Bottlenecks in the transmission ofPorcine reproductive and respiratory syndrome virus(PRRSV1) to naïve pigs and quasi-species variation during infection in partially immune pigs

Abstract

The existence of bottlenecks during infection of Porcine reproductive and respiratory syndrome virus (PRRSV) was studied in an experimental one-to-one model of transmission in pigs. Besides, the differences between viral quasi-species in vaccinated pigs that developed shorter or longer viremias after natural challenge were analysed. The results consistently reported the existence of bottlenecks during transmission. Several positions along the PRRSV genome were identified as being selected in partially immune animals that developed short viremias. Those positions accumulated in GP2, nsp9 and M proteins and resulted in changes in the protein structure and in the interactions of those proteins with their targets. The fact that the affected proteins are known targets of the immunity against PRRSV suggested that the immune response selected those changes. This pig model can be useful for the study of other pathogens of interest in animals and humans.Author summaryPorcine reproductive and respiratory syndrome (PRRS) is one of the most economically important disease of pigs. It is caused by PRRS virus (PRRSV), a positive-sense, single-stranded RNA virus in the Arteriviridae family within the order Nidovirales. Here, we study the existence of bottlenecks during disease transmission and the differences between viral quasi-species in vaccinated pigs that developed shorter or longer viremias after natural challenge. Our results consistently report the existence of bottlenecks during PRRSV1 transmission and identify several mutations along the viral genome selected by the host immune response that can be clear targets for new vaccine development.

Genetic diversification patterns in swine influenza A virus (H1N2) in vaccinated and nonvaccinated animals

“…Therefore, these mutations did not imply a benefit on viral fitness, so they were lost over time. Considering that virus was grown on MCDK cells before challenge, the nucleotide diversity loss of the inoculum could be explained by the virus readaptation of their natural host after a bottleneck effect (Sobel Leonard et al, 2016;Cortey et al, 2018).…”