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Published on: October 28, 2019
Interferon-gamma, macrophages, and virus spread after HSV-1 injection
Heather M Cathcart1, Mei Zheng, Jason J Covar
1Department of Cellular Biology and Anatomy, Medical College of Georgia, Augusta, Georgia 30912, USA.
Interferon-gamma and macrophages do not prevent herpes simplex virus type 1 (HSV-1) spread within the mouse eye. The innate immune response in the eye shows redundancy, not relying on a single factor for protection.
Area of Science:
- Ophthalmology
- Virology
- Immunology
Background:
- Herpes simplex virus type 1 (HSV-1) infection in the anterior chamber (AC) of the eye causes inflammation but typically does not spread to the posterior segment.
- The mechanisms preventing HSV-1 spread from the anterior to the posterior of the eye are not fully understood.
Purpose of the Study:
- To investigate the role of interferon-gamma (IFN-γ) and Mac-1(+) cells in preventing the direct anterior-to-posterior spread of HSV-1 within the injected eye.
- To determine if these factors influence the location or timing of viral spread.
Main Methods:
- BALB/c mice received uniocular AC injections of HSV-1.
- Interferon (IFN)-α, IFN-β, and IFN-γ localization and mRNA expression were analyzed using immunofluorescence and qPCR.
- HSV-1 spread was examined in IFN-γ knockout mice and macrophage-depleted mice.
Main Results:
- IFN-α, IFN-β, and IFN-γ were detected in the anterior segment of infected eyes up to 72 hours post-infection.
- Increased mRNA levels of IFN-β and IFN-γ were observed 48-120 hours after infection.
- Absence of IFN-γ or macrophages did not alter the sites or timing of HSV-1 spread in the injected eye.
Conclusions:
- Protection of the retina from HSV-1 in the injected eye does not rely on IFN-γ or Mac-1(+) macrophages alone.
- The innate immune response to viral infections in the eye exhibits redundancy, involving multiple protective mechanisms.
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