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TRPC1 participates in the HSV-1 infection process by facilitating viral entry

Published on Mar 18, 2020in Science Advances11.5
· DOI :10.1126/SCIADV.AAZ3367
Dongxu He9
Estimated H-index: 9
(Jiangnan University),
Aiqin Mao6
Estimated H-index: 6
(Jiangnan University)
+ 6 AuthorsXin Ma20
Estimated H-index: 20
(Jiangnan University)
Abstract
Mammalian transient receptor potential (TRP) channels are major components of Ca2+ signaling pathways and control a diversity of physiological functions. Here, we report a specific role for TRPC1 in the entry of herpes simplex virus type 1 (HSV-1) into cells. HSV-1–induced Ca2+ release and entry were dependent on Orai1, STIM1, and TRPC1. Inhibition of Ca2+ entry or knockdown of these proteins attenuated viral entry and infection. HSV-1 glycoprotein D interacted with the third ectodomain of TRPC1, and this interaction facilitated viral entry. Knockout of TRPC1 attenuated HSV-1–induced ocular abnormality and morbidity in vivo in TRPC1−/− mice. There was a strong correlation between HSV-1 infection and plasma membrane localization of TRPC1 in epithelial cells within oral lesions in buccal biopsies from HSV-1–infected patients. Together, our findings demonstrate a critical role for TRPC1 in HSV-1 infection and suggest the channel as a potential target for anti-HSV therapy.
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