Remodelling of the nuclear lamina during human cytomegalovirus infection: role of the viral proteins pUL50 and pUL53.

摘要: A fundamental step in the efficient production of human cytomegalovirus (HCMV) progeny is viral egress from nucleus to cytoplasm infected cells. In family Herpesviridae, this process involves alteration nuclear lamina components by two highly conserved proteins, whose homologues HCMV are named pUL50 and pUL53. This study showed that infection induced mislocalization lamins pUL53 play a role event. At late stages infection, both lamin A/C B an irregular distribution on rim, coincident with areas accumulation. No variations total amount could be detected, supporting view induces qualitative, rather than quantitative, these cellular components, as has been suggested previously for other herpesviruses. Interestingly, pUL53, absence products, localized diffusely nucleus, whilst co-expression interaction its partner, pUL50, restored rim localization distinct patches, thus indicating sufficient induce observed during virus infection. Importantly, analysis presence pUL50–pUL53 complexes at boundary products proteins were promote alterations lamins, strongly resembling those These results suggest may important exit virions inducing structural modifications lamina.