biostudies-literatureZhang XStrategic Priority Research Program of the Chinese Academy of SciencesEmergency Key Project of Guangzhou LaboratoryKey R&D Program of Hubei ProvinceHubei Science and Technology Major ProjectMOST | National Natural Science Foundation of China (NSFC)NIAID NIH HHSWuhan Ministry of Science and TechnologyKey R&D Program of Hubei ProvinceMOST | National Natural Science Foundation of Chinae0169523https://www.ebi.ac.uk/biostudies/studies/S-EPMC10949499biostudies-literatureUnknown98(3)Histone modifications function in both cellular and viral gene expression. However, the roles of acetyltransferases and histone acetylation in parvoviral infection remain poorly understood. In the current study, we found the histone deacetylase (HDAC) inhibitor, trichostatin A (TSA), promoted the replication and transcription of parvovirus minute virus of canines (MVC). Notably, the expression of host acetyltransferases KAT5, GTF3C4, and KAT2A was increased in MVC infection, as well as H4 acetylation (H4K12ac). KAT5 is not only responsible for H4K12ac but also crucial for viral replication and transcription. The viral nonstructural protein NS1 interacted with KAT5 and enhanced its expression. Further study showed that Y44 in KAT5, which may be tyrosine-phosphorylated, is indispensable for Journal of virologyNS1-mediated enhancement of MVC transcription and replication promoted by KAT5/H4K12ac.PMC10949499319701682021ACB004XDB04900002021BCD004EKPG21-30-2R01 AI1508772022020801020150Liu HHuang FQiu JYang JLiu LXu HSun YLiu YGuo JGuan WDing SChen ZZhang XHao HfalseNS1-mediated enhancement of MVC transcription and replication promoted by KAT5/H4K12ac.Histone modifications function in both cellular and viral gene expression. However, the roles of acetyltransferases and histone acetylation in parvoviral infection remain poorly understood. In the current study, we found the histone deacetylase (HDAC) inhibitor, trichostatin A (TSA), promoted the replication and transcription of parvovirus minute virus of canines (MVC). Notably, the expression of host acetyltransferases KAT5, GTF3C4, and KAT2A was increased in MVC infection, as well as H4 acetylation (H4K12ac). KAT5 is not only responsible for H4K12ac but also crucial for viral replication and transcription. The viral nonstructural protein NS1 interacted with KAT5 and enhanced its expression. Further study showed that Y44 in KAT5, which may be tyrosine-phosphorylated, is indispensable for 2024-01-01T00:00:00Z2024 Mar2026-03-27T16:29:15.257Z2024-11-15T04:12:19.786ZS-EPMC109494993834908510.1128/jvi.01695-23