Knockout of the Host Resistance Gene Pkr Fully Restores Replication of Murine Cytomegalovirus m142 and m143 Mutants In Vivo | Zendy

Eléonore Ostermann | Zendy; Gabriele Warnecke | Zendy; Zoe Waibler | Zendy; Wolfram Brune | Zendy

Open Access

Knockout of the Host Resistance Gene Pkr Fully Restores Replication of Murine Cytomegalovirus m142 and m143 Mutants In Vivo

Author(s) -

Eléonore Ostermann,

Gabriele Warnecke,

Zoe Waibler,

Wolfram Brune

Publication year - 2015

Publication title -

journal of virology

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 2.617

H-Index - 292

eISSN - 1070-6321

pISSN - 0022-538X

DOI - 10.1128/jvi.02003-15

Subject(s) - biology , protein kinase r , gene knockout , viral replication , human cytomegalovirus , virology , mutant , knockout mouse , gene , antiviral protein , protein kinase a , microbiology and biotechnology , rna , virus , kinase , genetics , mitogen activated protein kinase kinase

Murine cytomegalovirus (MCMV) proteins m142 and m143 are essential for viral replication. They bind double-stranded RNA and prevent protein kinase R-induced protein synthesis shutoff. Whether the two viral proteins have additional functions such as their homologs in human cytomegalovirus do remained unknown. We show that MCMV m142 and m143 knockout mutants attain organ titers equivalent to those attained by wild-type MCMV in Pkr knockout mice, suggesting that these viral proteins do not encode additional PKR-independent functions relevant for pathogenesis in vivo.

The content you want is available to Zendy users.

Already have an account? Click here to sign in.

Having issues? You can contact us here

Accelerating Research