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Background We conducted a retrospective study to explore molecular insights into human respiratory syncytial virus (HRSV) group B strains among patients attending outpatient clinics at government medical facilities both prior and during the onset of Influenza A/H1N1/2009 pandemic outbreak. Methods We screened 2300 nasopharyngeal swabs using multiplex real time reverse transcriptase polymerase chain reaction. We amplified a segment of the first and second hypervariable regions, as well as the conserved portion of the third domain of the G‐gene using HRSV‐B specific primers, sequenced by Sanger di‐deoxy chain termination method and thereafter analyzed the sequences. Results We characterized the circulating strains into three known genotypes: SAB4 (1.4%), BA7 (1.4%), and multiple variants of BA9 (97.2%). The majority of BA9 viruses were uniquely Kenyan with only 4% aligning with BA9 lineages found elsewhere. The mean evolutionary rate of the HRSV‐B was estimated to be 3.08 × 10−3 substitutions per site per year. Conclusion Our findings indicate that the circulating HRSV‐B viruses in Kenya underwent a slower evolution during the period of 2007–2010. Additionally, our findings reveal the existence of a unique lineage as well as new variants that have not been reported elsewhere to date.

Deformed wing virus (DWV) is an emerging infectious disease of the honey bee (Apis mellifera) that is considered a major cause of elevated losses of honey bee colonies. DWV comprises two widespread genotypes: the originally described genotype A, and genotype B. In adult honey bees, DWV-B has been shown to be more virulent than DWV-A. However, their comparative effects on earlier host developmental stages are unknown. Here, we experimentally inoculated honey bee pupae and tested for the relative impact of DWV-A versus DWV-B on mortality and wing deformities in eclosing adults. DWV-A and DWV-B caused similar, and only slightly elevated, pupal mortality (mean 18% greater mortality than control). Both genotypes caused similarly high wing deformities in eclosing adults (mean 60% greater wing deformities than control). Viral titer was high in all of the experimentally inoculated eclosing adults, and was independent of wing deformities, suggesting that the phenotype ‘deformed wings’ is not directly related to viral titer or viral genotype. These viral traits favor the emergence of both genotypes of DWV by not limiting the reproduction of its vector, the ectoparasitic Varroa destructor mite, in infected pupae, and thereby facilitating the spread of DWV in honey bees infested by the mite.

Enterobiasis, caused by the nematode Enterobius vermicularis, remains a widespread public health issue, yet data regarding its genetic structure in Southeast Europe are scarce. This study presents the first molecular and phylogenetic characterization of E. vermicularis isolates from Bulgaria. Between 2022 and 2025, perianal tape test samples were collected from 128 individuals (92.2% of whom were children) with enterobiasis from 17 regions of the country. Molecular identification was performed via nested PCR targeting a 324 bp fragment of the mitochondrial cytochrome c oxidase subunit 1 (cox1) gene, followed by Sanger sequencing. Phylogenetic relationships were analyzed using Maximum Likelihood (IQ-TREE), and population genetic indices were calculated using DnaSP v6. Phylogenetic analysis revealed that all 128 Bulgarian isolates belong to genotype B, clustering closely with sequences from other European and Asian countries. Genetic diversity analysis showed remarkably low variation, with a haplotype diversity (Hd) of 0.1507 ± 0.0416 and a nucleotide diversity (π) of 0.00082 ± 0.00015. Among the 11 identified haplotypes, a single dominant haplotype (Hap_1) accounted for 92.2% of all samples and was distributed across all sampled geographic regions. Tajima’s D was significantly negative (−2.314, < 0.05), suggesting a recent population expansion or purifying selection. The dominance of genotype B and the extremely low genetic diversity suggest a recent introduction or clonal expansion of E. vermicularis in Bulgaria. These findings provide essential baseline data for monitoring transmission dynamics and implementing effective control strategies in the Balkan region.

Background Hepatitis B virus (HBV) remains a major health concern particularly in regions with intermediate-to-high endemicity such as Vietnam. Occult hepatitis B infection (OBI) defined as the presence of replication-competent HBV DNA in the absence of detectable hepatitis B surface antigen (HBsAg) poses challenges for diagnosis and blood safety. However, data on OBI among Vietnam’s ethnic minority populations are scarce. Methods A cross-sectional study was conducted among 267 HBsAg-negative ethnic minority students at Thai Nguyen University of Medicine and Pharmacy in 2024. Serum samples were screened for HBV serological markers (anti-HBs, anti-HBc) using commercial ELISAs. HBV DNA was extracted, amplified by nested PCR targeting a conserved S/P region, and sequenced for genotyping and mutational analysis. Quantitative real-time PCR (qPCR) was used to assess viral loads. Results Among participants, 57% were susceptible (anti-HBs–/anti-HBc–), 27% exhibited vaccine-induced immunity, 12% had resolved infections, and 4% showed isolated anti-HBc positivity. Overall, 16% were anti-HBc positive, indicating prior exposure. HBV DNA was detected in two samples (0.7%), both with undetectable viral loads by qPCR. One case represented seronegative OBI and the other seropositive OBI. Phylogenetic analysis classified both isolates as genotype B. Mutational analysis identified substitutions K122R, F200Y, Y206C, and I187V, with S117N uniquely present in one isolate. Conclusions This study provides the first evidence of OBI among ethnic minority students in northern Vietnam. Although prevalence was low, the high proportion of HBV-susceptible individuals highlights ongoing vulnerability and underscores the need for strengthened immunization, awareness, and surveillance programs in underserved communities.

(1) The glycoprotein B (gB) on the viral envelope, encoded by the most widely characterised polymorphic gene, gpUL55, is responsible for cytomegalovirus (CMV) entry into the host and could serve as a potential marker of pathogenicity. The aim of the present study is to investigate the distribution of the CMV gB genotype in anterior segment infection in Taiwan and its correlation with clinical manifestations and outcomes. (2) Fifty-seven patients with CMV anterior segment infection were identified according to clinical features and positivity for CMV DNA in aqueous humour samples. CMV gB genotyping was performed through polymerase chain reaction assays. Patients’ medical records were retrospectively reviewed. (3) Among the 57 aqueous humour samples tested for gB, 40 (70.28%) had multiple gB genotypes, and only 17 (29.82%) had a single gB genotype. Compared with single-genotype infection, multiple-genotype infection was correlated with higher CMV loads (p < 0.001) but not correlated with outcome. A higher proportion of patients with the gB3 genotype had received filtering surgery before antiviral treatment than those without the gB3 genotype (p = 0.046). (4) Multiple-genotype infection was highly prevalent in CMV anterior segment infection in Taiwan, and gB1 and gB3 were predominant. Multiple-genotype infection was correlated with higher CMV loads but not with specific clinical manifestations or prognostic outcomes. The gB3 genotype may be correlated with poor intraocular pressure control.

Enterovirus D68 (EV-D68) is a leading cause of acute respiratory disease outbreaks, especially among children. EV-D68 infections can rapidly progress to severe clinical complications and potentially fatal outcomes. In Brazil, no diagnostic or genomic surveillance of this virus is currently performed. Between July and September 2023, cases of acute EV-D68 infection were identified among pediatric patients in several municipalities within the State of Alagoas, Northeast Brazil. Infections were confirmed by RT-qPCR using nasopharyngeal samples, and the complete EV-D68 genomes were sequenced and analyzed through phylogenetic inference. EV-D68 RNA was identified in four children aged 1–9 years from four geographically distinct municipalities in Alagoas. All infections were associated with lower respiratory tract symptoms, including dyspnea and wheezing; however, no fatalities were reported. Complete genomic sequencing revealed that the samples belonged to genotype B, subgenotype B3. This is the first study to report complete genomic data on EV-D68 infections from Brazil and South America. Enhanced genomic surveillance and focused EV-D68 diagnosis are critical to better understanding and managing the regional and national dissemination of this virus.

Background: Interaction between host transcription factors (TFs) and the viral genome is fundamental for hepatitis B virus (HBV) gene expression regulation. Additionally, the distinct interaction of the TFs’ network with the HBV genome determines the regulatory effect outcome. Hence, different HBV genotypes and their variants may display different viral replication/transcription regulation. Due to the lack of an efficient infection model suitable for all HBV genotypes, the hepatoma cell transfection model is primarily used in studies involving non-D HBV genotypes and variants. Methods: We explored the transcriptome profile of host TFs with a regulatory effect on HBV in eight liver-derived cell lines in comparison with primary human hepatocytes (PHH). We further analyzed the suitability of these models in supporting HBV genotype B replication/transcription. Results: Among studied models, HC-04, as a result of the close similarity of TFs transcriptome profile to PHH and the interaction of specific TFs including HNF4α and PPARα, showed the highest efficiency in regard to viral replication and antigen production. The absence of TFs expression in L02 transfection model resulted in its inefficiency in HBV replication/transcription. Conclusion: These observations help to better design studies on regulatory mechanisms involving non-D HBV genotypes and variants’ gene expression and the development of more efficient therapeutical approaches.

Hepatitis B virus (HBV) genotype C is a prevalent HBV genotype in the Chinese population. Although genotype C shows higher sequence heterogeneity and more severe liver disease than other genotypes, its pathogenesis and immunological traits are not yet fully elucidated. In this study, we first established and chemically synthesized the consensus sequence based on representative 138 full-length HBV genotype C genomes from the Chinese population. The pHBV1.3C plasmid system, containing a 1.3-fold full-length HBV genotype C consensus sequence, was constructed for subsequent validation. Next, we performed functional assays to investigate the replicative competence of pHBV1.3C in vitro through the transient transfection of HepG2 and Huh7 cells and validated the in vivo function via a hydrodynamic injection to BALB/c recipient mice. The in vitro investigation revealed that the extracellular HBV DNA and intracellular replicative intermediate (i.e., pregenomic RNA, pgRNA) were apparently measurable at 48 h, and the HBsAg and HBcAg were still positive in hepatoma cells at 96 h. We also found that HBsAg and HBeAg accumulated at the extracellular and intracellular levels in a time-dependent manner. The in vivo validation demonstrated that pHBV1.3C plasmids induced HBV viremia, triggered morphological changes and HBsAg- or HBcAg- positivity of hepatocytes, and ultimately caused inflammatory infiltration and focal or piecemeal necrosis in the livers of the murine recipients. HBV protein (HBsAg) colocalized with CD8+ T cells or CD4+ T cells in the liver. F4/80+ Kupffer cells were abundantly recruited around the altered murine hepatocytes. Taken together, our results indicate that the synthetic consensus sequence of HBV genotype C is replication-competent in vitro and in vivo. This genotype C consensus genome supports the full HBV life cycle, which is conducive to studying its pathogenesis and immune response, screening novel antiviral agents, and further optimizing testing and therapeutics.

HLA-B27 has an established relationship with the development of ankylosing spondylitis (AS). After reviewing the HLA-B genotype from 407 Chinese subjects (318 patients and 89 sex-matched controls), we found that 252 patients and 32 controls were HLA-B27(+) and that HLA-B * 27:04 was the dominant HLA-B27 subtype ( N = 224). In all participants, HLA * 27:04 homozygous were only detected in two patients. In the HLA-B27(+) group, HLA-B40 was observed in 51 cases and one control ( p < 0.05, OR = 7.87, 95% CI 1.05–59.0); of these, the most genotype was HLA-B * 27:04/B * 40:01( N = 38). Two hundred thirty-nine patients' clinical information was recorded. Cases with HLA-B27/B46 had more peripheral joint involvement (OR = 3.95, 95% CI 1.77–8.79) in HLA-B27(+) AS. HLA-B * 15:02 may be a significant risk element to peripheral joint involvement ( p < 0.05) in HLA-B27(−) patients. Therefore, we believe HLA-B * 40:01, HLA-B * 46:01, and HLA-B * 15:02 can be the test indicators for AS diagnostic value.

Background BabA is a Helicobacter pylori cell surface adhesin, which binds to the ABO/Le b histo-blood group antigens (Le b ) and serves as a virulence factor. Methods H. pylori single colonies were isolated from 156 [non-ulcer dyspepsia (NUD) = 97, duodenal ulcer (DU) = 34, gastric cancer (GC) = 25)] patients. babA and babB genes were evaluated by gene/locus-specific PCR. BabA protein expression and Le b binding activity were determined by immunoblotting and ELISA, respectively. Results The combined categorization of H. pylori strains based on high, low or no levels of BabA expression and Le b binding, produced 4 groups: (I) BabA-high/Le b -high (36 %), (II) BabA-low/Le b -low (26 %), (III) BabA-neg/Le b -low (30 %) and (IV) BabA-neg/Le b -neg (8 %) strains. The majority (63 %) of the BabA-low/Le b -low strains exhibited mixed babA/B genotypes as compared to merely 18 % of the BabA-high/Le b -high, 15 % of the BabA-neg/Le b -neg and 11 % of the BabA-neg/Le b -low ( P  = 0.0001) strains. In contrast to NUD strains, the great majority (70 %) of DU strains were BabA-low/Le b -low (11 %, P  = 0.0001), which compared to NUD strains, enhanced the risk of DU by 18.8-fold. In parallel, infection with babA/ B mixed genotype strains amplified the risk of DU by 3.6-fold ( vs . babA -positive: P  = 0.01) to 6.9-fold ( vs . babA -negative: P  = 0.007). Conclusions Here, we show higher prevalence of mixed babA/B genotypes among BabA-low/Le b -low clinical strains. Recombination of babA and babB genes across their loci may yield lower BabA expression and lower Le b binding activity. We conclude that H. pylori strains with lower Le b binding activity are better adapted for colonization of the gastric metaplastic patches in the duodenum and enhance the risk of duodenal ulcers.