Advances in African Swine Fever Virus

A special issue of Microorganisms (ISSN 2076-2607). This special issue belongs to the section "Virology".

Deadline for manuscript submissions: closed (30 November 2023) | Viewed by 954

Special Issue Editors

Harbin Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Harbin, China
Interests: virus; pathogenicity; innate immune; signaling pathway; host–virus interaction
Special Issues, Collections and Topics in MDPI journals
State Key Laboratory of Veterinary Etiological Biology and OIE/National Foot and Mouth Disease Reference Laboratory, Lanzhou Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Lanzhou, China
Interests: African Swine Fever Virus

Special Issue Information

Dear Colleagues,

African swine fever (ASF) is a highly contagious infectious disease caused by African swine fever virus (ASFV). ASFV-infected domestic pigs and wild boars have a mortality rate as high as 100%. Since there is no commercial vaccine available to prevent ASF, it has spread rapidly and caused a great challenge for the swine industry worldwide. ASFV encodes more than 167 proteins that not only execute their functions in virus replication, but also regulate host antiviral immune responses. The ASFV proteins E248R and E199L are involved in membrane fusion, and DP71L, A224L and EP424R regulate viral translation. Some ASFV proteins, such as MGF_505-7R, E120R, DP96R, A137R, I215L and MGF_360-12L, inhibit the innate immune response via different mechanisms. However, the pathogenesis, immune evasion and immune protection mechanism of ASFV are still not fully understood, limiting the development of safe and effective ASF vaccines. Therefore, it is urgent to study the molecular and cellular mechanisms of ASFV escaping innate and adaptive immune responses in the host.

This Special Issue aims to explore the pathogenesis, immune evasion and immune protective mechanism of ASFV and provide theoretical support for the design and development of novel effective ASFV vaccines.

Dr. Li Huang
Dr. Dan Li
Guest Editors

Manuscript Submission Information

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Published Papers (1 paper)

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Research

16 pages, 3213 KiB  
Article
African Swine Fever Virus I267L Is a Hemorrhage-Related Gene Based on Transcriptome Analysis
by Yuan Wen, Xianghan Duan, Jingjing Ren, Jing Zhang, Guiquan Guan, Yi Ru, Dan Li and Haixue Zheng
Microorganisms 2024, 12(2), 400; https://doi.org/10.3390/microorganisms12020400 - 17 Feb 2024
Viewed by 802
Abstract
African swine fever (ASF) is an acute and severe disease transmitted among domestic pigs and wild boars. This disease is notorious for its high mortality rate and has caused great losses to the world’s pig industry in the past few years. After infection, [...] Read more.
African swine fever (ASF) is an acute and severe disease transmitted among domestic pigs and wild boars. This disease is notorious for its high mortality rate and has caused great losses to the world’s pig industry in the past few years. After infection, pigs can develop symptoms such as high fever, inflammation, and acute hemorrhage, finally leading to death. African swine fever virus (ASFV) is the causal agent of ASF; it is a large DNA virus with 150–200 genes. Elucidating the functions of each gene could provide insightful information for developing prevention and control methods. Herein, to investigate the function of I267L, porcine alveolar macrophages (PAMs) infected with an I267L-deleted ASFV strain (named ∆I267L) and wild-type ASFV for 18 h and 36 h were taken for transcriptome sequencing (RNA-seq). The most distinct different gene that appeared at both 18 hpi (hours post-infection) and 36 hpi was F3; it is the key link between inflammation and coagulation cascades. KEGG analysis (Kyoto encyclopedia of genes and genomes analysis) revealed the complement and coagulation cascades were also significantly affected at 18 hpi. Genes associated with the immune response were also highly enriched with the deletion of I267L. RNA-seq results were validated through RT-qPCR. Further experiments confirmed that ASFV infection could suppress the induction of F3 through TNF-α, while I267L deletion partially impaired this suppression. These results suggest that I267L is a pathogenicity-associated gene that modulates the hemorrhages of ASF by suppressing F3 expression. This study provides new insights into the molecular mechanisms of ASFV pathogenicity and potential targets for ASFV prevention and control. Full article
(This article belongs to the Special Issue Advances in African Swine Fever Virus)
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