State Key Laboratory of Veterinary Biotechnology, Harbin Veterinary Research Institute, Chinese Academy of Agricultural Sciences, 427 Maduan Street, Harbin 150001, China.
Virology. 2013 Sep 1;443(2):321-8. doi: 10.1016/j.virol.2013.05.017. Epub 2013 Jun 12.
The contribution of S2 accessory gene of equine infectious anemia virus (EIAV) to the virulence of pathogenic strains was investigated in the present study by reverse mutation of all four consensus S2 mutation sites in an attenuated EIAV proviral strain, FDDV3-8, to the corresponding sequences of a highly pathogenic strain DV117. The S2 reverse-mutated recombinant strain FDDVS2r1-2-3-4 replicated with similar kinetics to FDDV3-8 in cultivated target cells. In contrast to the results of other studies of EIAV with dysfunctional S2, reverse mutation of S2 only transiently and moderately increased the plasma viral load of inoculated horses, and induction of transient immunosuppression did not boost viral pathogenicity. In addition, inoculation of FDDVS2r1-2-3-4 induced partial protection to a challenge pathogenic virus. These results suggest that the attenuated EIAV vaccine strain with multiple mutations in multiple genes will not easily revert to a virulent phenotype.
本研究通过将弱毒 FDDV3-8 株中 S2 基因的四个一致突变位点反向突变回高致病性 DV117 株的相应序列，研究了马传染性贫血病毒（EIAV） S2 辅助基因对致病株毒力的贡献。与其他研究中 S2 功能失调的 EIAV 不同，S2 的反向突变仅短暂且适度地增加了接种马的血浆病毒载量，并且免疫抑制的诱导并没有增强病毒的致病性。此外，接种 FDDVS2r1-2-3-4 可对挑战致病性病毒产生部分保护作用。这些结果表明，具有多个基因多处突变的减毒 EIAV 疫苗株不易回复为强毒表型。
