September 2016
Volume 57, Issue 12
ARVO Annual Meeting Abstract  |   September 2016
Lessons on immune evasion in the retina by viruses secondary to AIDS
Author Affiliations & Notes
  • Douglas A. Jabs
    Ophthalmology, Icahn School of Medicine at Mount Sinai, New York, New York, United States
    Epidemiology, Johns Hopkins University Bloomberg School of Public Health, Baltimore, Maryland, United States
  • Footnotes
    Commercial Relationships   Douglas Jabs, None
  • Footnotes
    Support  Cooperative agreements from the National Eye Institute, National Institutes of Health, U10 EY08052, U10 EY08057, and U10 EY08067
Investigative Ophthalmology & Visual Science September 2016, Vol.57, No Pagination Specified. doi:
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      Douglas A. Jabs; Lessons on immune evasion in the retina by viruses secondary to AIDS. Invest. Ophthalmol. Vis. Sci. 2016;57(12):No Pagination Specified.

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

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Presentation Description : Human cytomegalovirus (CMV) infection is common, typically manifesting as a “flu-like” illness, followed by establishment of latent infection. CMV uses a variety of mechanisms to evade host immune clearance mechanisms. It downregulates class I expression and interferes with antigen presentation to CD8+ T cells. CMV produces a class I homolog on the surface of infected cells and avoids NK cell clearance. CMV also produces an IL-10 homolog (cmv IL-10h) that binds to the human IL-10 receptor and downregulates Th1 responses, contributing to immune suppression and CMV evasion of the immune response. As such, host CD4+ T cell augmentation of CD8+ T cell and NK responses is required to control CMV infection. With immunodeficiency or immunosuppression, CMV can reactivate and replicate in the blood. Hematogenously disseminated CMV infects vascular endothelial cells in the retina, then retinal cells, resulting in full-thickness retinal destruction, as it spreads to contiguous retinal cells. Although CMV retinitis may occur with immunosuppression, such as for organ transplants and cancer, it most often is seen in the context of the acquired immune deficiency syndrome (AIDS). Human immunodeficiency virus (HIV) CMV interactions contribute to CMV and HIV disease pathogenesis and the increased incidence of CMV retinitis among patients with AIDS vs. other forms of immune compromise. HIV infects CD4+ cells, resulting in depletion of CD4+ T cells, the immunologic hallmark of AIDS. The primary risk of CMV retinitis is a low CD4+ T cell count, typically <50 cells/μL, although low CD8+ T cells also are a risk. HIV and CMV trans-activate each other, which together with CMV’s intrinsic immune suppression, result in increased disease burden from both viruses. Persons infected with HIV and CMV progress to AIDS more rapidly that those infected with HIV only. Among patients with AIDS, CMV retinitis is associated with increased mortality, as are greater amounts of CMV DNA circulating in the blood (CMV load). Treatment of CMV disease with systemic anti-CMV drugs results in improved survival. Sustained antiretroviral therapy-induced immune recovery of CD4+ T cells to >100 cells/μL results in control of CMV retinitis without specific anti-CMV therapy, indicating the importance of the immune response in controlling CMV disease.

This is an abstract that was submitted for the 2016 ARVO Annual Meeting, held in Seattle, Wash., May 1-5, 2016.


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