Skip to main content
U.S. Department of Energy
Office of Scientific and Technical Information

Investigation of host-cell influence on polyomavirus biological activity and the major virus-coded structural protein VP1

Thesis/Dissertation ·
OSTI ID:6997974

The host cell influence on polyomavirus biological activity and modification of the major virus-coded structural protein VP1 was investigated. Polyoma virions resulting from the permissive infections of primary mouse kidney cells, as compared to virus progeny from primary mouse embryo cells, exhibited a ten-fold greater ability to agglutinate guinea pig erythrocytes, a three-fold lower ability to become internalized into monopincytotic vesicles, and a two-fold lower ability to initiate a productive infection based on positive nuclear immunofluorescence when using mouse embryo host cells. Mouse kidney cell progeny were found to bind to host cells less specifically than mouse-embryo cell progeny. Two-dimensional gel electrophoresis of VP1, following in vivo labeling with /sup 32/P, revealed that species D and E of the mouse kidney cell progeny were phosphorylated to the same degree while mouse embryo cell progeny VP1 species E and F were phosphorylated equally. In vivo labeling of polyomavirus with /sup 35/S-sulfate, followed by gel electrophoretic analysis of the structural proteins and two-dimensional chromatographic analysis of the VP1 amino acids revealed that species E and F are modified by sulfation of tyrosine. These data suggest that host cells play a role in modulating biological activity of the virus by affecting the degree and site specific modification of the major capsid protein VP1. Modification of this protein may influence the recognition of virus attachment proteins for specific cellular receptors as well as other biological functions.

Research Organization:
Kansas State Univ., Manhattan (USA)
OSTI ID:
6997974
Country of Publication:
United States
Language:
English