Infection Genetics and Evolution最新文献

Although feline caliciviruses (FCVs) (Family Caliciviridae) have been studied extensively in household and shelter cats, limited information is available on FCVs in feral cat (Felis catus) populations. We report here high FCV detection rates (27.77%, 30/108) in oral samples from feral cats on the Caribbean island of St. Kitts. Fourteen (46.66%) of the FCV positive cats exhibited oral lesions that were characteristic of FCV infection. Based on analysis of VP1 sequences, the FCV strains from St. Kitts (FCP strains) formed two phylogenetically distinct clusters within FCV genotype-I, and exhibited significant genetic diversity between themselves, and with those of other FCVs (including the FCV vaccine strains). We identified genetically distinct FCV variants co-circulating in certain feral cat colonies, and hypothesized multiple-independent introductions of FCVs into the island feline population (especially from North America). Based on analysis of the putative VP1 E region, the FCP strains retained the conserved amino acid (aa) residues that are crucial for FCV binding to host receptor, whilst aa mismatches at the neutralizing and non-neutralizing epitopes, and at the virulence-related aa positions were observed between the FCP strains (and between the FCP strains and FCV vaccine strains). Taken together, our findings highlighted the complex molecular epidemiology of FCVs in the St. Kitts feral cat population, which might facilitate emergence of virulent pathotypes and/or antigenic variants. Considering these observations, and the potential risk of FCV transmission between feral and household cats, large-scale molecular epidemiological studies on FCVs in feral cat populations from different geographical regions are of utmost importance. To our knowledge, this is the first report on molecular prevalence and genetic diversity of FCVs from the Caribbean region.

Helicobacter pylori infects more than 50% of the global population. The diversity and severity of clinical outcomes are attributed to the complex interaction among pathogen, host, and environmental factors. This study investigated the association between H. pylori virulence genes (cagA, vacA, and dupA) and human host NOS2-954G/C polymorphism with clinical outcomes in H. pylori-infected Iranian patients. Polymerase chain reaction (PCR) was performed on 193H. pylori culture-positive biopsy samples to determine the presence of cagA, vacA, and dupA genotypes. The NOS2-954G/C polymorphism were assessed using PCR-restriction fragment length polymorphism (PCR-RFLP) on blood samples collected from 98 patients. The cagA and dupA genes were detected in 71.5% and 69.9% of isolates, respectively, and were more frequently found in strains derived from patients with peptic ulcer disease (PUD). The distribution of vacA polymorphisms was as follows: s1/s2 (82.9% / 17.1%), m1/m2 (44.6% / 55.4%), and i1/i2 (52.3% / 47.7%). Analysis of NOS2-954G/C polymorphism revealed the following genotypes: G/G (13.3%), G/C (81.6%), and C/C (5.1%). Notably, all 16 isolates obtained from gastric cancer (GC) patients exhibited the G/C genotype. Our findings suggest a borderline association between cagA-positive H. pylori isolates and disease severity, particularly PUD (p = 0.045), whereas a stronger and statistically significant association was observed for the human NOS2 - 954G/C polymorphism (p = 0.003). These results should be interpreted with caution, especially for outcomes with limited sample size.

Collateral sensitivity (CS) was first described by Szybalski and Bryson in 1952. It refers to the phenomenon where bacteria become more susceptible to one antibiotic when they develop resistance to another. Given the global rise of antimicrobial resistance (AMR) and advancements in next-generation sequencing and high-throughput experimental techniques, researchers aim to leverage CS to mitigate or even reverse the spread of AMR by elucidating the molecular mechanisms underlying CS. This paper reviews recent progress in CS research, focusing on laboratory methods, resistance mechanisms leading to CS, and the molecular characterization of CS across different bacterial species. Unlike previous overviews, this article synthesizes the intersection of experimental methodologies and molecular mechanisms to provide a cohesive framework for translating CS from evolutionary principles to clinical application.

Background: Pneumococcal serotypes 6A and 6B are serotypes of Streptococcus pneumoniae serogroup 6 that are most prevalent and cause invasive pneumococcal diseases (IPD). These serotypes are associated with unique clonal lineages, with some exhibiting antibiotic resistance and high virulence properties.

Objective: To explore the global spread of serotypes 6A and 6B clones, detailing their circulating patterns across regions.

Methods: Following the PRISMA guide, four databases were searched for English-language, peer-reviewed articles using molecular genotyping to determine sequence types (STs) of serotypes 6A and 6B.

Results: Thirty-seven studies from 23 countries were included, reporting 138 STs for serotype 6A and 106 for serotype 6B. Both were strongly associated with IPD. For serotype 6A, clonal complexes (CCs) 473 and 3173 were predominant. CC473, comprising ST473, ST1876, and ST471, exhibited widespread distribution across Europe, Asia, the Americas, and Oceania, while CC3173 (ST3173, ST361) was mainly reported in Africa and Asia. For serotype 6B, CC90 (ST90, ST273) and CC176 were the dominant lineages, with isolates recovered from all continents. Notably, ST395, ST1692, and ST3173 were identified in both serotypes. For example, ST395 was reported as 6A in Portugal, the United States, and Australia, and as 6B in Portugal; ST1692 was detected as 6B in Portugal and 6A in Australia; and ST3173 was observed as both 6A and 6B in China.

Conclusions: Serotypes 6A and 6B exhibit complex genetic variation and intercontinental widespread, with some lineages spanning both serotypes. This highlights their epidemiological significance and potential role in the spread of invasive pneumococcal diseases and antibiotic resistance globally.

The persistent global burden of herpes simplex virus type 2 (HSV-2) requires region-specific therapeutic strategies, yet the limited number of characterized clinical isolates from China has hindered accurate evaluation of local viral evolution and vaccine efficacy. To address this gap, we isolated and comprehensively characterized HSV-2/KM-1, a novel clinical strain obtained from a genital herpes patient in Kunming, China. Whole-genome sequencing showed 99.92% nucleotide identity with contemporary U.S. strains (MH790606, PP099973), which was markedly higher than its homology to China's reference strain HJ12 (128 amino acid differences). This unexpected phylogeographic similarity challenges existing models of geographically restricted HSV-2 evolution and suggests global viral gene flow facilitated by human mobility. Cell tropism analyses revealed accelerated replication in human foreskin fibroblasts (HFF-1), with early viral protein expression at 12 hpi, and high-titer production (7.0 log10 TCID₅₀/mL) in Vero cells at a low MOI (0.001). Comparative genomics identified 27 amino acid substitutions in virulence determinants (ICP4, UL52, UL36, etc.) compared with the U.S strain (PP099973), 14 of which altered residue polarity, potentially influencing viral-host interactions, as suggested by previous studies on these proteins' roles. As a phylogenetically U.S.-linked clinical isolate from China, HSV-2/KM-1 helps to fill a gap in regional pathogen resources and provides a critical tool for assessing globally circulating strains and developing targeted interventions.