Why the study?
The mechanism of viral adaptation to nonsusceptible hosts and the molecular basis for viral adaptation and attenuation remained largely unknown.
P108 and T109 on the E2 glycoprotein are critical for CSFV adaptation to rabbits but not for attenuation in pigs, providing insight into viral host adaptation mechanisms.
Provides mechanistic insight into CSFV host adaptation in animal models; leaves open implications for swine vaccine attenuation.
Historically, live attenuated vaccines produced by blind passage usually undergo adaptation in cell cultures or nonsusceptible hosts and attenuation in natural hosts, with a classical example being the classical swine fever virus (CSFV) lapinized vaccine C-strain, which was developed by hundreds of passages in rabbits. However, the mechanism of viral adaptation to nonsusceptible hosts and the molecular basis for viral adaptation and attenuation remain largely unknown. In this study, we demonstrated that P108 and T109 on the E2 glycoprotein together with the E rns glycoprotein of the rabbit-adaptive C-strain confer adaptation to rabbits on the highly virulent CSFV Shimen strain by affecting viral entry during infection but do not attenuate the Shimen strain in pigs. Our results provide vital information on the different molecular bases of CSFV adaptation to rabbits and attenuation in pigs.
No takes yet. Share an insight, caveat, or question.
Xie et al. (2020) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: