Abstract

In 2018, African swine fever broke out in China, and the death rate after infection was close to 100%. There is no effective and safe vaccine in the world. In order to better characterize and understand the virus–host-cell interaction, quantitative proteomics was performed on porcine alveolar macrophages (PAM) infected with ASFV through tandem mass spectrometry (TMT) technology, high-performance liquid chromatography (HPLC), and mass spectrometry (MS). The proteome difference between the simulated group and the ASFV-infected group was found at 24 h. A total of 4218 proteins were identified, including 306 up-regulated differentially expressed proteins and 238 down-regulated differentially expressed proteins. Western blot analysis confirmed changes in the expression level of the selected protein. Pathway analysis is used to reveal the regulation of protein and interaction pathways after ASFV infection. Functional network and pathway analysis can provide an insight into the complexity and dynamics of virus–host cell interactions. Further study combined with proteomics data found that ARG1 has a very important effect on ASFV replication. It should be noted that the host metabolic pathway of ARG1-polyamine is important for virus replication, revealing that the virus may facilitate its own replication by regulating the level of small molecules in the host cell.

Highlights

  • More than a hundred years ago, African Swine Fever (ASF) was first diagnosed inKenya and gradually spread to Europe and other places [1]

  • L-Arginine, ASFV replication was affected, proving that the ARG1-polyamine pathway is very important for ASFV replication. These results suggest that the ARG1-polyamines pathway contributes to the infectivity of ASFV, uncovering a case where the ASFV hijacks host metabolism to facilitate its own replication

  • We found that ASFV can cause a significant up-regulation of ARG1 after infecting porcine alveolar macrophages (PAM) cells, and this was further verified by Quantitative PCR (qPCR)

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Summary

Introduction

More than a hundred years ago, African Swine Fever (ASF) was first diagnosed inKenya and gradually spread to Europe and other places [1]. In 2018, the outbreak of African swine fever in China led to the death of a large number of pigs [2], seriously affecting the development of the pig farming industry. Its genome is a single molecule of linear double-stranded DNA (DsDNA), which is about 170 to 190 kbp in size and encodes 150 to 167 open reading frames (ORFs) [3,4]. It was recently reported, by cryo-electron microscope, that the diameter of ASFV BA71V isolates is about 208 nm [5]. ASFV mainly replicates in macrophages and monocytes [6]

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