Senecavirus A Enhances Its Adaptive Evolution via Synonymous Codon Bias Evolution

Synonymous codon bias in the viral genome affects protein translation and gene expression, suggesting that the synonymous codon mutant plays an essential role in influencing virulence and evolution. However, how the recessive mutant form contributes to virus evolvability remains elusive. In this paper, we characterize how the Senecavirus A (SVA), a picornavirus, utilizes synonymous codon mutations to influence its evolution, resulting in the adaptive evolution of the virus to adverse environments. The phylogenetic tree and Median-joining (MJ)-Network of these SVA lineages worldwide were constructed to reveal SVA three-stage genetic development clusters. Furthermore, we analyzed the codon bias of the SVA genome of selected strains and found that SVA could increase the GC content of the third base of some amino acid synonymous codons to enhance the viral RNA adaptive evolution. Our results highlight the impact of recessive mutation of virus codon bias on the evolution of the SVA and uncover a previously underappreciated evolutionary strategy for SVA. They also underline the importance of understanding the genetic evolution of SVA and how SVA adapts to the adverse effects of external stress

Global Infection Rate of Rotavirus C during 1980–2022 and Analysis of Critical Factors in the Host Range Restriction of Virus VP4

Information on rotavirus C (RVC) infection is lacking, partly because the prevalence of RVC among humans and animals worldwide is undefined. Data on the characteristics of the P genotype among RVC strains are also required. We performed systematic searches on the infection rates of RVC since 1980 based on the literature and gene sequences of the PubMed and GenBank databases. A phylogenetic tree of VP4 genes was constructed to evaluate the distribution of the P genotype of RVC from various hosts. The specific mutation motifs in VP8* with P [2]/P [4]/P [5] specificity were analyzed to elucidate their roles in host range restriction. The rate of RVC infection in humans has fallen from 3% before 2009 to 1%, whereas in animals it has risen from 10% to 25%. The P genotype of RVC showed strict host species specificity, and current human RVC infections are exclusively caused by genotype P [2]. In the VP8* hemagglutinin domain of the P [4]/P [5] genotype of swine RVC, specific insertion or deletion were found relative to the human P [2] genotype, and these motifs are a possible critical factor for host range restriction. Our findings highlight the need for further epidemiological surveillance, preventive strategies, and elucidation of the factors involved in the specific host range restriction of RVC-circulating strains

Correction to: Brucellosis seroprevalence in ovine and caprine flocks in China during 2000–2018: a systematic review and meta-analysis

The original article [1] contained a minor error whereby Table 1 was typeset incorrectly

A Soluble Bis-Chelated Gold(I) Diphosphine Compound with Strong Anticancer Activity and Low Toxicity

Gold-containing compounds have shown anticancer potential, but their clinical applications have been severely limited by poor stability and high toxicity in vivo. Here, we report a novel soluble bis-chelated gold­(I)–diphosphine compound (GC20) with strong anticancer activity and low toxicity. GC20 shows strong antiproliferation potency against a broad spectrum of cancer cell lines including cisplatin-resistant cancer cells (IC₅₀ ≈ 0.5 μM) and significantly reduces tumor growth in several tumor xenografts in mouse models at doses as low as 2 mg/kg. Studies of its mechanism revealed that GC20 specifically inhibits the enzymatic activity of thioredoxin reductase by binding to selenocysteine residue, without targeting other well-known selenol and thiol groups contained in biomolecules. Remarkably, in animal studies GC20 was shown to be well tolerated even at the high dose of 8 mg/kg. Our results strongly suggest that GC20 represents a promising candidate for the development of novel anticancer drugs