Abstract
African swine fever virus (ASFV) poses serious threats to the swine industry. The mortality rate of African swine fever (ASF) is 100%, and there is no effective vaccine currently available. Complex immune escape strategies of ASFV are crucial factors affecting immune prevention and vaccine development. CD2v and MGF360-505R genes have been implicated in the modulation of the immune response. The molecular mechanisms contributing to innate immunity are poorly understood. In this study, we discover the cytopathic effect and apoptosis of ΔCD2v/ΔMGF360-505R-ASFV after infection in porcine alveolar macrophages (PAMs) was significantly less than wild-type ASFV. We demonstrated that CD2v- and MGF360-505R-deficient ASFV decrease the level of apoptosis by inhibiting the NF-κB signaling pathway and IL-1β mRNA transcription. Compared with wild-type ASFV infection, the levels of phospho-NF-κB p65 and p-IκB protein decreased in CD2v- and MGF360-505R-deficient ASFV. Moreover, CD2v- and MGF360-505R-deficient ASFV induced less IL-1β production than wild-type ASFV and was attenuated in replication compared with wild-type ASFV. We further found that MGF360-12L, MGF360-13L, and MGF-505-2R suppress the promoter activity of NF-κB by reporter assays, and CD2v activates the NF-κB signaling pathway. These findings suggested that CD2v- and MGF360-505R-deficient ASFV could reduce the level of ASFV p30 and the apoptosis of PAMs by inhibiting the NF-κB signaling pathway and IL-1β mRNA transcription, which might reveal a novel strategy for ASFV to maintain the replication of the virus in the host.
Highlights
African swine fever (ASF) is a highly pathogenic animal infectious disease caused by the African swine fever virus (ASFV) infecting domestic pigs and wild boars, causing huge economic losses to the pig industry [1]
Deletion of MGF360 and MGF505 genes in ∆CD2v/∆MGF360-505R-ASFV does significantly affect the ability of the virus to replicate in primary swine macrophage cultures
Using a DNA homologous recombination technique [1], we constructed ∆CD2v/∆MGF360-505R-ASFV viruses by deleting gene segments encoding seven different proteins, includingMGF505-1R, MGF505-2R, MGF505-3R, MGF360-12L, MGF360-13L, MGF360-14L, and CD2v, which have previously been observed to be important for the virulence of different ASFVs [1,47]
Summary
African swine fever (ASF) is a highly pathogenic animal infectious disease caused by the African swine fever virus (ASFV) infecting domestic pigs and wild boars, causing huge economic losses to the pig industry [1]. ASFV was first reported in Kenya in 1921, and the disease is spreading in Africa, Europe, and Asia, posing a serious threat to the global economy and ecology [2,3]. There is currently no effective ASFV vaccine for prevention and control, and no drugs have been approved to treat ASF [5]. The huge genome and complex immune escape mechanism of ASFV pose a huge challenge to the development of high-efficiency ASFV vaccine [7]
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