The presence of abnormal hematologic findings such as lymphopenia, thrombocytopenia, and pancytopenia were diagnosed in severe cases of avian influenza A H5N1. Whether direct viral dissemination to bone marrow (BM) cells causes this phenomenon remains elusive. We explore the susceptibility of the two stem cell types; hematopoietic stem cells (HSCs) and mesenchymal stromal cells (MSCs) isolated from human BM cells or cord blood, to infection with avian H5N1 viruses. For the first time, we demonstrated that the H5N1 virus could productively infect and induce cell death in both human stem cell types. In contrast, these activities were not observed upon human influenza virus infection. We also determined whether infection affects the immunomodulatory function of MSCs. We noted a consequent dysregulation of MSC-mediated immune modulation as observed by high cytokine and chemokine production in H5N1 infected MSCs and monocytes cocultures. These findings provide a better understanding of H5N1 pathogenesis in terms of broad tissue tropism and systemic spread.

Norovirus (NoV), a leading cause of acute gastroenteritis worldwide, imposes significant morbidity and economic burdens across all age groups. Timely and accurate laboratory diagnosis is crucial for effective outbreak control and patient management. However, current diagnostic methods often require specialized equipment, technical expertise, and considerable time. To address these challenges, we developed a visual detection method utilizing gold nanoparticles (AuNPs) functionalized with the SMV25 aptamer specific to the NoV capsid protein. Detection relies on MgCl₂-induced changes in the color and absorbance of these aptamer-functionalized AuNPs. The assay exhibited a good linear relationship between the A630/A520 absorbance ratio and NoV capsid protein concentration. Specifically, in a buffer system, this linearity (R² = 0.9026) was observed over a 0–32 ng/µL range with a limit of detection (LOD) of 9.65 ng/µL. Similarly, for NoV spiked into stool suspensions, a strong linear correlation (R² = 0.9170) was found across a 0–100 ng/µL range, with an LOD of 37.11 ng/µL. Evaluation with real stool samples yielded 77% sensitivity and 65% specificity. Notably, the assay demonstrated the highest sensitivity towards NoV GII.2 (100%), followed by GII.4 (78%). Scanning transmission electron microscopy confirmed the underlying aggregation and dispersion patterns of the aptamer-functionalized AuNPs. This colorimetric assay provides a simple, rapid, and visual method for NoV detection. Nevertheless, further enhancements are necessary to improve its performance in the direct testing of complex specimens, paving the way for future on-site detection applications, especially in resource-limited settings.

Two primary vaccines for coronavirus disease 2019 (COVID-19) have been rolled out in the mass vaccination campaign that started simultaneously with the spread of the delta variant. To explore the vaccines’ effect on reducing viral load and disease severity, we conducted a retrospective cohort study in Thai patients aged ≥18 years who were confirmed COVID-19 positive by RT-PCR. Compared to unvaccinated patients, Ct values and the number of severe cases among vaccine regimens were analyzed. Ct values of vaccinated patients were not significantly different from unvaccinated patients, despite an increase of Ct values in a booster dose. The adjusted odd ratio for prevention of delta-related severe diseases was 0.47, 95% CI: 0.30–0.76 and 0.06, 95% CI: 0.01–0.45 after receiving one dose and two doses, respectively. No severe illness was found in booster-vaccinated individuals. Focusing on the vaccine types, one dose of ChAdOx1 nCoV-19 gave significant protection, whereas one dose of CoronaVac did not (0.49, 95% CI: 0.30–0.79, p = 0.003 vs. 0.28, 95% CI: 0.04–2.16, p = 0.223). Two-dose vaccination showed robust protective effects in all subpopulations regardless of vaccine type. Vaccinations with two primary vaccines could not reduce viral load in patients with COVID-19, but could prevent severe illness.

Vancomycin-resistant Enterococcus faecium (VREfm) is a significant cause of hospital-acquired infections due to its multidrug resistance, environmental persistence, and high transmissibility. This study aimed to characterize clinical and surveillance VREfm isolates by examining antimicrobial resistance profiles, virulence gene distribution, biofilm formation, and genetic background. A total of 107 VREfm isolates (43 clinical, 64 surveillance) were collected from Maharaj Nakorn Chiang Mai Hospital. Antimicrobial susceptibility testing, PCR detection of resistance and virulence genes, and biofilm formation using the crystal violet assay were performed. Whole genome sequencing (WGS) was conducted on four representative isolates. Most clinical isolates (88.4%) were from urine samples, while all surveillance isolates were obtained from rectal swabs. The majority of patients (74-75%) were over 60 years old. All isolates exhibited resistance to ampicillin, penicillin, ciprofloxacin, levofloxacin, and vancomycin, with some showing high-level gentamicin resistance. The vanA gene was detected in all isolates, corresponding with vancomycin MICs ≥64 µg/mL. Virulence genes esp, hyl, acm, and sagA were detected in 96.9-100% of isolates. Moderate biofilm formation was observed in 83.7% of clinical and 68.7% of surveillance isolates, particularly among those carrying multiple virulence genes. WGS identified two sequence types; ST17 and ST262, which shared similar resistance and virulence profiles. Clinical and surveillance VREfm isolates exhibited comparable resistance and virulence characteristics. These findings underscore the need for continuous surveillance of VREfm in hospitals, particularly among high-risk populations, to prevent infections and improve treatment strategies.

Background: Multiple severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) variants emerged globally during the recent coronavirus disease (COVID-19) pandemic. From April 2020 to April 2021, Thailand experienced three COVID-19 waves, and each wave was driven by different variants. Therefore, we aimed to analyze the genetic diversity of circulating SARS-CoV-2 using whole-genome sequencing analysis. Methods: A total of 33 SARS-CoV-2 positive samples from three consecutive COVID-19 waves were collected and sequenced by whole-genome sequencing, of which, 8, 10, and 15 samples were derived from the first, second, and third waves, respectively. The genetic diversity of variants in each wave and the correlation between mutations and disease severity were explored. Results: During the first wave, A.6, B, B.1, and B.1.375 were found to be predominant. The occurrence of mutations in these lineages was associated with low asymptomatic and mild symptoms, providing no transmission advantage and resulting in extinction after a few months of circulation. B.1.36.16, the predominant lineage of the second wave, caused more symptomatic COVID-19 cases and contained a small number of key mutations. This variant was replaced by the VOC alpha variant, which later became dominant in the third wave. We found that B.1.1.7 lineage-specific mutations were crucial for increasing transmissibility and infectivity, but not likely associated with disease severity. There were six additional mutations found only in severe COVID-19 patients, which might have altered the virus phenotype with an inclination toward more highly pathogenic SARS-CoV-2. Conclusion: The findings of this study highlighted the importance of whole-genome analysis in tracking newly emerging variants, exploring the genetic determinants essential for transmissibility, infectivity, and pathogenicity, and helping better understand the evolutionary process in the adaptation of viruses in humans.