About: A natural polymorphism in Zika virus NS2A protein responsible of virulence in mice

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About: A natural polymorphism in Zika virus NS2A protein responsible of virulence in mice Goto Sponge NotDistinct Permalink

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

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	A natural polymorphism in Zika virus NS2A protein responsible of virulence in mice
Creator	Park, Jun-Gyu Martínez-Sobrido, Luis Nogales, Aitor Márquez-Jurado, Silvia Almazan, Fernando Iborra, Francisco
Source	PMC
abstract	Zika virus (ZIKV) infection is currently one of the major concerns in human public health due to its association with neurological disorders. Intensive effort has been implemented for the treatment of ZIKV, however there are not currently approved vaccines or antivirals available to combat ZIKV infection. In this sense, the identification of virulence factors associated with changes in ZIKV virulence could help to develop safe and effective countermeasures to treat ZIKV or to prevent future outbreaks. Here, we have compared the virulence of two related ZIKV strains from the recent outbreak in Brazil (2015), Rio Grande do Norte Natal (RGN) and Paraiba. In spite of both viruses being identified in the same period of time and region, significant differences in virulence and replication were observed using a validated mouse model of ZIKV infection. While ZIKV-RGN has a 50% mouse lethal dose (MLD(50)) of ~10(5) focus forming units (FFUs), ZIKV-Paraiba infection resulted in 100% of lethality with less than 10 FFUs. Combining deep-sequencing analysis and our previously described infectious ZIKV-RGN cDNA clone, we identified a natural polymorphism in the non-structural protein 2 A (NS2A) that increase the virulence of ZIKV. Moreover, results demonstrate that the single amino acid alanine to valine substitution at position 117 (A117V) in the NS2A was sufficient to convert the attenuated rZIKV-RGN in a virulent Paraiba-like virus (MLD(50) < 10 FFU). The mechanism of action was also evaluated and data indicate that substitution A117V in ZIKV NS2A protein reduces host innate immune responses and viral-induced apoptosis in vitro. Therefore, amino acid substitution A117V in ZIKV NS2A could be used as a genetic risk-assessment marker for future ZIKV outbreaks.
has issue date	2019-12-27(xsd:dateTime)
bibo:doi	10.1038/s41598-019-56291-4
bibo:pmid	31882898
has license	cc-by
sha1sum (hex)	a72473db86f1e26d0d1e6db3e7078a3536b9ba65
schema:url	https://doi.org/10.1038/s41598-019-56291-4
resource representing a document's title	A natural polymorphism in Zika virus NS2A protein responsible of virulence in mice
has PubMed Central identifier	PMC6934710
has PubMed identifier	31882898
schema:publication	Sci Rep
resource representing a document's body	covid:a72473db86f1e26d0d1e6db3e7078a3536b9ba65#body_text
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