Abstract
Coronaviruses have brought severe challenges to public health all over the world in the past 20years. SARS-CoV-2, the causative agent of the COVID-19 pandemic that has led to millions of deaths, belongs to the genus beta-coronavirus. Alpha- and beta-coronaviruses encode a unique protein, nonstructural protein 1 (Nsp1) that both suppresses host immune responses and reduces global gene expression levels in the host cells. As a key pathogenicity factor of coronaviruses, Nsp1 redirects the host translation machinery to increase synthesis of viral proteins. Through multiple mechanisms, coronaviruses impede host protein expression through Nsp1, while escaping inhibition to allow the translation of viral RNA. In this review, we discuss current data about suppression of the immune responses and inhibition of protein synthesis induced by coronavirus Nsp1, as well as the prospect of live-attenuated vaccine development with virulence-attenuated viruses with mutations in Nsp1.
Highlights
Three highly pathogenic human coronaviruses have emerged in the last two decades, including severe acute respiratory syndrome coronavirus (SARS-CoV; Ksiazek et al, 2003; Rota et al, 2003), Middle East respiratory syndrome coronavirus (MERS-CoV; Bermingham et al, 2012; Zaki et al, 2012), and severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which caused the worldwide pandemic COVID-19 since late 2019 (Coronaviridae Study Group of the International Committee on Taxonomy of Viruses, 2020)
It has been observed that the SARS-CoV nonstructural protein 1 (Nsp1) binds the small ribosomal subunit (40S) directly during translation initiation and inhibits translation of both endogenous mRNA and exogenous genes, including those, whose translation is initiated by the viral internal ribosome entry site (IRES; Kamitani et al, 2009)
Coronavirus Nsp1, among the first viral proteins to be expressed after virus entering into the host cells, is a major viral pathogenicity factor of the alpha- and beta-CoVs
Summary
Three highly pathogenic human coronaviruses (hCoVs) have emerged in the last two decades, including severe acute respiratory syndrome coronavirus (SARS-CoV; Ksiazek et al, 2003; Rota et al, 2003), Middle East respiratory syndrome coronavirus (MERS-CoV; Bermingham et al, 2012; Zaki et al, 2012), and severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which caused the worldwide pandemic COVID-19 since late 2019 (Coronaviridae Study Group of the International Committee on Taxonomy of Viruses, 2020). It has been observed that the SARS-CoV Nsp1 binds the small ribosomal subunit (40S) directly during translation initiation and inhibits translation of both endogenous mRNA and exogenous genes, including those, whose translation is initiated by the viral internal ribosome entry site (IRES; Kamitani et al, 2009).
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
