Analysis of mouse polyomavirus mutants with lesions in the minor capsid proteins
Jazyk angličtina Země Velká Británie, Anglie Médium print
Typ dokumentu srovnávací studie, časopisecké články, práce podpořená grantem
- MeSH
- antigeny virové biosyntéza MeSH
- buněčné linie MeSH
- DNA virů biosyntéza MeSH
- fibroblasty virologie MeSH
- kapsida genetika MeSH
- kodon iniciační MeSH
- kyselina myristová metabolismus MeSH
- mutace MeSH
- myši MeSH
- Polyomavirus genetika imunologie fyziologie MeSH
- replikace DNA MeSH
- replikace viru MeSH
- transfekce MeSH
- virové plášťové proteiny MeSH
- zvířata MeSH
- Check Tag
- myši MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- srovnávací studie MeSH
- Názvy látek
- antigeny virové MeSH
- DNA virů MeSH
- kodon iniciační MeSH
- kyselina myristová MeSH
- virové plášťové proteiny MeSH
- VP2 protein, Polyomavirus MeSH Prohlížeč
Polyomavirus mutants E, Q and H, expressing non-myristylated VP2, were generated by replacing the N-terminal glycine residue with glutamic acid, glutamine or histidine, respectively. Viruses mutated in either VP2 or VP3 translation initiation codons were also prepared. All mutated genomes, when transfected into murine host cells, gave rise to viral particles. Infectivity of VP2- and VP3- viruses, as measured by the number of cells expressing viral antigens, was dramatically diminished, indicative of defects in the early stages of infection. In contrast, the absence of a myristyl moiety on VP2 did not substantially affect the early steps of virus infection. No differences in numbers of cells expressing early or late viral antigens were observed between wild-type (wt) and E or Q myr- viruses during the course of a life cycle. Furthermore, no delay in virus DNA replication was detected. However, when cells were left for longer in culture, the number of infected cells, measured by typical virus bursts, was much lower when mutant rather than wt genomes were used. In situ, cell fractionation studies revealed differences in the interaction of viral particles with host cell structures. The infectivity of mutants was affected not only by loss of the myristyl group on VP2, but also, and to a greater extent, by alterations of the N-terminal amino acid composition.
Citace poskytuje Crossref.org
Mouse polyomavirus infection induces lamin reorganisation