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Interaction of herpes simplex virus type 2 (HSV-2) glycoprotein D with the host cell surface is sufficient to induce

J Vanover1, J Kintner1, J Whittimore1

  • 1Department of Microbiology, East Tennessee State University, James H. Quillen College of Medicine, Johnson City, TN 37614, USA.

Microbiology (Reading, England)
|January 30, 2010
PubMed

Insights

Herpes simplex virus type 2 (HSV-2) glycoprotein D (gD) interaction with host cells triggers a novel anti-chlamydial response, inducing Chlamydia trachomatis persistence. This persistence is reversible and mediated by HSV-2 gD, not productive viral replication.

Area of Science:

  • Microbiology
  • Virology
  • Cell Biology

Background:

  • Chlamydia trachomatis can enter a viable, non-cultivable persistent state under unfavorable conditions.
  • Previous work established a co-infection model of C. trachomatis and herpes simplex virus type 2 (HSV-2), showing viral co-infection stimulates chlamydial persistence.
  • HSV-induced persistence is not dependent on productive viral replication and is not mediated by known anti-chlamydial pathways.

Purpose of the Study:

  • To investigate the mechanism of HSV-2-induced Chlamydia trachomatis persistence.
  • To determine if HSV-induced chlamydial persistence is reversible.
  • To identify the specific HSV-2 component responsible for inducing chlamydial persistence.

Main Methods:

  • Utilized an in vitro co-infection model with C. trachomatis and HSV-2.
  • Employed UV-inactivated HSV-2 and chemically fixed infected cells to dissect viral and cellular contributions.
  • Used HSV-2 glycoprotein D (gD)-specific neutralizing antibodies and a recombinant HSV-2 gD:Fc fusion protein to assess gD's role.

Main Results:

  • HSV-2-induced chlamydial persistence is reversible, with infectivity recovering within 44 hours of co-infection with UV-inactivated HSV-2.
  • Interaction between HSV-2-infected cells and C. trachomatis induced persistence, suppressing infectious progeny and causing aberrant reticulate body (RB) formation.
  • Neutralizing antibodies against HSV-2 gD and treatment with a soluble HSV-2 gD:Fc fusion protein both prevented or mimicked HSV-2-induced chlamydial persistence.

Conclusions:

  • HSV-2 glycoprotein D interaction with the host cell surface is sufficient to trigger a novel host anti-chlamydial response.
  • This response restricts C. trachomatis development, leading to a persistent state.
  • The findings elucidate a new mechanism of host-pathogen interaction influencing bacterial survival strategies.

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