Ca2+ plays an antiviral role by increasing p53 expression to achieve protection against spring viraemia of carp virus infection. Issue 102 (July 2020)

• Record Type: Journal Article
• Authors: Lu, Long-Feng; Zhou, Xiao-Yu; Zhang, Can; Li, Zhuo-Cong; Chen, Dan-Dan; Zhang, Yong-An; Li, Shun
• Is Part Of: Fish & shellfish immunology. Issue 102(2020)
• Page Start: 449
• Page End: 459
• Publication Date: 2020-07
• Subjects: Ca2+ -- Antiviral -- p53 -- Ubiquitination -- SVCV; Fishes -- Immunology -- Periodicals; Shellfish -- Immunology -- Periodicals; Poissons -- Immunologie -- Périodiques; Crustacés -- Immunologie -- Périodiques; 571.9617
• DOI: 10.1016/j.fsi.2020.05.023
• Languages: English
• ISSNs: 1050-4648

Abstract

Abstract: Calcium (Ca) is a messenger that regulates a multitude of physiological processes, but its functions in antiviral progress remain undefined. In this study, we found that Ca 2+ enhances fish survival to defend against spring viraemia of carp virus (SVCV) infection by reversing the instability of p53 mediated by the viral protein. First, Ca 2+ significantly protected cells and fish against SVCV infection by inducing early apoptosis. Additionally, p53 expression, which was inhibited by SVCV N protein, was upregulated by Ca 2+ treatment. Then, the mechanism underlying the reduction of K63-linked p53 ubiquitination by SVCV N protein via the K358 site was completely prevented by Ca 2+ . These findings reveal the role of Ca 2+ in lower vertebrates in the antiviral response, which is connected to and corresponds with viral immune evasion, providing a solution to fish diseases caused by pathogens. Highlights: Ca 2+ significantly strengthens the survival of cells and fish to defend against SVCV infection. Ca 2+ blunts the expression of viral genes and induces the expression of fish p53. Ca 2+ treatment rescues the reduced K63-linked ubiquitination of p53 which degraded by SVCV N protein.