April 2014
Volume 55, Issue 13
Free
ARVO Annual Meeting Abstract  |   April 2014
Stimulation of Suppressor of Cytokine Signaling (SOCS)1 and SOCS3 Expression by Murine Cytomegalovirus (MCMV) Does Not Necessarily Require Productive Virus Replication
Author Affiliations & Notes
  • Christine Iris Alston
    Department of Biology, Georgia State University, Atlanta, GA
  • Hsin Chien
    Department of Biology, Georgia State University, Atlanta, GA
  • Moon Kwon Han
    Department of Biology, Georgia State University, Atlanta, GA
  • Jessica E Fleming
    Department of Biology, Georgia State University, Atlanta, GA
  • Richard D Dix
    Department of Biology, Georgia State University, Atlanta, GA
    Department of Ophthalmology, Emory University School of Medicine, Atlanta, GA
  • Footnotes
    Commercial Relationships Christine Alston, None; Hsin Chien, None; Moon Han, None; Jessica Fleming, None; Richard Dix, None
  • Footnotes
    Support None
Investigative Ophthalmology & Visual Science April 2014, Vol.55, 2822. doi:
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      Christine Iris Alston, Hsin Chien, Moon Kwon Han, Jessica E Fleming, Richard D Dix; Stimulation of Suppressor of Cytokine Signaling (SOCS)1 and SOCS3 Expression by Murine Cytomegalovirus (MCMV) Does Not Necessarily Require Productive Virus Replication. Invest. Ophthalmol. Vis. Sci. 2014;55(13):2822.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Purpose: SOCS family proteins govern the regulation of immune responses to pathogen invasion by a negative feedback regulatory mechanism to dampen cytokine expression and thereby favor pathogenesis and disease development. SOCS1 is an inhibitor of antiviral interferon (IFN-α/β) signaling, whereas SOCS3 regulates signaling by the proinflammatory interleukin-6 (IL-6) cytokine family. We have shown previously that SOCS1 and SOCS3 mRNAs and proteins are robustly upregulated within MCMV-infected eyes of mice susceptible to retinitis during retrovirus-induced immunodeficiency (MAIDS). To determine with greater precision the mechanisms by which MCMV upregulates SOCS1 and SOCS3 expression during MAIDS-related MCMV retinitis, we performed in vitro experiments to determine if SOCS1 and/or SOCS3 expression requires productive (lytic) virus replication.

Methods: Monolayers of IC-21 mouse macrophages or murine embryonic fibroblast (MEF) cells were inoculated with either infectious MCMV (moi = 3), noninfectious UV-inactivated MCMV, or maintenance medium (control), harvested at 10 min to 48 hr postinfection (pi), and compared by quantitative real-time RT-PCR assay for SOCS1 and SOCS3 mRNA production.

Results: MCMV infection of both IC-21 and MEF monolayers resulted in significant upregulation of SOCS1 and SOCS3 mRNA production that peaked between 2 to 6 hr pi. In comparison, inoculation of both cell lines with UV-inactivated MCMV also resulted in upregulation of SOCS1 and SOCS3 mRNA production albeit at lower levels than that observed during MCMV infection.

Conclusions: Although UV-inactivated MCMV stimulated SOCS1 and SOCS3 mRNA production, productive (lytic) MCMV replication resulted in more robust stimulation of SOCS1 and SOCS3 mRNA production. That UV-inactivated MCMV stimulated SOCS1 and SOCS3 mRNA production albeit at moderate levels when compared with infectious MCMV nonetheless suggests a role for parental virus tegument protein(s) in SOCS1 and SOCS3 stimulation.

Keywords: 492 cytomegalovirus • 415 AIDS/HIV • 702 retinitis  
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