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.
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.
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DOI:
10.1016/j.virol.2013.04.028
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发表时间:
2013-08-15
期刊:
影响因子:
3.7
通讯作者:
Dixon LK
中科院分区:
文献类型:
--
作者:
Abrams CC;Goatley L;Fishbourne E;Chapman D;Cooke L;Oura CA;Netherton CL;Takamatsu HH;Dixon LK
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. Attenuated strain OUR T88/3 protects pigs against challenge with virulent strain OUR T88/1. OUR T88/3 encodes virulence associated genes DP71L and DP96R. Construction of recombinant virus OUR T88/3ΔDP2 with DP71L and DP96R genes deleted. Growth of recombinant virus OUR T88/3ΔDP2 in vitro is similar to OUR T88/3. Pigs inoculated with OUR T88/3ΔDP2 show reduced protection when challenged with OUR T88/1
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