Author: Vlad Petrovan, Anusyah Rathakrishnan, Muneeb Islam, Lynnette C. Goatley, Katy Moffat, Pedro J. Sanchez-Cordon, Ana L. Reis, Linda K. Dixon
About this Publication:
The limited knowledge on the role of many of the approximately 170 proteins encoded by African swine fever virus restricts progress towards vaccine development. Previously, the DP148R gene was deleted from the genome of genotype I virulent Benin 97/1 isolate. This virus, Benin?DP148R, induced transient moderate clinical signs after immunization and high levels of protection against challenge. However, the Benin?DP148R virus and genome persisted in blood over a prolonged period. In the current study deletion of either EP402R or EP153R genes individually or in combination from Benin?DP148R genome was shown not to reduce virus replication in macrophages in vitro. However, deletion of EP402R dramatically reduced the period of infectious virus persistence in blood in immunized pigs from 28 to 14 days and virus genome from 59 to 14 days, whilst maintaining high levels of protection against challenge. The additional deletion of EP153R (Benin?DP148R?EP153R?EP402R) further attenuated the virus and no viremia or clinical signs were observed post-immunization. This was associated with decreased protection and detection of moderate levels of challenge virus in blood. Interestingly, the deletion of EP153R alone from Benin?DP148R did not result in further virus attenuation and did not reduce the period of virus persistence in blood. These results show that EP402R and EP153R have a synergistic role in reducing clinical signs and levels of virus in blood.
Subject Areas: Research and Development
Diseases: African Swine Fever