For some viruses, a persistent infection confers resistance to host cells against the virus or closely related viruses. This effect is well-documented; for example, retroviruses and hepatitis B lead to superinfection exclusion by downregulating host cell surface entry receptors, and Rift valley fever virus induces RNA silencing. In this study, the researchers elucidated the mechanism of persistence infection using mouse models, plasmid recombinations, human cell culture, immunofluorescence assays, Western blotting and Northern blotting.
This study presents evidence that superinfection exclusion occurs for Borna disease virus (BDV) in vitro and in rats, and that BDV nucleocapsid proteins P, N, or X confers resistance against BDV in humans by blocking viral polymerase. Overexpression of P also resulted in resistance, suggesting that balance of nucleocapsid components may be important for a virus to establish infection.
These results not only provide a mechanism for superinfection exclusion in BDV, but also suggest that changing the balance of nucleocapsid components should be researched as a novel strategy for future antiviral therapeutics.