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Influenza A virus-induced autophagy contributes to enhancement of virus infectivity by SOD1 downregulation in alveolar epithelial cells.

Abstract Infection with influenza A virus (IAV) A/WSN/1933 (H1N1) causes oxidative stress and severe lung injury. We have demonstrated that the generation of reactive oxygen species (ROS) during IAV infection is tightly regulated by superoxide dismutase 1 (SOD1) and correlated with viral replication in alveolar epithelial cells. However, the molecular mechanism underlying SOD1 reduction during IAV infection is uncertain. Here we demonstrate that the autophagy pathway is activated by IAV infection and involved in enhanced ROS generation in the early phase of infection. We observed that IAV infection induced autophagic vacuolation, leading to autophagic degradation of cellular proteins, including the protease sensitive antioxidant SOD1. Silencing of the microtubule-associated protein 1A/1B-light chain 3 (LC3) gene in A549 cells supported the critical role of autophagy in the ROS increase. The decrease in viral titer and viral polymerase activity caused by LC3 silencing or the autophagy inhibitor clearly evidenced the involvement of autophagy in the control of ROS generation and viral infectivity. Therefore, we concluded that early stage IAV infection induces autophagic degradation of antioxidant enzyme SOD1, thereby contributing to increased ROS generation and viral infectivity in alveolar epithelial cells.
PMID
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Authors

Mayor MeshTerms
Keywords

Autophagy

Infectivity

Influenza

ROS

SOD1

Journal Title biochemical and biophysical research communications
Publication Year Start




PMID- 29548827
OWN - NLM
STAT- MEDLINE
DCOM- 20180413
LR  - 20180413
IS  - 1090-2104 (Electronic)
IS  - 0006-291X (Linking)
VI  - 498
IP  - 4
DP  - 2018 Apr 15
TI  - Influenza A virus-induced autophagy contributes to enhancement of virus
      infectivity by SOD1 downregulation in alveolar epithelial cells.
PG  - 960-966
LID - S0006-291X(18)30581-3 [pii]
LID - 10.1016/j.bbrc.2018.03.089 [doi]
AB  - Infection with influenza A virus (IAV) A/WSN/1933 (H1N1) causes oxidative stress 
      and severe lung injury. We have demonstrated that the generation of reactive
      oxygen species (ROS) during IAV infection is tightly regulated by superoxide
      dismutase 1 (SOD1) and correlated with viral replication in alveolar epithelial
      cells. However, the molecular mechanism underlying SOD1 reduction during IAV
      infection is uncertain. Here we demonstrate that the autophagy pathway is
      activated by IAV infection and involved in enhanced ROS generation in the early
      phase of infection. We observed that IAV infection induced autophagic
      vacuolation, leading to autophagic degradation of cellular proteins, including
      the protease sensitive antioxidant SOD1. Silencing of the microtubule-associated 
      protein 1A/1B-light chain 3 (LC3) gene in A549cells supported the critical role
      of autophagy in the ROS increase. The decrease in viral titer and viral
      polymerase activity caused by LC3 silencing or the autophagy inhibitor clearly
      evidenced the involvement of autophagy in the control of ROS generation and viral
      infectivity. Therefore, we concluded that early stage IAV infection induces
      autophagic degradation of antioxidant enzyme SOD1, thereby contributing to
      increased ROS generation and viral infectivity in alveolar epithelial cells.
CI  - Copyright (c) 2018 Elsevier Inc. All rights reserved.
FAU - Jung, Kwang Il
AU  - Jung KI
AD  - Department of Life Sciences, Korea University, Seoul 136-701, South Korea.
FAU - Pyo, Chul Woong
AU  - Pyo CW
AD  - Department of Life Sciences, Korea University, Seoul 136-701, South Korea.
FAU - Choi, Sang-Yun
AU  - Choi SY
AD  - Department of Life Sciences, Korea University, Seoul 136-701, South Korea.
      Electronic address: [email protected]
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20180317
PL  - United States
TA  - Biochem Biophys Res Commun
JT  - Biochemical and biophysical research communications
JID - 0372516
RN  - 0 (Microtubule-Associated Proteins)
RN  - 0 (Reactive Oxygen Species)
RN  - 0 (SOD1 protein, human)
RN  - 0 (light chain 3, human)
RN  - EC 1.15.1.1 (Superoxide Dismutase-1)
SB  - IM
MH  - A549 Cells
MH  - Alveolar Epithelial Cells/*enzymology/*virology
MH  - Autophagy/*physiology
MH  - Down-Regulation
MH  - Gene Silencing
MH  - Host-Pathogen Interactions
MH  - Humans
MH  - Influenza A virus/*pathogenicity
MH  - Influenza, Human/*etiology
MH  - Microtubule-Associated Proteins/genetics
MH  - Reactive Oxygen Species
MH  - Superoxide Dismutase-1/*metabolism
OTO - NOTNLM
OT  - *Autophagy
OT  - *Infectivity
OT  - *Influenza
OT  - *ROS
OT  - *SOD1
EDAT- 2018/03/20 06:00
MHDA- 2018/04/14 06:00
CRDT- 2018/03/18 06:00
PHST- 2018/02/15 00:00 [received]
PHST- 2018/03/13 00:00 [accepted]
PHST- 2018/03/20 06:00 [pubmed]
PHST- 2018/04/14 06:00 [medline]
PHST- 2018/03/18 06:00 [entrez]
AID - S0006-291X(18)30581-3 [pii]
AID - 10.1016/j.bbrc.2018.03.089 [doi]
PST - ppublish
SO  - Biochem Biophys Res Commun. 2018 Apr 15;498(4):960-966. doi:
      10.1016/j.bbrc.2018.03.089. Epub 2018 Mar 17.