March 2012
Volume 53, Issue 14
Free
ARVO Annual Meeting Abstract  |   March 2012
Characteristics of Suppressor of Cytokine Signaling (SOCS)1 and SOCS3 Expression in Response to Murine Cytomegalovirus (MCMV) Infection During Health and Retrovirus-Induced Immunosuppression (MAIDS)
Author Affiliations & Notes
  • Christine I. Alston
    Department of Biology, Viral Immunology Center, Georgia State University, Atlanta, Georgia
  • Hsin Chien
    Department of Biology, Viral Immunology Center, Georgia State University, Atlanta, Georgia
  • Emily L. Blalock
    Department of Biology, Viral Immunology Center, Georgia State University, Atlanta, Georgia
  • Richard D. Dix
    Department of Biology, Viral Immunology Center, Georgia State University, Atlanta, Georgia
    Department of Ophthalmology, Emory University School of Medicine, Atlanta, Georgia
  • Footnotes
    Commercial Relationships  Christine I. Alston, None; Hsin Chien, None; Emily L. Blalock, None; Richard D. Dix, None
  • Footnotes
    Support  NIH Grant EY010568, NIH/NEI Core Grant P30/EY006360, Research to Prevent Blindness, and Fight for Sight
Investigative Ophthalmology & Visual Science March 2012, Vol.53, 6227. doi:
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      Christine I. Alston, Hsin Chien, Emily L. Blalock, Richard D. Dix; Characteristics of Suppressor of Cytokine Signaling (SOCS)1 and SOCS3 Expression in Response to Murine Cytomegalovirus (MCMV) Infection During Health and Retrovirus-Induced Immunosuppression (MAIDS). Invest. Ophthalmol. Vis. Sci. 2012;53(14):6227.

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

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Abstract

Purpose: : Suppressor of Cytokine Signaling (SOCS) proteins are induced upon cytokine signaling and act as negative feedback regulators by interfering with the JAK/STAT pathway. Whereas SOCS1 inhibits signaling induced by Type 1 and Type 2 interferon (IFN), SOCS3 inhibits signaling by IL-6 family cytokines. Previous work by us determined that SOCS1 and SOCS3 mRNA and protein levels were significantly upregulated in MCMV-infected eyes of mice with MAIDS during progression of retinitis suggesting a pathogenic role for these cytokine regulators during MAIDS-related MCMV retinitis. Studies were therefore performed to characterize SOCS1 and SOCS3 expression during systemic MCMV infection of healthy mice versus MAIDS mice with focus on splenic cells.

Methods: : Groups of healthy C57BL/6 mice or C57BL/6 mice with MAIDS were injected intraperitonally with MCMV or mock-injected. At 1 - 10 days after injection, splenic cells were collected from all mice and subjected to real time RT-PCR assay for quantification of SOCS1, SOCS3, MCMV IE1, MCMV gH, IFN-β, IFN-γ, and/or IL-6 mRNA levels.

Results: : When compared with splenic cells from mock-infected healthy mice, splenic cells from MCMV-infected healthy mice showed detectable SOCS1 and SOCS3 mRNA levels that peaked significantly at day 2 postinfection (pi), but declined thereafter, and by days 7 and 10 pi were at levels less than those found in mock-infected mice. Splenic cells collected from MAIDS animals with systemic MCMV infection showed a similar pattern of SOCS1 and SOCS3 mRNA synthesis including a significant decrease in mRNA levels late in the course of infection. Splenic cells collected from healthy mice at 2 days pi also showed a significant increase in levels of IFN-γ and IL-6 mRNAs, but not IFN-β mRNA. MCMV infection of splenic cells as assessed by detection of MCMV-specific IE1 and gH mRNAs was observed at days 1 - 4 pi, but was undetectable at days 7 and 10 pi.

Conclusions: : SOCS1 and SOCS3 may play a role in the pathogenesis of systemic MCMV infection during health and MAIDS by affecting IFN-γ and IL-6 production, respectively. Our findings serve to set baseline data for future studies on the mechanism(s) by which SOCS1 and SOCS3 impact onset and progression of MAIDS-related MCMV retinitis.

Keywords: cytomegalovirus • retinitis • microbial pathogenesis: experimental studies 
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