Human parainfluenza virus type 1 regulates cholesterol biosynthesis and establishes quiescent infection in human airway cells.

Human parainfluenza virus type 1 (hPIV1) and 3 (hPIV3) cause seasonal epidemics, but little is known about their interaction with human airway cells. In this study, we determined cytopathology, replication, and progeny virion release from human airway cells during long-term infection in vitro. Both...

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Autores principales:	Yuki Kurebayashi, Shringkhala Bajimaya, Masahiro Watanabe, Nicholas Lim, Michael Lutz, Megan Dunagan, Toru Takimoto
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2021
Materias:	Immunologic diseases. Allergy RC581-607 Biology (General) QH301-705.5
Acceso en línea:	https://doaj.org/article/281ac0e84f124cd19fb45c37104a36e9
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spelling	oai:doaj.org-article:281ac0e84f124cd19fb45c37104a36e92021-12-02T20:00:10ZHuman parainfluenza virus type 1 regulates cholesterol biosynthesis and establishes quiescent infection in human airway cells.1553-73661553-737410.1371/journal.ppat.1009908https://doaj.org/article/281ac0e84f124cd19fb45c37104a36e92021-09-01T00:00:00Zhttps://doi.org/10.1371/journal.ppat.1009908https://doaj.org/toc/1553-7366https://doaj.org/toc/1553-7374Human parainfluenza virus type 1 (hPIV1) and 3 (hPIV3) cause seasonal epidemics, but little is known about their interaction with human airway cells. In this study, we determined cytopathology, replication, and progeny virion release from human airway cells during long-term infection in vitro. Both viruses readily established persistent infection without causing significant cytopathic effects. However, assembly and release of hPIV1 rapidly declined in sharp contrast to hPIV3 due to impaired viral ribonucleocapsid (vRNP) trafficking and virus assembly. Transcriptomic analysis revealed that both viruses induced similar levels of type I and III IFNs. However, hPIV1 induced specific ISGs stronger than hPIV3, such as MX2, which bound to hPIV1 vRNPs in infected cells. In addition, hPIV1 but not hPIV3 suppressed genes involved in lipid biogenesis and hPIV1 infection resulted in ubiquitination and degradation of 3-hydroxy-3-methylglutaryl-coenzyme A reductase, a rate limiting enzyme in cholesterol biosynthesis. Consequently, formation of cholesterol-rich lipid rafts was impaired in hPIV1 infected cells. These results indicate that hPIV1 is capable of regulating cholesterol biogenesis, which likely together with ISGs contributes to establishment of a quiescent infection.Yuki KurebayashiShringkhala BajimayaMasahiro WatanabeNicholas LimMichael LutzMegan DunaganToru TakimotoPublic Library of Science (PLoS)articleImmunologic diseases. AllergyRC581-607Biology (General)QH301-705.5ENPLoS Pathogens, Vol 17, Iss 9, p e1009908 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Immunologic diseases. Allergy RC581-607 Biology (General) QH301-705.5
spellingShingle	Immunologic diseases. Allergy RC581-607 Biology (General) QH301-705.5 Yuki Kurebayashi Shringkhala Bajimaya Masahiro Watanabe Nicholas Lim Michael Lutz Megan Dunagan Toru Takimoto Human parainfluenza virus type 1 regulates cholesterol biosynthesis and establishes quiescent infection in human airway cells.
description	Human parainfluenza virus type 1 (hPIV1) and 3 (hPIV3) cause seasonal epidemics, but little is known about their interaction with human airway cells. In this study, we determined cytopathology, replication, and progeny virion release from human airway cells during long-term infection in vitro. Both viruses readily established persistent infection without causing significant cytopathic effects. However, assembly and release of hPIV1 rapidly declined in sharp contrast to hPIV3 due to impaired viral ribonucleocapsid (vRNP) trafficking and virus assembly. Transcriptomic analysis revealed that both viruses induced similar levels of type I and III IFNs. However, hPIV1 induced specific ISGs stronger than hPIV3, such as MX2, which bound to hPIV1 vRNPs in infected cells. In addition, hPIV1 but not hPIV3 suppressed genes involved in lipid biogenesis and hPIV1 infection resulted in ubiquitination and degradation of 3-hydroxy-3-methylglutaryl-coenzyme A reductase, a rate limiting enzyme in cholesterol biosynthesis. Consequently, formation of cholesterol-rich lipid rafts was impaired in hPIV1 infected cells. These results indicate that hPIV1 is capable of regulating cholesterol biogenesis, which likely together with ISGs contributes to establishment of a quiescent infection.
format	article
author	Yuki Kurebayashi Shringkhala Bajimaya Masahiro Watanabe Nicholas Lim Michael Lutz Megan Dunagan Toru Takimoto
author_facet	Yuki Kurebayashi Shringkhala Bajimaya Masahiro Watanabe Nicholas Lim Michael Lutz Megan Dunagan Toru Takimoto
author_sort	Yuki Kurebayashi
title	Human parainfluenza virus type 1 regulates cholesterol biosynthesis and establishes quiescent infection in human airway cells.
title_short	Human parainfluenza virus type 1 regulates cholesterol biosynthesis and establishes quiescent infection in human airway cells.
title_full	Human parainfluenza virus type 1 regulates cholesterol biosynthesis and establishes quiescent infection in human airway cells.
title_fullStr	Human parainfluenza virus type 1 regulates cholesterol biosynthesis and establishes quiescent infection in human airway cells.
title_full_unstemmed	Human parainfluenza virus type 1 regulates cholesterol biosynthesis and establishes quiescent infection in human airway cells.
title_sort	human parainfluenza virus type 1 regulates cholesterol biosynthesis and establishes quiescent infection in human airway cells.
publisher	Public Library of Science (PLoS)
publishDate	2021
url	https://doaj.org/article/281ac0e84f124cd19fb45c37104a36e9
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Human parainfluenza virus type 1 regulates cholesterol biosynthesis and establishes quiescent infection in human airway cells.

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