African Swine Fever Virus Regulates Host Energy and Amino Acid Metabolism To Promote Viral Replication
Xue Qiao, Huisheng Liu, Zixiang Zhu, Fan Yang, Yingying Song, Zongqiang Li, Zhaoning Xue, Weijun Cao, Xiangtao Liu, Haixue Zheng
Abstract
In order to promote viral replication, viruses often cause severe immunosuppression and seize organelles to synthesize a large number of metabolites required for self-replication. African swine fever virus (ASFV) has developed many strategies to evade host innate immune responses. However, the impact of ASFV infection on host cellular metabolism remains unknown. Here, for the first time, we analyzed the metabolomic profiles of ASFV-infected PAMs. ASFV infection increased host TCA cycle and amino acid metabolism. Aspartate, glutamate, and TCA cycle promoted ASFV replication. ASFV infection also induced the increase of lactate production to inhibit innate immune responses for self-replication. This study identified novel immune evasion mechanisms utilized by ASFV and provided insights into ASFV-host interactions, which is critical for guiding the design of new prevention strategies against ASFV targeting the altered metabolic pathways.