Infection by agnoprotein-negative mutants of polyomavirus JC and SV40 results in the release of virions that are mostly deficient in DNA content

摘要: Background: Human polyomavirus JC (JCV) is the etiologic agent of a brain disease, known as progressive multifocal leukoencephalopathy (PML). The JCV genome encodes small multifunctional phospho-protein, agnoprotein, from late coding region virus, whose regulatory functions in viral replication cycle remain elusive. In this work, functional role and SV40 agnoproteins virion release was investigated using point mutant (Pt) each where ATG codon agnoprotein mutated to abrogate its expression. Results: Analysis both protein expression Pt virus revealed that processes were substantially down-regulated absence compared wild-type (WT) virus. Complementation studies cells, which are constitutively expressing transfected with genome, showed an elevation level DNA near observed for WT. Constitutive large T antigen found be not sufficient compensate loss efficient neither nor vivo. Examination process mutants particles efficiently released infected cells but mostly deficient content. Conclusions: results study provide evidence plays important life cycle. Infection by agnoprotein-negative viruses virions