Abstract
The ORF75c tegument protein of murine gammaherpesvirus 68 (MHV68) promotes the degradation of the antiviral promyelocytic leukemia (PML) protein. Surprisingly, MHV68 expressing a degradation-deficient ORF75c replicated in cell culture and in mice similar to the wild-type virus. However, in cells infected with this mutant virus, PML formed novel track-like structures that are induced by ORF61, the viral ribonucleotide reductase large subunit. These findings may explain why ORF75c mutant viruses unable to degrade PML had no demonstrable phenotype after infection.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Cell Line
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Herpesviridae Infections / genetics
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Herpesviridae Infections / metabolism
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Herpesviridae Infections / veterinary*
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Herpesviridae Infections / virology
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Mice
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Nuclear Proteins / genetics
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Nuclear Proteins / metabolism*
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Promyelocytic Leukemia Protein
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Proteolysis
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Rhadinovirus / enzymology*
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Rhadinovirus / genetics
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Ribonucleotide Reductases / genetics
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Ribonucleotide Reductases / metabolism*
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Rodent Diseases / genetics
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Rodent Diseases / metabolism*
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Rodent Diseases / virology*
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Transcription Factors / genetics
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Transcription Factors / metabolism*
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Tumor Suppressor Proteins / genetics
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Tumor Suppressor Proteins / metabolism*
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Viral Proteins / genetics
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Viral Proteins / metabolism*
Substances
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Nuclear Proteins
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Pml protein, mouse
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Promyelocytic Leukemia Protein
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Transcription Factors
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Tumor Suppressor Proteins
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Viral Proteins
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Ribonucleotide Reductases