Deletion of virulence associated genes from attenuated African swine fever virus isolate OUR T88/3 decreases its ability to protect against challenge with virulent virus

Abstract

African swine fever virus (ASFV) causes an acute haemorrhagic disease of domestic pigs against which there is no effective vaccine. The attenuated ASFV strain OUR T88/3 has been shown previously to protect vaccinated pigs against challenge with some virulent strains including OUR T88/1. Two genes, DP71L and DP96R were deleted from the OUR T88/3 genome to create recombinant virus OUR T88/3ΔDP2. Deletion of these genes from virulent viruses has previously been shown to reduce ASFV virulence in domestic pigs. Groups of 6 pigs were immunised with deletion virus OUR T88/3ΔDP2 or parental virus OUR T88/3 and challenged with virulent OUR T88/1 virus. Four pigs (66%) were protected by inoculation with the deletion virus OUR T88/3ΔDP2 compared to 100% protection with the parental virus OUR T88/3. Thus the deletion of the two genes DP71L and DP96R from OUR T88/3 strain reduced its ability to protect pigs against challenge with virulent virus.

Different routes and doses influence protection in pigs immunised with the naturally attenuated African swine fever virus isolate OURT88/3

“…Pigs inoculated intramuscularly with 10 4 TCID 50 were protected to a similar degree (66%) as previously described (Boinas et al., 2004, Oura et al., 2005, King et al., 2011, Abrams et al., 2013). However, the level of protection induced when pigs were immunised intramuscularly with 10 3 and 10 5 TCID 50 was lower (50 and 33% respectively).…”

“…So, although pigs immunised with low and moderate doses by intramuscular route displayed lower protection, the low or non-existent viral loads together with the asymptomatic clinical courses observed in protected pigs, similar to those described in previous studies with OURT88/3 (Boinas et al., 2004, Oura et al., 2005, King et al., 2011, Abrams et al., 2013), suggested this route as the most feasible and safe for immunisations against ASFV.…”

“…The present study extends previous studies on protection induced by intramuscular administration of OURT88/3 (Boinas et al., 2004, Oura et al., 2005, King et al., 2011, Abrams et al., 2013). Here, different combinations of doses (10 3 , 10 4 and 10 5 TCID 50 ) and routes of immunisation of OURT88/3, including the intranasal route which had not been previously tested, were evaluated.…”

African swine fever: a global view of the current challenge

“…These data together the advances on the molecular and biological characteristics of the virus [11, 13], and on the immune mechanism that could be involved in protection [92], have led to the development of new promising vaccine candidates. Currently, a number of different approaches are under study [96–100], the most promising of which are based on stimulating the cytolytic CD8+ T-cell and antibody response [92, 98, 99]. These strategies include the construction of deletion mutants from virulent or moderate to low virulent virus isolates, by deleting genes involved in i.e replication, virulence, cellular transport or innate immune response [96, 97, 100].…”

“…Currently, a number of different approaches are under study [96–100], the most promising of which are based on stimulating the cytolytic CD8+ T-cell and antibody response [92, 98, 99]. These strategies include the construction of deletion mutants from virulent or moderate to low virulent virus isolates, by deleting genes involved in i.e replication, virulence, cellular transport or innate immune response [96, 97, 100]. These vaccine candidates are in a first assessment step, so studies for safety, adverse reactions, potential persistence and transmission in the field are far to be evaluated.…”