The cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING) pathway plays a significant role in health and disease. In this pathway, cGAS, one of the major cytosolic DNA sensors in mammalian cells, regulates innate immunity and the STING-dependent production of pro-inflammatory cytokines, including type-I interferon. Moreover, the cGAS–STING pathway is integral to other cellular processes, such as cell death, cell senescence, and autophagy. Activation of the cGAS–STING pathway by “self” DNA is also attributed to various infectious diseases and autoimmune or inflammatory conditions. In addition, the cGAS–STING pathway activation functions as a link between innate and adaptive immunity, leading to the inhibition or facilitation of tumorigenesis; therefore, research targeting this pathway can provide novel clues for clinical applications to treat infectious, inflammatory, and autoimmune diseases and even cancer. In this review, we focus on the cGAS–STING pathway and its corresponding cellular and molecular mechanisms in health and disease.

Summary: The formation of aliphatic carboxylic acids during soda-AQ pulping of kenaf bark was studied. In addition to formic and acetic acids, a variety of hydroxy monocarboxylic and dicarboxylic acids were monitored. The results showed that the formation of hydroxy acids and formic acid significantly depend, in contrast to acetic acid, on the cooking conditions employed. Detailed gas chromatographic studies revealed that the most abundant hydroxy carboxylic acids were glucoisosaccharinic, lactic, glycolic, 3-deoxypentonic, 2-hydroxybutanoic, xyloisosaccharinic, 3,4-dideoxypentonic, 2-hydroxyglutaric, and glucoisosaccharinaric acids. The total amount of aliphatic carboxylic acids corresponded to 12–16% of o.d. kenaf bark.

Swine acute diarrhea syndrome coronavirus (SADS-CoV) is a virulent pathogen that causes acute diarrhea in piglets. The virus was first discovered in Guangdong Province, China, in 2017 and has since emerged in Jiangxi, Fujian, and Guangxi Provinces. The outbreak exhibited a localized and sporadic pattern, with no discernable temporal continuity. The virus can infect human progenitor cells and demonstrates considerable potential for cross-species transmission, representing a potential risk for zoonotic transmission. Therefore, continuous surveillance of and comprehensive research on SADS-CoV are imperative. This review provides an overview of the temporal and evolutionary features of SADS-CoV outbreaks, focusing on the structural characteristics of the virus, which serve as the basis for discussing its potential for interspecies transmission. Additionally, the review summarizes virus–host interactions, including the effects on host cells, as well as apoptotic and autophagic behaviors, and discusses prevention and treatment modalities for this viral infection.

Porcine epidemic diarrhea virus (PEDV), a member of the Alpha-coronavirus genus in the Coronaviridae family, induces acute diarrhea, vomiting, and dehydration in neonatal piglets. This study aimed to investigate the genetic dependencies of PEDV and identify potential therapeutic targets by using a single-guide RNA (sgRNA) lentiviral library to screen host factors required for PEDV infection. Protein kinase C θ (PKCθ), a calcium-independent member of the PKC family localized in the cell membrane, was found to be a crucial host factor in PEDV infection. The investigation of PEDV infection was limited in Vero and porcine epithelial cell-jejunum 2 (IPEC-J2) due to defective interferon production in Vero and the poor replication of PEDV in IPEC-J2. Therefore, identifying suitable cells for PEDV investigation is crucial. The findings of this study reveal that human embryonic kidney (HEK) 293T and L929 cells, but not Vero and IPEC-J2 cells, were suitable for investigating PEDV infection. PKCθ played a significant role in endocytosis and the replication of PEDV, and PEDV regulated the expression and phosphorylation of PKCθ. Apoptosis was found to be involved in PEDV replication, as the virus activated the PKCθ-B-cell lymphoma 2 (BCL-2) ovarian killer (BOK) axis in HEK293T and L929 cells to increase viral endocytosis and replication via mitochondrial apoptosis. This study demonstrated the suitability of HEK293T and L929 cells for investigating PEDV infection and identified PKCθ as a host factor essential for PEDV infection. These findings provide valuable insights for the development of strategies and drug targets for PEDV infection.

African swine fever (ASF) leads to high mortality in domestic pigs and wild boar, and it is caused by the African swine fever virus (ASFV). Currently, no commercially available vaccine exists for its prevention in China. In this study, we engineered a pseudorabies recombinant virus (PRV) expressing ASFV CD2v and p54 proteins (PRV-∆TK-(CD2v)-∆gE-(p54)) using CRISPR/Cas9 and homologous recombination technology. PRV-∆TK-(CD2v)-∆gE-(p54) effectively delivers CD2v and p54, and it exhibits reduced virulence. Immunization with PRV-∆TK-(CD2v)-∆gE-(p54) neither induces pruritus nor causes systemic infection and inflammation. Furthermore, a double knockout of the TK and gE genes eliminates the depletion of T, B, and monocytes/macrophages in the blood caused by wild-type viral infection, decreases the proliferation of granulocytes to eliminate T-cell immunosuppression from granulocytes, and enhances the ability of the immune system against PRV infection. An overexpression of CD2v and p54 proteins does not alter the characteristics of PRV-∆TK/∆gE. Moreover, PRV-∆TK-(CD2v)-∆gE-(p54) successfully induces antibody production via intramuscular (IM) vaccination and confers effective protection for vaccinated mice upon challenge. Thus, PRV-∆TK-(CD2v)-∆gE-(p54) demonstrates good immunogenicity and safety, providing highly effective protection against PRV and ASFV. It potentially represents a suitable candidate for the development of a bivalent vaccine against both PRV and ASFV infections.

Porcine epidemic diarrhea virus (PEDV) presents a substantial challenge to the global swine industry. However, the origin, host range, and potential cross-species transmission of PEDV remain poorly understood. This study characterizes a novel PEDV strain, CHFJFQ, isolated from diarrheic piglets in Fuqing, Fujian, China. Through sequencing and phylogenetic analysis, we determined that CHFJFQ belongs to the GIIa subgroup and is a recombinant with CH/HNXX/2016 as the major parent and NW17 as the minor parent. Compared to CV777, CHFJFQ exhibits multiple base deletions and insertions across the 5′UTR, ORF1a/b, S, and ORF3 genes. Phylogenetic analysis indicates shared ancestry with bat coronaviruses, though a direct zoonotic origin remains uncertain. Interestingly, CHFJFQ demonstrated its ability to infect human and mouse cell lines in vitro and, more significantly, caused in vivo infection in both pigs and mice. The primary target organs were the intestines, lungs, and spleen, resulting in 100% mortality in suckling piglets. PEDV CHFJFQ was detected in mouse tissues, but no clinical signs were observed, indicating limited cross-species pathogenicity. Overall, these findings offer crucial insights into the epidemiology, genetics, infectivity, and pathogenicity of PEDV and provide valuable information for vaccine development.