Abstract
African swine fever (ASF) is an emerging disease threat to the swine industry worldwide. There is no vaccine against ASF, and progress is hindered by a lack of knowledge concerning the extent of ASFV strain diversity and the viral antigens conferring type-specific protective immunity in pigs. We have previously demonstrated that homologous ASFV serotype-specific proteins CD2v (EP402R) and/or C-type lectin are required for protection against challenge with the virulent ASFV strain Congo (Genotype I, Serogroup 2), and we have identified T-cell epitopes on CD2v which may be associated with serotype-specific protection. Here, using a cell-culture adapted derivative of the ASFV strain Congo (Congo-a) with specific deletion of the EP402R gene (ΔCongoCD2v) in swine vaccination/challenge experiments, we demonstrated that deletion of the EP402R gene results in the failure of ΔCongoCD2v to induce protection against challenge with the virulent strain Congo (Congo-v). While ΔCongoCD2v growth kinetics in COS-1 cells and primary swine macrophage culture were almost identical to parental Congo-a, replication of ΔCongoCD2v in vivo was significantly reduced compared with parental Congo-a. Our data support the idea that the CD2v protein is important for the ability of homologous live-attenuated vaccines to induce protective immunity against the ASFV strain Congo challenge in vivo.
Highlights
African swine fever (ASF) is an acute viral haemorrhagic disease of domestic swine with a mortality rate close to 100% [1,2,3]
We have previously demonstrated that ASFV CD2v (EP402R) and/or C-type lectin (EP153R) proteins are sufficient to mediate serologic specificity determined by a hemadsorption inhibition assay (HAI) and are important for protection against homologous ASFV
We report for the first time the generation of a recombinant ASFV with a deletion of the EP402R gene based on the attenuated ASFV of Genotype I and Serogroup
Summary
African swine fever (ASF) is an acute viral haemorrhagic disease of domestic swine with a mortality rate close to 100% [1,2,3]. It was shown that immunization of pigs using various viral vectors carrying the CD2v protein can induce strong humoral and cellular immunity [22,23,24], and DNA vaccines expressing the CD2v gene can effectively activate the cytotoxic T lymphocyte (CTL) immune response [25,26,27] While this immunization did not result in full protection against ASFV, partial protective effects after the virus challenge have been reported in some studies [28,29,30]. Mutants with a CD2v deletion have been generated for several ASFV strains (BA71, Malawi, and Georgia), the data on the role of the CD2v protein in virus virulence for domestic pigs and in protecting animals from ASF are contradictory [34,35,36,37]. We found that the deletion of the EP402R gene did not significantly affect the ability of the virus to replicate in vitro; it resulted in an inability to induce a protective immune response to infection with the parental (i.e., homologous) virulent ASFV strain
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