Tibetan sheep, a Chinese indigenous breed, are mainly distributed in plateau and mountain-valley areas at a terrestrial elevation between 2260 and 4100 m. The herd is genetically distinct from the other domestic sheep and undergoes acclimatization to adapt to the hypoxic environment. To date, whether the mitochondrial DNA modification of Tibetan sheep shares the same feature as the other domestic breed remains unknown. In this study, we compared the whole mitogenome sequences from 32 Tibetan sheep, 22 domestic sheep and 24 commercial sheep to identify the selection signatures of hypoxic-tolerant in Tibetan sheep. Nucleotide diversity analysis using the sliding window method showed that the highest level of nucleotide diversity was observed in the control region with a peak value of π = 0.05215, while the lowest π value was detected in the tRNAs region. qPCR results showed that the relative mtDNA copy number in Tibetan sheep was significantly lower than that in Suffolk sheep. None of the mutations in 12S rRNA were fixed in Tibetan sheep, which indicated that there has been less artificial selection in this herd than the other domestic and commercial breeds. Although one site (1277G) might undergo the purifying selection, it was not identified as the breed-specific allele in Tibetan sheep. We proposed that nature selection was the main drive during the domestication of Tibetan sheep and single mutation (or locus) could not reveal the signature of selection as for the high diversity in the mitogenome of Tibetan sheep.

Proteins can be chemically altered after translation, a process known as posttranslational modification (PTM). PTMs can control protein function, localization, folding, and interactions with other biological macromolecules. The amino acid lysine is frequently modified, including succinylation, acetylation, butyrylation, malonylation, and ubiquitination. A recently discovered PTM of lysine residues is succinylation (1). Lysine succinylation occurs in people, yeast, mice, and bacteria (2, 3). With an enzymatic or nonenzymatic process, the succinyl group is covalently linked to the lysine residue through the succinyl donor. Lysine succinylation generally controls a number of critical biological processes, for example, cell cycle, growth, and signal transduction pathways. For instance, protein succinylation can change the activity of enzymes involved in lipid and glucose metabolism, thus influencing the cell life cycle (4). Desuccinylation inhibits activation of the signaling adaptor mitochondrial antiviral signaling protein (MAVS), which in turn prevents type I interferon production and antiviral gene expression (5). Most recently, severe acute respiratory syndrome coronavirus 2 and influenza virus infections are regulated by succinylation through different mechanisms (6, 7). However, the understanding of how succinylation influences other viruses has not been studied.

Porcine reproductive and respiratory syndrome virus (PRRSV), a significant pathogen affecting the swine industry globally, has been shown to manipulate host cell processes, including autophagy, to facilitate its replication and survival within the host. Autophagy, an intracellular degradation process crucial for maintaining cellular homeostasis, can be hijacked by viruses for their own benefit. During PRRSV infection, autophagy plays a complex role, both as a defense mechanism of the host and as a tool exploited by the virus. This review explores the current understanding of the molecular mechanisms underlying autophagy induction under PRRSV infection, its impact on virus replication, and the potential implications for viral pathogenesis and antiviral strategies. By synthesizing the latest research findings, this article aims to enhance our understanding of the intricate relationship between autophagy and PRRSV, paving the way for novel therapeutic approaches against this swine pathogen.

The pseudorabies virus (PRV), also known as suid alphaherpesvirus 1 (SuAHV-1), has garnered significant attention due to its broad host range and the economic losses it incurs in the swine industry. This review aims to provide a comprehensive understanding of the intricate virus–host interactions during PRV infection, focusing on the evasion strategies of the virus against the host responses. We also summarize the mechanisms by which PRV manipulates the host cell machinery to facilitate its replication and spread, while simultaneously evading detection and clearance by the immune system. Furthermore, we discuss the latest advancements, such as metabolic, autophagic, and apoptotic pathways in studying these interactions, highlighting the role of various cellular factors and pathways in elucidating virus–host dynamics. By integrating these insights, the article aims to provide a comprehensive overview of the molecular mechanisms underlying PRV pathogenesis and host response, paving the way for the development of novel therapeutic strategies against this virus.