Dual control of tick-borne encephalitis virus replication by autophagy in mouse macrophages

Result code in IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F60076658%3A12310%2F22%3A43904778" target="_blank" >RIV/60076658:12310/22:43904778 - isvavai.cz</a>

Result on the web

<a href="https://www.sciencedirect.com/science/article/pii/S016817022200106X?via%3Dihub" target="_blank" >https://www.sciencedirect.com/science/article/pii/S016817022200106X?via%3Dihub</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1016/j.virusres.2022.198778" target="_blank" >10.1016/j.virusres.2022.198778</a>

Result language

angličtina

Original language name

Dual control of tick-borne encephalitis virus replication by autophagy in mouse macrophages

Original language description

Autophagy is a lysosomal degradative pathway responsible for recycling cytosolic proteins and organelles and also functions as an innate defense mechanism that host cells use against viral infection. While many viruses have evolved mechanisms to antagonize the antiviral effects of the autophagy pathway, others subvert autophagy to facilitate replication. For flaviviruses, both the positive and negative role of autophagy in virus replication has been reported. The interplay between autophagy and tick-borne encephalitis virus (TBEV) in innate immune cells is largely unknown. Here we report the relationship between an autophagy and TBEV replication in mouse macrophage cell line PMJ2-R using Hypr strain of TBEV. First, we examined the effect of Hypr infection on the autophagy pathway. We detected a mild and a temporary increase of autophagy marker LC3-II in Hypr-infected cells. The role of autophagy in TBEV replication was evaluated in autophagy related gene 5 (Atg5) knockdown cells (shAtg5). Our results showed that during an early stage of Hypr infection the viral titers were increased, while later on, at 72 hpi, the titers have declined in shAtg5 cells compared to control. Moreover, the higher number of virus-positive cells was observed in shAtg5 cells in early stage of infection and correlated with enhanced virus entry. Finally, we found an increased production of IFN-beta in Hypr-infected shAtg5 cells in comparison to control at 48 and 72 hpi implicating that autophagy restricts the amount of IFN produced by TBEV-infected macrophages. To conclude, in mouse macrophages TBEV replication is controlled by autophagy in time dependent manner, having temporally an antiviral and then a pro-viral role during infection. Our study points out to a delicate and complex involvement of autophagy machinery at level of virus entry and IFN-beta production when controlling TBEV infection.

Czech name

—

Czech description

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Type

J_imp - Article in a specialist periodical, which is included in the Web of Science database

CEP classification

—

OECD FORD branch

10607 - Virology

Project

<a href="/en/project/GA19-15678S" target="_blank" >GA19-15678S: The effect of tick saliva and salivary sialostatins on cellular stres responses and its implication to tick-borne enecephalitis virus transmission</a><br>

Continuities

P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)

Publication year

2022

Confidentiality

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Name of the periodical

Virus Research

ISSN

0168-1702

e-ISSN

—

Volume of the periodical

315

Issue of the periodical within the volume

JUL 2 2022

Country of publishing house

NL - THE KINGDOM OF THE NETHERLANDS

Number of pages

8

Pages from-to

nestrankovano

UT code for WoS article

000793363000001

EID of the result in the Scopus database

2-s2.0-85128939697