Virus-lymphocyte interactions: inductive signals necessary to render B lymphocytes susceptible to vesicular stomatitis virus infection.
We examined the inductive signals necessary to render B lymphocytes capable of supporting a productive vesicular stomatitis virus infection. Small murine splenic B cells in the G0 phase of the cell cycle were cultured with stimulators which allow progression through various stages in the activation and/or differentiation pathway leading to antibody secretion. We found that vesicular stomatitis virus expression is dependent on the state of B-cell activation and that three distinct phases can be defined. A nonsupportive state, which is defined by the failure to produce infection centers, viral proteins, or PFUs, is characteristic of freshly isolated small B cells, B cells cultured 48 h without further stimulation, or B cells in the G1 phase of the cell cycle induced by culture with T-cell-derived lymphokines. This refractory state was not due to a failure of virus uptake. Activation of G0 B cells with anti-immunoglobulin at doses which allow entry into the S phase rendered them capable of synthesizing viral proteins and increased the number of B cells producing infection centers, without enhancing PFU production on a per cell basis. In contrast, B cells stimulated with multiple inductive signals provided by anti-immunoglobulin and lymphokines showed increased infectious particle production (7 PFU per infection center). Lipopolysaccharide stimulation, acting through another induction pathway, caused the maximum increase in the number of infected B cells and production of infectious particles (25 PFU per infection center).
Schmidt
M R
MR
Department of Molecular Genetics and Microbiology, University of Massachusetts Medical School, Worcester 01655.
Woodland
R T
RT
D000818:Animals; D001402:B-Lymphocytes / Q000382:microbiology*; D008213:Lymphocyte Activation; D008222:Lymphokines / Q000494:pharmacology; D051379:Mice; D013154:Spleen / Q000166:cytology; D014721:Vesicular stomatitis Indiana virus / Q000254:growth & development*; D014764:Viral Proteins / Q000096:biosynthesis; D014777:Virus Diseases / Q000382:microbiology; D014779:Virus Replication
D008222:Lymphokines; D014764:Viral Proteins