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Epstein-Barr virus internalization and infectivity are blocked by selective protein kinase C inhibitors
M Cirone1, A Angeloni, G Barile
1Dipartimento di Medicina Sperimentale, Università La Sapienza, Rome, italy.
Abstract:
Selective protein kinase C inhibitors can either block or significantly reduce Epstein-Barr virus infectivity: inhibition of transformation and decreased 3H-thymidine (3H-TdR) incorporation in human B lymphocytes infected with B95-8 EBV, as well as a significant reduction in the induction of early antigens in Raji cells superinfected by P3HRI EBV was achieved by pre-treating the cells with the inhibitors. The inhibitors do not act by blocking binding of the virus to its cellular receptor CR 2, but rather are effective in the viral internalization process. Our results suggest that protein kinase C may be involved in the process of viral entry into cells.
Insights
Selective protein kinase C inhibitors reduce Epstein-Barr virus (EBV) infectivity by blocking viral entry into cells. These findings suggest protein kinase C plays a role in EBV internalization.
Area of Science:
- Virology
- Cell Biology
- Biochemistry
Background:
- Epstein-Barr virus (EBV) is a human herpesvirus that infects B lymphocytes, leading to transformation and potential oncogenesis.
- Protein kinase C (PKC) is a family of enzymes involved in various cellular processes, including signal transduction and cell proliferation.
Purpose of the Study:
- To investigate the role of protein kinase C in Epstein-Barr virus infectivity and entry into human B lymphocytes.
- To determine if selective protein kinase C inhibitors can modulate EBV infection.
Main Methods:
- Human B lymphocytes (Raji cells) were pre-treated with selective protein kinase C inhibitors.
- Cells were infected with Epstein-Barr virus (B95-8 EBV and P3HRI EBV strains).
- Viral infectivity was assessed by measuring transformation, 3H-thymidine incorporation, and early antigen induction. Viral binding to the CR2 receptor and internalization were also examined.
Main Results:
- Selective protein kinase C inhibitors significantly reduced Epstein-Barr virus infectivity, including inhibition of transformation and decreased 3H-thymidine incorporation.
- A significant reduction in the induction of early antigens in superinfected Raji cells was observed.
- Inhibitors did not block viral binding to the CR2 receptor but were effective in the viral internalization process.
Conclusions:
- Protein kinase C is implicated in the process of Epstein-Barr virus entry into host cells.
- Selective protein kinase C inhibitors represent a potential therapeutic strategy for controlling EBV infection by targeting viral internalization.