June 2021
Volume 62, Issue 8
Open Access
ARVO Annual Meeting Abstract  |   June 2021
Optineurin is a novel host defense factor against viral infections of the eye and infection-associated nerve damage
Author Affiliations & Notes
  • Deepak Shukla
    Illinois Eye and Ear Infirmary, Chicago, Illinois, United States
  • Joshua Ames
    Illinois Eye and Ear Infirmary, Chicago, Illinois, United States
  • Tejabhiram Yadavalli
    Illinois Eye and Ear Infirmary, Chicago, Illinois, United States
  • Rahul K Suryawanshi
    Illinois Eye and Ear Infirmary, Chicago, Illinois, United States
  • James Hopkins
    Illinois Eye and Ear Infirmary, Chicago, Illinois, United States
  • Alex Agelidis
    Illinois Eye and Ear Infirmary, Chicago, Illinois, United States
  • Tibor Valyi-Nagy
    Pathology, University of Illinois at Chicago, Chicago, Illinois, United States
  • Footnotes
    Commercial Relationships   Deepak Shukla, None; Joshua Ames, None; Tejabhiram Yadavalli, None; Rahul Suryawanshi, None; James Hopkins, None; Alex Agelidis, None; Tibor Valyi-Nagy, None
  • Footnotes
    Support  NIH grants: R01EY029426; R01EY024710; P30EY001792
Investigative Ophthalmology & Visual Science June 2021, Vol.62, 2689. doi:
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      Deepak Shukla, Joshua Ames, Tejabhiram Yadavalli, Rahul K Suryawanshi, James Hopkins, Alex Agelidis, Tibor Valyi-Nagy; Optineurin is a novel host defense factor against viral infections of the eye and infection-associated nerve damage. Invest. Ophthalmol. Vis. Sci. 2021;62(8):2689.

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

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Abstract

Purpose : Our main goal was to identify intrinsic host factors responsible for defending against viral infections of the eye. We used herpes simplex virus-1 (HSV-1) as a model virus to characterize a mammalian protein, optineurin. Optineurin is a glaucoma-associated gene, and mutations in this gene are also commonly reported in many other neurodegenerative diseases.

Methods : Cell types including human corneal epithelial, HeLa, Vero cells as well as primary cultures of neurons were used for infection with various HSV-1 strains. Viral plaque assays, viral genome counts by real-time PCR, and virus growth was estimated over time using time lapse fluorescence microscopy. TIRF/Super-resolution microscopy was used to demonstrate degradation of HSV-1 proteins and HSV-1 xenophagy. Immunohistochemistry was performed to detect optineurin localization in postmortem human nervous system tissues from patients with HSV encephalitis and ALS disease. Flow cytometry was performed to estimate cell death. Novel object recognition test was used to determine cognitive decline in mice.

Results : We provide the very first evidence that lack of optineurin results in measurably enhanced HSV-1 infection of the cells of ocular and non-ocular origins. We demonstrate that optineurin selectively binds to and degrades HSV-1 viral proteins via autophagy. In addition to selective degradation of HSV-1 proteins, optineurin may potentially participate in xenophagy of HSV-1 virions, which significantly restricts viral spread in wild-type compared to optineurin knockout cells. Loss of optineurin in intact animals demonstrates a more robust effect on nerve damage and potential loss of optimal vision in HSV-1 infected eyes. These animals show significantly reduced corneal sensitivity and succumb to HSV-1 infection due to rapid onset of encephalitis. Most interestingly, HSV-1 infected animals lacking optineurin show significantly lower scores in object recognition tests, suggesting a rapid loss of cognitive functions compared to wild-type animals

Conclusions : Optineurin is an important host defense factor that prevents severe damage to corneal cells and innervating nerves as well as the brain upon HSV-1 infection. Ours may be the first demonstration to explain an important protective role for this protein in infection as well as neurodegeneration.

This is a 2021 ARVO Annual Meeting abstract.

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