Analysis of protein synthesis by two-dimensional gel electrophoresis in T cells persistently infected with coxsackie B virus.
Coxsackie B viruses (CBV) have been implicated in various human diseases that present as either limited acute infections or prolonged chronic infections. A number of investigations have suggested that a virus-induced immune dysfunction might play a role in in vivo pathogenesis. In the current study, we describe CBV infection of two human T cell-derived cell lines (Jurkat and MOLT-4 cells) as potential models for CBV infection of lymphocytes. Short term (up to 144 h post-infection) CBV infection of either cell line resulted in a decline in the viability of the cell population together with an approximate 10-fold rise in the titre of infectious virus during the period of incubation. Analyses of the intracellular proteins by two-dimensional polyacrylamide gel electrophoresis (2-D PAGE) demonstrated that although putative virus proteins were detectable there was minimal inhibition of the cellular protein synthesis following CBV infection. This contrasted with the more permissive and highly lytic CBV infection of HEp-2C cells (Cash, Electrophoresis 1991, 10, 793-800). Persistently infected cell lines from both Jurkat and MOLT-4 cells (piJURKAT-3673 and piMOLT-2667 cells) were established. Analyses of intracellular protein synthesis of these persistently infected cell lines showed the synthesis of novel proteins not detected for the corresponding uninfected parental cell line. There were no significant alterations in overall cellular protein synthesis detectable by the small format 2-D PAGE system employed in these investigations. The data presented in the current investigation will contribute towards studies on virus-induced responses of specific biological functions associated with T cells.
Gimenez
B
B
Department of Molecular and Cell Biology, University of Aberdeen, Marischal College, UK.
Amarasekera
D
D
Argo
E
E
Cash
P
P
D002460:Cell Line; D015180:Electrophoresis, Gel, Two-Dimensional; D029822:Enterovirus B, Human / Q000502:physiology*; D006801:Humans; D014176:Protein Biosynthesis; D013601:T-Lymphocytes / Q000378:metabolism* / Q000821:virology*; D014779:Virus Replication