p53 Activation following Rift Valley fever virus infection contributes to cell death and viral production.

Rift Valley fever virus (RVFV) is an emerging viral zoonosis that is responsible for devastating outbreaks among livestock and is capable of causing potentially fatal disease in humans. Studies have shown that upon infection, certain viruses have the capability of utilizing particular cellular signa...

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Autores principales:	Dana Austin, Alan Baer, Lindsay Lundberg, Nazly Shafagati, Annalise Schoonmaker, Aarthi Narayanan, Taissia Popova, Jean Jacques Panthier, Fatah Kashanchi, Charles Bailey, Kylene Kehn-Hall
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2012
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/18754295d1b048c0a9f6e162e78beb36
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spelling	oai:doaj.org-article:18754295d1b048c0a9f6e162e78beb362021-11-18T07:19:39Zp53 Activation following Rift Valley fever virus infection contributes to cell death and viral production.1932-620310.1371/journal.pone.0036327https://doaj.org/article/18754295d1b048c0a9f6e162e78beb362012-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/22574148/pdf/?tool=EBIhttps://doaj.org/toc/1932-6203Rift Valley fever virus (RVFV) is an emerging viral zoonosis that is responsible for devastating outbreaks among livestock and is capable of causing potentially fatal disease in humans. Studies have shown that upon infection, certain viruses have the capability of utilizing particular cellular signaling pathways to propagate viral infection. Activation of p53 is important for the DNA damage signaling cascade, initiation of apoptosis, cell cycle arrest and transcriptional regulation of multiple genes. The current study focuses on the role of p53 signaling in RVFV infection and viral replication. These results show an up-regulation of p53 phosphorylation at several serine sites after RVFV MP-12 infection that is highly dependent on the viral protein NSs. qRT-PCR data showed a transcriptional up-regulation of several p53 targeted genes involved in cell cycle and apoptosis regulation following RVFV infection. Cell viability assays demonstrate that loss of p53 results in less RVFV induced cell death. Furthermore, decreased viral titers in p53 null cells indicate that RVFV utilizes p53 to enhance viral production. Collectively, these experiments indicate that the p53 signaling pathway is utilized during RVFV infection to induce cell death and increase viral production.Dana AustinAlan BaerLindsay LundbergNazly ShafagatiAnnalise SchoonmakerAarthi NarayananTaissia PopovaJean Jacques PanthierFatah KashanchiCharles BaileyKylene Kehn-HallPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 7, Iss 5, p e36327 (2012)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Dana Austin Alan Baer Lindsay Lundberg Nazly Shafagati Annalise Schoonmaker Aarthi Narayanan Taissia Popova Jean Jacques Panthier Fatah Kashanchi Charles Bailey Kylene Kehn-Hall p53 Activation following Rift Valley fever virus infection contributes to cell death and viral production.
description	Rift Valley fever virus (RVFV) is an emerging viral zoonosis that is responsible for devastating outbreaks among livestock and is capable of causing potentially fatal disease in humans. Studies have shown that upon infection, certain viruses have the capability of utilizing particular cellular signaling pathways to propagate viral infection. Activation of p53 is important for the DNA damage signaling cascade, initiation of apoptosis, cell cycle arrest and transcriptional regulation of multiple genes. The current study focuses on the role of p53 signaling in RVFV infection and viral replication. These results show an up-regulation of p53 phosphorylation at several serine sites after RVFV MP-12 infection that is highly dependent on the viral protein NSs. qRT-PCR data showed a transcriptional up-regulation of several p53 targeted genes involved in cell cycle and apoptosis regulation following RVFV infection. Cell viability assays demonstrate that loss of p53 results in less RVFV induced cell death. Furthermore, decreased viral titers in p53 null cells indicate that RVFV utilizes p53 to enhance viral production. Collectively, these experiments indicate that the p53 signaling pathway is utilized during RVFV infection to induce cell death and increase viral production.
format	article
author	Dana Austin Alan Baer Lindsay Lundberg Nazly Shafagati Annalise Schoonmaker Aarthi Narayanan Taissia Popova Jean Jacques Panthier Fatah Kashanchi Charles Bailey Kylene Kehn-Hall
author_facet	Dana Austin Alan Baer Lindsay Lundberg Nazly Shafagati Annalise Schoonmaker Aarthi Narayanan Taissia Popova Jean Jacques Panthier Fatah Kashanchi Charles Bailey Kylene Kehn-Hall
author_sort	Dana Austin
title	p53 Activation following Rift Valley fever virus infection contributes to cell death and viral production.
title_short	p53 Activation following Rift Valley fever virus infection contributes to cell death and viral production.
title_full	p53 Activation following Rift Valley fever virus infection contributes to cell death and viral production.
title_fullStr	p53 Activation following Rift Valley fever virus infection contributes to cell death and viral production.
title_full_unstemmed	p53 Activation following Rift Valley fever virus infection contributes to cell death and viral production.
title_sort	p53 activation following rift valley fever virus infection contributes to cell death and viral production.
publisher	Public Library of Science (PLoS)
publishDate	2012
url	https://doaj.org/article/18754295d1b048c0a9f6e162e78beb36
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p53 Activation following Rift Valley fever virus infection contributes to cell death and viral production.

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