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10.1128/JVI.03571-13

http://scihub22266oqcxt.onion/10.1128/JVI.03571-13
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24478444!3993736!24478444
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suck abstract from ncbi


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pmid24478444      J+Virol 2014 ; 88 (8): 4251-64
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  • Attenuation and restoration of severe acute respiratory syndrome coronavirus mutant lacking 2 -o-methyltransferase activity #MMPMID24478444
  • Menachery VD; Yount BL Jr; Josset L; Gralinski LE; Scobey T; Agnihothram S; Katze MG; Baric RS
  • J Virol 2014[Apr]; 88 (8): 4251-64 PMID24478444show ga
  • The sudden emergence of severe acute respiratory syndrome coronavirus (SARS-CoV) in 2002 and, more recently, Middle Eastern respiratory syndrome CoV (MERS-CoV) underscores the importance of understanding critical aspects of CoV infection and pathogenesis. Despite significant insights into CoV cross-species transmission, replication, and virus-host interactions, successful therapeutic options for CoVs do not yet exist. Recent identification of SARS-CoV NSP16 as a viral 2'-O-methyltransferase (2'-O-MTase) led to the possibility of utilizing this pathway to both attenuate SARS-CoV infection and develop novel therapeutic treatment options. Mutations were introduced into SARS-CoV NSP16 within the conserved KDKE motif and effectively attenuated the resulting SARS-CoV mutant viruses both in vitro and in vivo. While viruses lacking 2'-O-MTase activity had enhanced sensitivity to type I interferon (IFN), they were not completely restored in their absence in vivo. However, the absence of either MDA5 or IFIT1, IFN-responsive genes that recognize unmethylated 2'-O RNA, resulted in restored replication and virulence of the dNSP16 mutant virus. Finally, using the mutant as a live-attenuated vaccine showed significant promise for possible therapeutic development against SARS-CoV. Together, the data underscore the necessity of 2'-O-MTase activity for SARS-CoV pathogenesis and identify host immune pathways that mediate this attenuation. In addition, we describe novel treatment avenues that exploit this pathway and could potentially be used against a diverse range of viral pathogens that utilize 2'-O-MTase activity to subvert the immune system. IMPORTANCE: Preventing recognition by the host immune response represents a critical aspect necessary for successful viral infection. Several viruses, including SARS-CoV, utilize virally encoded 2'-O-MTases to camouflage and obscure their viral RNA from host cell sensing machinery, thus preventing recognition and activation of cell intrinsic defense pathways. For SARS-CoV, the absence of this 2'-O-MTase activity results in significant attenuation characterized by decreased viral replication, reduced weight loss, and limited breathing dysfunction in mice. The results indicate that both MDA5, a recognition molecule, and the IFIT family play an important role in mediating this attenuation with restored virulence observed in their absence. Understanding this virus-host interaction provided an opportunity to design a successful live-attenuated vaccine for SARS-CoV and opens avenues for treatment and prevention of emerging CoVs and other RNA virus infections.
  • |Adaptor Proteins, Signal Transducing[MESH]
  • |Amino Acid Motifs[MESH]
  • |Animals[MESH]
  • |Carrier Proteins/genetics/metabolism[MESH]
  • |DEAD-box RNA Helicases/genetics/metabolism[MESH]
  • |Female[MESH]
  • |Humans[MESH]
  • |Interferon-Induced Helicase, IFIH1[MESH]
  • |Male[MESH]
  • |Methyltransferases/chemistry/genetics/*metabolism[MESH]
  • |Mice[MESH]
  • |Mice, Inbred BALB C[MESH]
  • |Mice, Inbred C57BL[MESH]
  • |Mutation[MESH]
  • |RNA-Binding Proteins[MESH]
  • |Severe Acute Respiratory Syndrome/genetics/metabolism/*virology[MESH]
  • |Severe acute respiratory syndrome-related coronavirus/*enzymology/genetics/pathogenicity/physiology[MESH]
  • |Viral Nonstructural Proteins/chemistry/genetics/*metabolism[MESH]
  • |Virulence[MESH]


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