mediates antiviral defenses by inducing interferon (IFN) and IFN-stimulated genes.

Purpose of the Study:

  • To review recent advancements in understanding HSV's interaction with the STING pathway.
  • To elucidate how STING influences HSV replication and pathogenesis.
  • To highlight viral mechanisms that counteract STING-mediated immunity.

Main Methods:

  • Review of existing literature on HSV and STING pathway interactions.
  • Analysis of studies detailing STING activation by viral and host DNA during HSV infection.
  • Examination of viral evasion strategies targeting STING signaling.

Main Results:

  • HSV infection activates STING signaling through viral or host-derived dsDNA.
  • HSV has evolved mechanisms to inhibit or neutralize the STING-mediated antiviral response.
  • STING plays a significant role in controlling HSV replication and disease progression.

Conclusions:

  • The STING pathway is a critical host defense against HSV.
  • HSV actively subverts STING signaling to facilitate its own replication and persistence.
  • Further research into HSV-STING interactions may reveal novel therapeutic targets.