About: Activation of COX-2/PGE(2) Promotes Sapovirus Replication via the Inhibition of Nitric Oxide Production

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About: Activation of COX-2/PGE(2) Promotes Sapovirus Replication via the Inhibition of Nitric Oxide Production Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : covidontheweb.inria.fr associated with source document(s)

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Activation of COX-2/PGE(2) Promotes Sapovirus Replication via the Inhibition of Nitric Oxide Production
Creator	Cho, Kyoung-Oh Kang, Mun-Il Park, Su-Jin Kim, Deok-Song Kwon, Hyung-Jun Park, Jun-Gyu Goodfellow, Ian Baek, Yeong-Bin Cho, Eun-Hyo Choi, Jong-Soon Hosmillo, Myra Kim, Ji-Yun Kwon, Joseph Seo, Ja-Young Soliman, Mahmoud López, Susana Alfajaro, Mia Kang, Lee, Woo Baek, Soliman Cho, Y-B Choi, J-S Kim, J-Y Mm, Alfajaro Park, J-Y Ws, Lee
Source	Medline; PMC
abstract	Enteric caliciviruses in the genera Norovirus and Sapovirus are important pathogens that cause severe acute gastroenteritis in both humans and animals. Cyclooxygenases (COXs) and their final product, prostaglandin E(2) (PGE(2)), are known to play important roles in the modulation of both the host response to infection and the replicative cycles of several viruses. However, the precise mechanism(s) by which the COX/PGE(2) pathway regulates sapovirus replication remains largely unknown. In this study, infection with porcine sapovirus (PSaV) strain Cowden, the only cultivable virus within the genus Sapovirus, markedly increased COX-2 mRNA and protein levels at 24 and 36 h postinfection (hpi), with only a transient increase in COX-1 levels seen at 24 hpi. The treatment of cells with pharmacological inhibitors, such as nonsteroidal anti-inflammatory drugs or small interfering RNAs (siRNAs) against COX-1 and COX-2, significantly reduced PGE(2) production, as well as PSaV replication. Expression of the viral proteins VPg and ProPol was associated with activation of the COX/PGE(2) pathway. We observed that pharmacological inhibition of COX-2 dramatically increased NO production, causing a reduction in PSaV replication that could be restored by inhibition of nitric oxide synthase via the inhibitor N-nitro-l-methyl-arginine ester. This study identified a pivotal role for the COX/PGE(2) pathway in the regulation of NO production during the sapovirus life cycle, providing new insights into the life cycle of this poorly characterized family of viruses. Our findings also reveal potential new targets for treatment of sapovirus infection. IMPORTANCE Sapoviruses are among the major etiological agents of acute gastroenteritis in both humans and animals, but little is known about sapovirus host factor requirements. Here, using only cultivable porcine sapovirus (PSaV) strain Cowden, we demonstrate that PSaV induced the vitalization of the cyclooxygenase (COX) and prostaglandin E(2) (PGE(2)) pathway. Targeting of COX-1/2 using nonsteroidal anti-inflammatory drugs (NSAIDs) such as the COX-1/2 inhibitor indomethacin and the COX-2-specific inhibitors NS-398 and celecoxib or siRNAs targeting COXs, inhibited PSaV replication. Expression of the viral proteins VPg and ProPol was associated with activation of the COX/PGE(2) pathway. We further demonstrate that the production of PGE(2) provides a protective effect against the antiviral effector mechanism of nitric oxide. Our findings uncover a new mechanism by which PSaV manipulates the host cell to provide an environment suitable for efficient viral growth, which in turn can be a new target for treatment of sapovirus infection.
has issue date	2017-01-18(xsd:dateTime)
bibo:doi	10.1128/jvi.01656-16
bibo:pmid	27881647
has license	cc-by
sha1sum (hex)	bd78c67dd1bf9aea39f8fb3a1fe1761628dbe422
schema:url	https://doi.org/10.1128/jvi.01656-16
resource representing a document's title	Activation of COX-2/PGE(2) Promotes Sapovirus Replication via the Inhibition of Nitric Oxide Production
has PubMed Central identifier	PMC5244346
has PubMed identifier	27881647
schema:publication	J Virol
resource representing a document's body	covid:bd78c67dd1bf9aea39f8fb3a1fe1761628dbe422#body_text
is schema:about of	named entity 'sapovirus' named entity 'sapovirus' named entity 'RNAs' named entity 'sapovirus' named entity 'pharmacological' named entity 'genus' named entity 'demonstrate' named entity 'specific' named entity 'Here' named entity 'celecoxib' named entity 'severe' named entity 'porcine' named entity 'strain' named entity 'REPLICATION' named entity 'COX-2' named entity 'HUMANS' named entity 'VIRAL PROTEINS' named entity 'CELLS' named entity 'ANTIVIRAL' named entity 'ANIMALS' named entity 'NS-398' named entity 'TARGETING' named entity 'MAJOR' named entity 'PORCINE' named entity 'ANTI-INFLAMMATORY DRUGS' named entity 'INHIBITOR' named entity 'HOST FACTOR' named entity 'UNKNOWN' named entity 'PROVIDES' named entity 'TURN' named entity 'ROLES' named entity 'FINAL' named entity 'TO PROVIDE' named entity 'VIRUS' named entity 'MECHANISM' named entity 'NITRO' named entity 'PROPOL' named entity 'NO PRODUCTION' named entity 'SEVERE' named entity 'ROLE' named entity 'PHARMACOLOGICAL' named entity 'POTENTIAL' named entity 'FINDINGS' named entity 'VIRAL' named entity 'SIRNAS' named entity 'STUDY' named entity 'PRODUCTION' named entity 'ACTIVATION' named entity 'KNOWN' named entity 'ABOUT' named entity 'TARGETS' named entity 'INFECTION' named entity 'PRODUCT' named entity 'EFFECTOR' named entity 'SEEN' named entity 'HPI'

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