Endoplasmic Reticulum-Shaping Atlastin Proteins Facilitate KSHV Replication

Kaposi's sarcoma-associated herpesvirus (KSHV) has two life cycle modes: the latent and lytic phases. The endoplasmic reticulum (ER) is the site for KSHV production. Furthermore, ER stress can trigger reactivation of KSHV. Little is known about the nature of the ER factors that regulate KSHV re...

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Published inFrontiers in cellular and infection microbiology Vol. 11; p. 790243
Main Authors Long, Wen-Ying, Zhao, Guo-Hua, Wu, Yao
Format Journal Article
LanguageEnglish
Published Switzerland Frontiers Media S.A 13.01.2022
Subjects
atlastin
Cellular and Infection Microbiology
Endoplasmic Reticulum
ER stress
Gene Expression Regulation, Viral
Herpesviridae Infections
Herpesvirus 8, Human - genetics
Humans
KSHV
lytic activation
Virus Activation - physiology
Virus Replication - physiology
ER stress
lytic activation
atlastin
KSHV
endoplasmic reticulum
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Summary:Kaposi's sarcoma-associated herpesvirus (KSHV) has two life cycle modes: the latent and lytic phases. The endoplasmic reticulum (ER) is the site for KSHV production. Furthermore, ER stress can trigger reactivation of KSHV. Little is known about the nature of the ER factors that regulate KSHV replication. Atlastin proteins (ATLs which include ATL1, ATL2, and ATL3) are large dynamin-related GTPases that control the structure and the dynamics of the ER membrane. Here, we show that ATLs can regulate KSHV lytic activation and infection. Overexpression of ATLs enhances KSHV lytic activation, whereas ATLs silence inhibits it. Intriguingly, we find that silencing of ATLs impairs the response of cells to ER stress, and ER stress can promote the lytic activation of KSHV. Our study establishes that ATLs plays a critically regulatory role in KSHV infection, thus expanding the known scope of biological processes controlled by ATLs to include KSHV infection.
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Reviewed by: Henri Gruffat, Institut National de la Santé et de la Recherche Médicale (INSERM), France; Kun Zhang, Virginia Commonwealth University, United States
Edited by: Marc Servant, Université de Montréal, Canada
These authors share first authorship
This article was submitted to Virus and Host, a section of the journal Frontiers in Cellular and Infection Microbiology
ISSN:2235-2988
2235-2988
DOI:10.3389/fcimb.2021.790243