Analysis of the relationship between replication of the Hokkaido genotype of Puumala orthohantavirus and autophagy.

Autor: Tamiya K; Laboratory of Public Health, Faculty of Veterinary medicine, Hokkaido University, Sapporo, Japan., Kobayashi S; Laboratory of Public Health, Faculty of Veterinary medicine, Hokkaido University, Sapporo, Japan. Electronic address: shin-kobayashi@vetmed.hokudai.ac.jp., Yoshii K; Laboratory of Public Health, Faculty of Veterinary medicine, Hokkaido University, Sapporo, Japan; National Research Center for the Control and Prevention of Infectious diseases (CCPID), Nagasaki University, Nagasaki, Japan., Kariwa H; Laboratory of Public Health, Faculty of Veterinary medicine, Hokkaido University, Sapporo, Japan.
Jazyk: angličtina
Zdroj: Virus research [Virus Res] 2022 Sep; Vol. 318, pp. 198830. Date of Electronic Publication: 2022 May 28.
DOI: 10.1016/j.virusres.2022.198830
Abstrakt: Hantaviruses are potentially fatal zoonotic pathogens of the family Hantaviridae. No human infection by the Hokkaido genotype of Puumala orthohantavirus (PUUV-Hok) has been reported. However, other PUUV genotypes cause hemorrhagic fever with renal syndrome (HFRS) in humans. Autophagy is a highly conserved lysosomal degradation process in eukaryotic cells that affects the replication of various viruses. In this study, we examined the role of autophagy in PUUV-Hok replication. PUUV-Hok infection induced the expression of LC3-II, an autophagosome marker, and the nucleocapsid protein (NP) of PUUV-Hok was colocalized with punctate structures of LC3. Inhibition of autophagy using an siRNA for Atg5, an autophagy-related gene, increased the replication of PUUV-Hok, whereas an autophagy inducer decreased its replication. Inhibition of lysosomal degradation increased the expression of NP and LC3-II. In summary, autophagy was induced by PUUV-Hok infection, which inhibited PUUV-Hok replication in a manner related to the degradation of the NP in lysosomes.
(Copyright © 2022. Published by Elsevier B.V.)
Databáze: MEDLINE
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