期刊
VIRUSES-BASEL
卷 13, 期 8, 页码 -出版社
MDPI
DOI: 10.3390/v13081473
关键词
African swine fever virus; macrophage; replication; virulence
类别
资金
- UKRI Biotechnology and Biosciences Science Research Council (BBSRC) [BBS/E/I/00007039/7031/7034]
- Pirbright flow cytometry and sequencing facilities
- Zoetis
- BBSRC [BBS/E/I/00007031, BBS/E/I/00007034, BBS/E/I/00007039] Funding Source: UKRI
The study evaluated the role of two virus proteins, K145R and DP148R, in virus replication in macrophages and virulence in pigs. The deletion of DP148R did not attenuate the virus, while the additional deletion of the K145R gene delayed the onset of clinical signs in pigs. Further gene deletions would be necessary to attenuate the virus.
African swine fever virus causes a frequently fatal disease of domestic pigs and wild boar that has a high economic impact across 3 continents. The large double-stranded DNA genome codes for approximately 160 proteins. Many of these have unknown functions and this hinders our understanding of the virus and host interactions. The purpose of the study was to evaluate the role of two virus proteins, K145R and DP148R, in virus replication in macrophages and virulence in pigs. To do this, the DP148R gene, alone or in combination with the K145R gene, was deleted from the virulent genotype II Georgia 2007/1 isolate. Neither of these deletions reduced the ability of the viruses to replicate in porcine macrophages compared to the parental wild-type virus. Pigs infected with Georgia Delta DP148R developed clinical and post-mortem signs and high viremia, typical of acute African swine fever, and were culled on day 6 post-infection. The additional deletion of the K145R gene delayed the onset of clinical signs and viremia in pigs by 3 days, but pigs showed signs of acute African swine fever and were culled on days 10 or 13 post-infection. The results show that the deletion of DP148R did not attenuate the genotype II Georgia 2007/1 isolate, contrary to the results obtained with the genotype I Benin97/1 isolate. Additional deletion of the K145R gene delayed clinical signs, but infected pigs reached the humane endpoint. The deletion of additional genes would be required to attenuate the virus.
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