Immune Escape Mechanism and Vaccine Research Progress of African Swine Fever Virus

Abstract

African swine fever virus (ASFV) is the causative agent of the epidemic of African swine fever (ASF), with virulent strains having a mortality rate of up to 100% and presenting devastating impacts on animal farming. Since ASF was first reported in China in 2018, ASFV still exists and poses a potential threat to the current pig industry. Low-virulence and genotype I strains of ASFV have been reported in China, and the prevention and control of ASF is more complicated. Insufficient understanding of the interaction of ASFV with the host immune system hinders vaccine development. Physical barriers, nonspecific immune response and acquired immunity are the three barriers of the host against infection. To escape the innate immune response, ASFV invades monocytes/macrophages and dendritic cells, thereby inhibiting IFN expression, regulating cytokine expression and the body’s inflammatory response process. Meanwhile, in order to evade the adaptive immune response, ASFV inhibits antigen presentation, induces the production of non-neutralizing antibodies, and inhibits apoptosis. Recently, significant advances have been achieved in vaccine development around the world. Live attenuated vaccines (LAVs) based on artificially deleting specific virulence genes can achieve 100% homologous protection and partial heterologous protection. The key of subunit vaccines is identifying the combination of antigens that can effectively provide protection and selecting carriers that can effectively deliver the antigens. In this review, we introduce the epidemic trend of ASF and the impact on the pig industry, analyze the interaction mechanism between ASFV and the body’s immune system, and compare the current status of potential vaccines in order to provide a reference for the development of effective ASF vaccines.

Oronasal or Intramuscular Immunization with a Thermo-Attenuated ASFV Strain Provides Full Clinical Protection against Georgia 2007/1 Challenge

“…As recently reviewed, different vaccine development strategies have been attempted with varying success [17][18][19][20][21][22]. The administration of the inactivated virus in the absence or presence of modern adjuvants did not induce any protection, even if the candidate vaccines induced seroconversion [23,24].…”

Assessment of the Impact of a Toll-like Receptor 2 Agonist Synthetic Lipopeptide on Macrophage Susceptibility and Responses to African Swine Fever Virus Infection

“…In this study, we observed that all three synthetic lipopeptides also drastically downregulated cGAS expression. As recently reviewed, PRRs involved in recognition of ASFV include TLR3, which senses viral dsRNA, and cGAS-STING, which senses viral DNA in the cytoplasm [ 49 ]. Indeed, ASFV encodes genes that inhibit the actions of both TLR3 and cGAS-STING [ 49 , 50 , 51 ].…”

“…As recently reviewed, PRRs involved in recognition of ASFV include TLR3, which senses viral dsRNA, and cGAS-STING, which senses viral DNA in the cytoplasm [ 49 ]. Indeed, ASFV encodes genes that inhibit the actions of both TLR3 and cGAS-STING [ 49 , 50 , 51 ]. Interestingly, moM1 polarization, which is instead associated with impairment of ASFV’s ability to replicate at early time points [ 21 ] and characterized by enhanced release of pro-inflammatory cytokines [ 14 ], downregulated TLR3 , TLR7 , TLR8 , and TLR9 , but it did not modulate cGAS expression.…”

Structure and function of African swine fever virus proteins: Current understanding

“…In conclusion, A224L and A179L proteins suppress ASFV infectioninduced apoptosis. By inhibiting apoptosis, the virus avoids being exposed to the immune system by host cells, thus facilitating immune escape and viral proliferation (Wang Z. et al, 2022). In addition, studies of A224L and A179L proteins have demonstrated that apoptosis and the survival of ASFV-infected host cells are tightly regulated processes (Figure 7B).…”