Parvovirus minute virus of mice induces a DNA damage response that facilitates viral replication.

Infection by DNA viruses can elicit DNA damage responses (DDRs) in host cells. In some cases the DDR presents a block to viral replication that must be overcome, and in other cases the infecting agent exploits the DDR to facilitate replication. We find that low multiplicity infection with the autono...

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Autores principales:	Richard O Adeyemi, Sebastien Landry, Meredith E Davis, Matthew D Weitzman, David J Pintel
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2010
Materias:	Immunologic diseases. Allergy RC581-607 Biology (General) QH301-705.5
Acceso en línea:	https://doaj.org/article/6bf81769819e4433a09e7f932d152cd7
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spelling	oai:doaj.org-article:6bf81769819e4433a09e7f932d152cd72021-11-18T06:03:50ZParvovirus minute virus of mice induces a DNA damage response that facilitates viral replication.1553-73661553-737410.1371/journal.ppat.1001141https://doaj.org/article/6bf81769819e4433a09e7f932d152cd72010-10-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/20949077/?tool=EBIhttps://doaj.org/toc/1553-7366https://doaj.org/toc/1553-7374Infection by DNA viruses can elicit DNA damage responses (DDRs) in host cells. In some cases the DDR presents a block to viral replication that must be overcome, and in other cases the infecting agent exploits the DDR to facilitate replication. We find that low multiplicity infection with the autonomous parvovirus minute virus of mice (MVM) results in the activation of a DDR, characterized by the phosphorylation of H2AX, Nbs1, RPA32, Chk2 and p53. These proteins are recruited to MVM replication centers, where they co-localize with the main viral replication protein, NS1. The response is seen in both human and murine cell lines following infection with either the MVMp or MVMi strains. Replication of the virus is required for DNA damage signaling. Damage response proteins, including the ATM kinase, accumulate in viral-induced replication centers. Using mutant cell lines and specific kinase inhibitors, we show that ATM is the main transducer of the signaling events in the normal murine host. ATM inhibitors restrict MVM replication and ameliorate virus-induced cell cycle arrest, suggesting that DNA damage signaling facilitates virus replication, perhaps in part by promoting cell cycle arrest. Thus it appears that MVM exploits the cellular DNA damage response machinery early in infection to enhance its replication in host cells.Richard O AdeyemiSebastien LandryMeredith E DavisMatthew D WeitzmanDavid J PintelPublic Library of Science (PLoS)articleImmunologic diseases. AllergyRC581-607Biology (General)QH301-705.5ENPLoS Pathogens, Vol 6, Iss 10, p e1001141 (2010)
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 Richard O Adeyemi Sebastien Landry Meredith E Davis Matthew D Weitzman David J Pintel Parvovirus minute virus of mice induces a DNA damage response that facilitates viral replication.
description	Infection by DNA viruses can elicit DNA damage responses (DDRs) in host cells. In some cases the DDR presents a block to viral replication that must be overcome, and in other cases the infecting agent exploits the DDR to facilitate replication. We find that low multiplicity infection with the autonomous parvovirus minute virus of mice (MVM) results in the activation of a DDR, characterized by the phosphorylation of H2AX, Nbs1, RPA32, Chk2 and p53. These proteins are recruited to MVM replication centers, where they co-localize with the main viral replication protein, NS1. The response is seen in both human and murine cell lines following infection with either the MVMp or MVMi strains. Replication of the virus is required for DNA damage signaling. Damage response proteins, including the ATM kinase, accumulate in viral-induced replication centers. Using mutant cell lines and specific kinase inhibitors, we show that ATM is the main transducer of the signaling events in the normal murine host. ATM inhibitors restrict MVM replication and ameliorate virus-induced cell cycle arrest, suggesting that DNA damage signaling facilitates virus replication, perhaps in part by promoting cell cycle arrest. Thus it appears that MVM exploits the cellular DNA damage response machinery early in infection to enhance its replication in host cells.
format	article
author	Richard O Adeyemi Sebastien Landry Meredith E Davis Matthew D Weitzman David J Pintel
author_facet	Richard O Adeyemi Sebastien Landry Meredith E Davis Matthew D Weitzman David J Pintel
author_sort	Richard O Adeyemi
title	Parvovirus minute virus of mice induces a DNA damage response that facilitates viral replication.
title_short	Parvovirus minute virus of mice induces a DNA damage response that facilitates viral replication.
title_full	Parvovirus minute virus of mice induces a DNA damage response that facilitates viral replication.
title_fullStr	Parvovirus minute virus of mice induces a DNA damage response that facilitates viral replication.
title_full_unstemmed	Parvovirus minute virus of mice induces a DNA damage response that facilitates viral replication.
title_sort	parvovirus minute virus of mice induces a dna damage response that facilitates viral replication.
publisher	Public Library of Science (PLoS)
publishDate	2010
url	https://doaj.org/article/6bf81769819e4433a09e7f932d152cd7
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Parvovirus minute virus of mice induces a DNA damage response that facilitates viral replication.

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