Interplay between autophagy and herpes simplex virus type 1: ICP34.5, one of the main actors
EntityUAM. Departamento de Biología Molecular
10.3390/ijms232113643International Journal of Molecular Sciences 23.21 (2022): 13643
ISSN1661-6596 (print); 1422-0067 (online)
ProjectGobierno de España. PID2019-110570GB-I00
SubjectsAutophagy; Herpes Simplex; Herpesvirus 1, Human; Virus Replication; Antivirus Agent; Viral Proteins; Biología y Biomedicina / Biología
Rights© 2022 by the authors
Esta obra está bajo una Licencia Creative Commons Atribución 4.0 Internacional.
Herpes simplex virus type 1 (HSV-1) is a neurotropic virus that occasionally may spread to the central nervous system (CNS), being the most common cause of sporadic encephalitis. One of the main neurovirulence factors of HSV-1 is the protein ICP34.5, which although it initially seems to be relevant only in neuronal infections, it can also promote viral replication in non-neuronal cells. New ICP34.5 functions have been discovered during recent years, and some of them have been questioned. This review describes the mechanisms of ICP34.5 to control cellular antiviral responses and debates its most controversial functions. One of the most discussed roles of ICP34.5 is autophagy inhibition. Although autophagy is considered a defense mechanism against viral infections, current evidence suggests that this antiviral function is only one side of the coin. Different types of autophagic pathways interact with HSV-1 impairing or enhancing the infection, and both the virus and the host cell modulate these pathways to tip the scales in its favor. In this review, we summarize the recent progress on the interplay between autophagy and HSV-1, focusing on the intricate role of ICP34.5 in the modulation of this pathway to fight the battle against cellular defenses
Google Scholar:Ripa Peralta, Inés - Andreu Satué, Sabina - López Guerrero, José Antonio - Bello-Morales Arroyo, Ángeles Raquel
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