African swine fever (ASF) is a viral disease with a high fatality rate in both domestic pigs and wild boars. ASF has greatly challenged pig-raising countries and also negatively impacted regional and national trade of pork products. To date, ASF has spread throughout Africa, Europe, and Asia. The development of safe and effective ASF vaccines is urgently required for the control of ASF outbreaks. The ASF virus (ASFV), the causative agent of ASF, has a large genome and a complex structure. The functions of nearly half of its viral genes still remain to be explored. Knowledge on the structure and function of ASFV proteins, the mechanism underlying ASFV infection and immunity, and the identification of major immunogenicity genes will contribute to the development of an ASF vaccine. In this context, this paper reviews the available knowledge on the structure, replication, protein function, virulence genes, immune evasion, inactivation, vaccines, control, and diagnosis of ASFV.

Mitochondria are important organelles involved in metabolism and programmed cell death in eukaryotic cells. In addition, mitochondria are also closely related to the innate immunity of host cells against viruses. The abnormality of mitochondrial morphology and function might lead to a variety of diseases. A large number of studies have found that a variety of viral infections could change mitochondrial dynamics, mediate mitochondria-induced cell death, and alter the mitochondrial metabolic status and cellular innate immune response to maintain intracellular survival. Meanwhile, mitochondria can also play an antiviral role during viral infection, thereby protecting the host. Therefore, mitochondria play an important role in the interaction between the host and the virus. Herein, we summarize how viral infections affect microbial pathogenesis by altering mitochondrial morphology and function and how viruses escape the host immune response.

Classical swine fever (CSF), caused by CSF virus (CSFV), is a highly contagious swine disease with high morbidity and mortality, which has caused significant economic losses to the pig industry worldwide. Biosecurity measures and vaccination are the main methods for prevention and control of CSF since no specific drug is available for the effective treatment of CSF. Although a series of biosecurity and vaccination strategies have been developed to curb the outbreak events, it is still difficult to eliminate CSF in CSF-endemic and re-emerging areas. Thus, in addition to implementing enhanced biosecurity measures and exploring more effective CSF vaccines, other strategies are also needed for effectively controlling CSF. Currently, more and more research about anti-CSFV strategies was carried out by scientists, because of the great prospects and value of anti-CSFV strategies in the prevention and control of CSF. Additionally, studies on anti-CSFV strategies could be used as a reference for other viruses in the Flaviviridae family, such as hepatitis C virus, dengue virus, and Zika virus. In this review, we aim to summarize the research on anti-CSFV strategies. In detail, host proteins affecting CSFV replication, drug candidates with anti-CSFV effects, and RNA interference (RNAi) targeting CSFV viral genes were mentioned and the possible mechanisms related to anti-CSFV effects were also summarized.

Porcine parvovirus (PPV) infection is the primary cause of SMEDI (stillbirth; mummification; embryonic death; infertility) syndrome, which is a global burden for the swine industry. Thus, it is crucial to establish a rapid and efficient detection method against PPV infection. In the present work, we developed a recombinase-aided amplification (RAA) assay, coupled with a lateral flow dipstick (LFD), to achieve an amplification of PPV DNA at 37 °C within 15 min. The detection limits of PPV RAA-LFD assay were 10² copies/μL recombinant plasmid pMD19-T-VP1, 6.38 × 10⁻⁷ ng/μL PPV DNA, and 10⁻¹ TCID₅₀/mL virus, respectively. This method was highly specific for PPV detection with no cross-reactivity for other swine pathogens. In contrast to polymerase chain reaction (PCR), the PPV RAA-LFD assay is more sensitive and cost-saving. Hence, the established PPV RAA-LFD assay provided an alternative for PPV detection, especially in resource-limited regions.

Senecavirus A (SVA), formerly known as Seneca Valley virus (SVV), causes vesicular symptoms in adult pigs and acute death of neonatal piglets. This pathogen has emerged in major swine producing countries around the world and caused significant economic losses to the pig industry. Thus, it is necessary to develop strategies to prevent and control SVA infection. Herein, an SVA strain (named GD-ZYY02-2018) was isolated from a pig herd with vesicular symptoms in Guangdong province of China in 2018. The present study aimed to carry out the phylogenetic analysis of the GD-ZYY02-2018 strain, determine its pathogenicity in finishing pigs, and assess the protective efficacy of the inactivated GD-ZYY02-2018 strain against virus challenge. The results of phylogenetic analysis showed that the SVA GD-ZYY02-2018 strain belonged to the USA-like strains and had a close genetic relationship with recent Chinese SVA strains. Animal challenge experiment showed that 100-day-old pigs inoculated intranasally with SVA GD-ZYY02-2018 strain developed vesicular lesion, low fever, viremia, and virus shedding in feces. The immunization challenge experiment showed that pigs vaccinated with inactivated GD-ZYY02-2018 strain could produce a high titer of anti-SVA neutralizing antibody and no vesicular lesion, fever, viremia, and virus shedding in feces was observed in vaccinated pigs after challenge with GD-ZYY02-2018 strain, indicating that inactivated GD-ZYY02-2018 could protect finishing pigs against the challenge of homologous virus. In conclusion, preliminary results indicated that inactivated GD-ZYY02-2018 could be used as a candidate vaccine for in-depth research and might be conducive to the prevention and control of SVA infection.