Reverse mutation of the virulence-associated S2 gene does not cause an attenuated equine infectious anemia virus strain to revert to pathogenicity.

The research article investigates whether the S2 accessory gene of Equine Infectious Anemia Virus (EIAV) contributes to the virulence of pathogenic strains. By reverse mutating the gene in an attenuated EIAV strain, the researchers identify that the virulence does not easily revert back.

Objective of the Study

• The study’s primary objective is to examine the contribution of the S2 accessory gene to the virulence of pathogenic strains in the Equine Infectious Anemia Virus (EIAV).

Approach

• The researchers reverse mutated all four consensus S2 mutation sites in an attenuated EIAV proviral strain, FDDV3-8, switching them back to the corresponding sequences of a highly pathogenic strain, DV117.
• The S2 reverse-mutated recombinant strain created through this process is designated as FDDVS2r1-2-3-4.

Findings

• The scientists observed that FDDVS2r1-2-3-4 displayed similar replication kinetics in cultivated target cells to the original FDDV3-8 strain.
• Unlike other studies involving EIAV with dysfunctional S2, reverse mutation of S2 only transiently and moderately increased the plasma viral load of infected horses.
• In terms of immunosuppression, temporary induction failed to boost viral pathogenicity in these horses, which differs from conventional outcomes in viral infection studies.

Conclusion

• The research concludes that inoculation of horses with FDDVS2r1-2-3-4 induced a partial protection against a challenge pathogenic virus. This suggests that an attenuated EIAV vaccine strain with multiple mutations in numerous genes will not easily revert to a lethal phenotype. Therefore, it might be effective as a potential vaccine for EIAV.