A viral lncRNA tethers HSV-1 genomes at the nuclear periphery to establish viral latency.

Autor:	Grams TR; Department of Molecular Genetics and Microbiology, University of Florida, Gainesville, Florida, USA., Edwards TG; Department of Molecular Genetics and Microbiology, University of Florida, Gainesville, Florida, USA., Bloom DC; Department of Molecular Genetics and Microbiology, University of Florida, Gainesville, Florida, USA.
Jazyk:	angličtina
Zdroj:	Journal of virology [J Virol] 2023 Dec 21; Vol. 97 (12), pp. e0143823. Date of Electronic Publication: 2023 Nov 22.
DOI:	10.1128/jvi.01438-23
Abstrakt:	Importance: Herpes simplex virus 1 (HSV-1) establishes lifelong latency in neuronal cells. Following a stressor, the virus reactivates from latency, virus is shed at the periphery and recurrent disease can occur. During latency, the viral lncRNA termed the latency-associated transcript (LAT) is known to accumulate to high abundance. The LAT is known to impact many aspects of latency though the molecular events involved are not well understood. Here, we utilized a human neuronal cell line model of HSV latency and reactivation (LUHMES) to identify the molecular-binding partners of the LAT during latency. We found that the LAT binds to both the cellular protein, TMEM43, and HSV-1 genomes in LUHMES cells. Additionally, we find that knockdown of TMEM43 prior to infection results in a decreased ability of HSV-1 to establish latency. This work highlights a potential mechanism for how the LAT facilitates the establishment of HSV-1 latency in human neurons. Competing Interests: The authors declare no conflict of interest.
Databáze:	MEDLINE
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