5 research outputs found
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SARS-CoV-2 Orf6 hijacks Nup98 to block STAT nuclear import and antagonize interferon signaling.
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the causative agent of the ongoing coronavirus disease 2019 (COVID-19) pandemic that is a serious global health problem. Evasion of IFN-mediated antiviral signaling is a common defense strategy that pathogenic viruses use to replicate and propagate in their host. In this study, we show that SARS-CoV-2 is able to efficiently block STAT1 and STAT2 nuclear translocation in order to impair transcriptional induction of IFN-stimulated genes (ISGs). Our results demonstrate that the viral accessory protein Orf6 exerts this anti-IFN activity. We found that SARS-CoV-2 Orf6 localizes at the nuclear pore complex (NPC) and directly interacts with Nup98-Rae1 via its C-terminal domain to impair docking of cargo-receptor (karyopherin/importin) complex and disrupt nuclear import. In addition, we show that a methionine-to-arginine substitution at residue 58 impairs Orf6 binding to the Nup98-Rae1 complex and abolishes its IFN antagonistic function. All together our data unravel a mechanism of viral antagonism in which a virus hijacks the Nup98-Rae1 complex to overcome the antiviral action of IFN
Recommended from our members
SARS-CoV-2 Orf6 hijacks Nup98 to block STAT nuclear import and antagonize interferon signaling.
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the causative agent of the ongoing coronavirus disease 2019 (COVID-19) pandemic that is a serious global health problem. Evasion of IFN-mediated antiviral signaling is a common defense strategy that pathogenic viruses use to replicate and propagate in their host. In this study, we show that SARS-CoV-2 is able to efficiently block STAT1 and STAT2 nuclear translocation in order to impair transcriptional induction of IFN-stimulated genes (ISGs). Our results demonstrate that the viral accessory protein Orf6 exerts this anti-IFN activity. We found that SARS-CoV-2 Orf6 localizes at the nuclear pore complex (NPC) and directly interacts with Nup98-Rae1 via its C-terminal domain to impair docking of cargo-receptor (karyopherin/importin) complex and disrupt nuclear import. In addition, we show that a methionine-to-arginine substitution at residue 58 impairs Orf6 binding to the Nup98-Rae1 complex and abolishes its IFN antagonistic function. All together our data unravel a mechanism of viral antagonism in which a virus hijacks the Nup98-Rae1 complex to overcome the antiviral action of IFN
Growth curve of Atlantoscia floridana (van Name) (Crustacea, Isopoda, Philosciidae) from a Brazilian Restinga Forest
The terrestrial isopod Atlantoscia floridana (van Name, 1940) occurs from the U.S.A. (Florida) to Brazil and Argentina. In the southernmost Brazilian State, Rio Grande do Sul, the species is recorded in many localities, in urban and in non-urban areas. The growth curve of Atlantoscia floridana based on field data is presented. The specimens were sampled from April, 2000 to October, 2001 at the Reserva Biológica do Lami (RBL), Rio Grande do Sul. Captured individuals were sexed and had their cephalothorax width measured, with the data analyzed with von Bertalanffy's model. The growth curves for males and females are described, respectively, by the equations: Wt = 1.303 [1 - e-0.00941 (t + 50.37)] and Wt = 1.682 [1 - e-0.00575 (t + 59.13)]. The curves showed differential growth between sexes, where females reach a higher Wµ with a slower growth rate. Based on the growth curves it was also possible to estimate life expectancy for males and females.<br>O isópodo terrestre Atlantoscia floridana (van Name, 1940) ocorre desde os Estados Unidos (Flórida) até o Brasil e Argentina. No Rio Grande do Sul a espécie é registrada em muitas localidades, em áreas urbanas e não-urbanas. Este trabalho apresenta a curva de crescimento de Atlantoscia floridana, baseada em dados de campo. Os espécimes foram amostrados desde abril, 2000 a outubro, 2001 na Reserva Biológica do Lami (RBL), Rio Grande do Sul. Os indivíduos capturados foram sexados e tiveram o cefalotórax medido. Os dados foram analisados utilizando-se o modelo de von Bertalanffy. A curva de crescimento para machos e fêmeas são descritas, respectivamente, pelas equações Wt = 1.303 [1 - e-0.00941 (t + 50.37)] e Wt = 1.682 [1 - e -0.00575 (t + 59.13)]. As curvas mostraram crescimento diferencial entre os sexos, onde as fêmeas atingem o maior Wµ com uma taxa de crescimento menor. Com base nas curvas de crescimento também foi possível estimar a expectativa de vida para machos e fêmeas