Jaturong SewatanonPaul D. LingBaylor College of MedicineMahidol University2018-11-092018-11-092014-01-01Journal of Virology. Vol.88, No.6 (2014), 3591-3597109855140022538X2-s2.0-84894545833https://repository.li.mahidol.ac.th/handle/20.500.14594/34023The 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. © 2014, American Society for Microbiology.Mahidol UniversityImmunology and MicrobiologyArticleSCOPUS10.1128/JVI.03081-13