Function investigation of p11.5 in ASFV infection  

作　　者：Dan Yin Bin Shi Renhao Geng Yingnan Liu Lang Gong Hongxia Shao Kun Qian Hongjun Chen Aijian Qin 

机构地区：[1]Ministry of Education Key Laboratory for Avian Preventive Medicine,Yangzhou University,Jiangsu 225009,China [2]Jiangsu Co-innovation Center for Prevention and Control of Important Animal Infectious Diseases and Zoonoses,Jiangsu 225009,China [3]Joint International Research Laboratory of Agriculture and Agri-Product Safety of Ministry of Education of China,Jiangsu 225009,China [4]Shanghai Veterinary Research Institute,CAAS,Shanghai,200241,China [5]South China Agricultural University,Guangzhou 510642,China

出　　处：《Virologica Sinica》2024年第3期469-477,共9页中国病毒学（英文版）

基　　金：supported by the National Key Research and Development Program(Grant No.2021YFD1800100);the National Natural Science Foundation of China(Grant No.31941016);the Priority Academic Program Development of Jiangsu Higher Education Institutions,and the Jiangsu Co-innovation Center for the Prevention and Control of Important Animal Infectious Diseases and Zoonoses.

摘　　要：Virus replication relies on complex interactions between viral proteins.In the case of African swine fever virus(ASFV),only a few such interactions have been identified so far.In this study,we demonstrate that ASFV protein p72 interacts with p11.5 using co-immunoprecipitation and liquid chromatography-mass spectrometry(LC-MS).It was found that protein p72 interacts specifically with p11.5 at sites amino acids(aa)1–216 of p72 and aa 1–68 of p11.5.To assess the importance of p11.5 in ASFV infection,we developed a recombinant virus(ASFVGZΔA137R)by deleting the A137R gene from the ASFVGZ genome.Compared with ASFVGZ,the infectious progeny virus titers of ASFVGZΔA137R were reduced by approximately 1.0 logs.In addition,we demonstrated that the growth defect was partially attributable to a higher genome copies-to-infectious virus titer ratios produced in ASFVGZΔA137R-infected MA104 cells than in those infected with ASFVGZ.This finding suggests that MA104 cells infected with ASFVGZΔA137R may generate larger quantities of noninfectious particles.Importantly,we found that p11.5 did not affect virus-cell binding or endocytosis.Collectively,we show for the first time the interaction between ASFV p72 and p11.5.Our results effectively provide the relevant information of the p11.5 protein.These results extend our understanding of complex interactions between viral proteins,paving the way for further studies of the potential mechanisms and pathogenesis of ASFV infection.

关 键 词：African swine fever virus p72 protein p11.5 protein Protein interactions 

分 类 号：S852.651[农业科学—基础兽医学]