Title

Virus-lymphocyte interactions: inductive signals necessary to render B lymphocytes susceptible to vesicular stomatitis virus infection

Academic Program

Biochemistry & Molecular Pharmacology

UMMS Affiliation

Graduate School of Biomedical Sciences; Department of Molecular Genetics and Microbiology

Publication Date

1990-07-01

Document Type

Article

Disciplines

Life Sciences | Medicine and Health Sciences

Abstract

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).

Source

J Virol. 1990 Jul;64(7):3289-96.

Journal/Book/Conference Title

Journal of virology

Related Resources

Link to Article in PubMed

PubMed ID

2161942

Link to Full Text

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