The rapid evolution of viral pathogens presents significant challenges for global health, as traditional methods for virus detection often fail to identify novel or genetically diverse viruses. The emergence and reemergence of viral pathogens necessitate more advanced and inclusive diagnostic approaches. This review aims to explore the role of metagenomics in overcoming the limitations of traditional viral detection methods and to assess its impact on the discovery, characterization, and surveillance of viral pathogens. A comprehensive review of recent studies employing metagenomic approaches to viral detection was conducted. High-throughput sequencing technologies and bioinformatics tools were highlighted as key components in enabling broad-spectrum viral identification and characterization. Metagenomic approaches have successfully identified novel pathogens, including new arboviruses and reemerging strains of known viruses. These techniques provide a more complete understanding of viral diversity and dynamics, surpassing the limitations of targeted assays and culturing methods. Key findings emphasize the capability of metagenomics to detect viruses previously undetected by conventional methods, improving the scope of surveillance. Metagenomics offers transformative advantages for viral surveillance and outbreak management. It enhances early detection, allows for better-informed responses to viral threats, and contributes to more effective strategies for managing emerging and reemerging viral pathogens. Integration of metagenomic techniques into public health practices is crucial for combating the evolving landscape of viral diseases.

Severe fever with thrombocytopenia syndrome (SFTS) is an emerging zoonotic disease caused by the tick-borne SFTS virus (SFTSV), with a case fatality rate of 16.2-32.6% in East Asia. Currently, no approved vaccines or antiviral treatments exist. Monoclonal antibody (mAb) therapy offers rapid immune protection and is a promising strategy against SFTSV. This review outlines advances in SFTSV neutralizing mAb research, covering conventional generation methods (hybridoma, phage display) and innovative approaches such as single B cell sequencing. We also introduce computational tools like artificial intelligence -assisted epitope prediction and mAb design. Furthermore, we discuss the structure-function relationships of mAbs targeting Gn and Gc glycoproteins, their mechanisms (e.g., fusion inhibition, receptor blockade), and key functional attributes including breadth, potency, and cross-reactivity. Challenges such as limited epitope accessibility, immune interference, and antibody-dependent enhancement are highlighted. Finally, we propose a multipronged strategy integrating structure-guided engineering, high-throughput screening, and rigorous preclinical evaluation to accelerate the development of safe and effective SFTSV therapeutics.

The hepatitis delta virus (HDV) is a defective and small, blood-borne viroid-like pathogen that coinfects with the hepatitis B virus (HBV) in about 5% of the infected individuals as it is a satellite virus of HBV. The treatment of HDV infection is quite challenging because there is no vaccine against HDV. Several commercial PCR and in-house assays have been developed, but there are greater variations in the results of these assays because they are not standardized properly. Studies are also delayed because of the unavailability of commercial HDV-specific antibodies for the diagnosis of HDV infection, even for the research devotions. To fill this gap, the recombinant antigenic HDAg protein of genotype I of HDV from the local isolate was successfully expressed and purified in the Escherichia coli () system, followed by anti-HDAg antibodies production in rabbits. After determining and amplifying the antigenic region of of HDV, the fragment was cloned into the pET-28a vector and expressed in TOP10 cells. Following the successful expression of recombinant protein with a His-tag at its C-terminal end, we purified the protein using affinity chromatography. Both the expression and purification of HDAg-An protein were confirmed through SDS-PAGE and Western blot analysis. Through proper optimization, the HDAg-An protein was obtained with more than 90% purity. The next step involved immunizing Japanese White rabbits with the purified . The immunization protocol included 80 µg of HDAg-An in two subcutaneous priming doses and four 40 µg booster doses, followed by blood collection two weeks after each boost to monitor antibody production. The level of anti-HDAg antibodies in the rabbit serum was assessed using a quantitative ELISA technique. In the future, these antibodies could be used for the development of HDV-specific in-house assays as well as vaccines against the HDV genotype I that is locally predominant, potentially decreasing the burden of imported diagnostic tools and reagents.

Interleukin-37 (IL-37) can prevent liver damage and may be an important candidate for use as a novel therapeutic tool in hepatitis B virus (HBV) infection. This study aimed to evaluate the serum levels of IL-37 in individuals with chronic HBV (CHB) infection, those who spontaneously cleared (SC) HBV infection, compared with healthy control (HC) subjects. This case-control study included 30 patients with CHB (17 males, 13 females; mean age, 50.13 ± 14.51), 30 subjects with SC HBV infection (16 males, 14 females; mean age, 51.50 ± 16.85), and 42 HC subjects (22 males, 20 females; mean age, 53.52 ± 14.44). Blood samples were collected, and then serum IL-37 levels were measured using an enzyme-linked immunosorbent assay kit. Our results showed that serum IL-37 levels were significantly higher in the CHB (96.99 ± 13.39 pg/mL) than in the HC group (37.85 ± 2.99 pg/mL, = 0.02). No statistically significant differences were found in IL-37 serum levels between CHB group and SC group (91.93 ± 17.11 pg/mL, = 0.43). Correlation analysis showed a significant negative correlation between serum IL-37 levels and age in SC subjects ( = 0.02, = -0.42). Our results suggest that increased production of IL-37 may biologically act as a negative feedback loop to attenuate the release of pro-inflammatory cytokines and subsequently alleviate disease symptoms in CHB. The negative correlation between the cytokine and age may indicate that higher levels of IL-37 in younger individuals may lead to the spontaneous clearance of HBV.

As a key component of innate immunity, natural killer (NK) cells initiate rapid effector responses against various viral pathogens. However, their role in the pathogenesis of hemorrhagic fever with renal syndrome (HFRS) remains unclear. In this study, NK cell subsets and receptor expression were analyzed by flow cytometry in patients with HFRS. Enzyme-linked immunosorbent assay was used to measure soluble HLA-G (sHLA-G) levels in plasma. In experimental models of acute viral infection, changes in the expression of several NK cell receptor ligands were also detected by flow cytometry. Flow cytometry revealed a redistribution of NK cell subsets in patients with HFRS, characterized by the expansion of CD56CD16 NK cells, which remained elevated from the acute phase to the convalescent phase. In addition, sustained overexpression of NK cell receptors (NCR p30, NCR p44, NCR p46, KIR2DL2/3, and KIR2DL4) was observed beyond the acute phase. Higher plasma concentrations of sHLA-G were detected in mild-type cases compared with moderate-type, severe-type, and critical-type patients. Hantaan virus infection was also found to upregulate intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), CD62E, CD62P, human leukocyte antigen-A, B, C (HLA-A, B, C), HLA-E, and HLA-G. These findings suggest that NK cells undergo rapid expansion following viral infection and maintain elevated levels throughout the clinical course, accompanied by persistent overexpression of NK receptors. Lower concentrations of soluble HLA-G (sHLA-G) in moderate-type, severe-type, and critical-type patients may indicate a potential mechanism contributing to increased vascular permeability in HFRS.

The immunological properties of recombinant hepatitis B surface antigen (rHBsAg), prepared using yeast ( [SC]) and Chinese hamster ovary (CHO) cells, were evaluated through and assays to support the efficacy of recombinant hepatitis B vaccines. , antigenicity was assessed by measuring the affinity of rHBsAg to anti-HB antibodies using surface plasmon resonance. mice were intraperitoneally injected with 3 µg of simulated vaccines containing anti-HB antibodies absorbed onto aluminum hydroxide adjuvant. Humoral responses were evaluated by measuring serum anti-HB antibody titers and seroconversion rates on days 7, 14, 21, and 28. Cellular immune responses were assessed based on cytokine (Interferon-γ-IFN-γ) and (Tumor Necrosis Factor-α- TNF-α) production from splenic lymphocytes on day 28 postimmunization. A recombinant Huh-7-HBsAg cell line, developed to analyze cellular immune responses, was established through cytotoxicity and apoptosis assays. , the equilibrium dissociation constant (K) of rHBsAg from CHO cells was significantly lower than that from yeast cells, indicating stronger antibody affinity. , rHBsAg-CHO induced faster and higher antibody titers compared with rHBsAg-SC. Cellular responses showed higher levels of TNF-α and IFN-γ for rHBsAg-CHO. In addition, the rHBsAg-CHO group exhibited higher late apoptosis rates in target cells. The rates induced in the rHBsAg-CHO and rHBsAg-SC groups were 25.0% and 19.2%, respectively. In conclusion, this study demonstrates that the immunological properties of rHBsAg vary based on the expression systems and provides nonclinical data supporting the evaluation of vaccine efficacy.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the causative agent of coronavirus disease 2019 (COVID-19), has led to a global health crisis by triggering extensive systemic and immune dysregulation. Granulocytes, including neutrophils, eosinophils, and basophils, are critical components of the innate immune system that play dual roles in protection and pathogenesis during infection. In this review, we examine the multifaceted roles of granulocytes in COVID-19 and their impact on disease severity through excessive inflammation, cytokine storm, and tissue damage. Neutrophil extracellular traps (NETs) and the overactivation of neutrophil subtypes contribute to the development of thrombosis and acute respiratory distress syndrome. In contrast, eosinophils and basophils modulate T helper 2-type and allergic responses that may influence recovery or disease progression. We further summarize the therapeutic strategies targeting granulocyte activation and signaling pathways, including IL-1, IL-6, IL-17, IL-5 receptor, granulocyte-macrophage colony-stimulating factor inhibitors, and antihistamines, emphasizing their clinical outcomes, approval status, and the global regions in which they are studied. Understanding the regulatory mechanisms of granulocyte activation and inhibition provides new insights into COVID-19 immunopathology and opens pathways for targeted immunomodulatory therapy. These findings underscore the importance of balancing protective immune functions with controlled anti-inflammatory interventions to mitigate the severe complications of SARS-CoV-2 infection.

The objective of this study is to examine the general characteristics, clinical manifestations, laboratory findings, and imaging features of patients with lung adenocarcinoma who develop influenza pneumonia while undergoing immunotherapy. A retrospective analysis was conducted on the clinical data of 48 patients with lung adenocarcinoma and pulmonary infections who received immunotherapy as a stand-alone treatment between September 2022 and September 2024 at the Affiliated Hospital of North China University of Science and Technology. Clinical characteristics of patients with concurrent influenza pneumonia were assessed. When compared with the non-influenza pneumonia group, patients in the influenza pneumonia group demonstrated significantly more severe systemic symptoms, elevated urea nitrogen levels, reduced platelet counts, decreased serum albumin levels, lower Prognostic Nutritional Index values, and higher prevalence of bilateral and multilobed lung involvement. Chest imaging frequently revealed ground glass opacities, reticular patterns, and the "crazy paving" sign. Additionally, this group exhibited higher CURB-65 scores and an increased need for intensive care unit admission, with all comparisons yielding values <0.05. Hypotension emerged as a potential factor influencing mortality in both groups (odds ratio = 9.094, = 0.041). Among the 19 patients with lung adenocarcinoma and influenza pneumonia, 89.5% had coinfections with other pathogens. Gram-negative bacterial infections were the most common (64.7%), with subspecies, , and identified as the leading pathogens. Fungal infections, primarily involving species, accounted for 23.5% of cases. General characteristics, clinical manifestations, laboratory findings, and imaging features are essential references for the diagnosis and management of lung adenocarcinoma complicated by influenza pneumonia. Particular attention should be directed to blood pressure fluctuations, with careful monitoring of low blood pressure, especially when accompanied by bacterial infections.

Chronic hepatitis B (CHB) drives liver fibrosis, contributing to chronic liver disease. Galectin-3 (Gal-3), a lectin linked to inflammation and fibrosis, was investigated for its association with liver injury severity in HBeAg-negative CHB and chronic hepatitis B virus (HBV) infection (CHI) patients. We enrolled 25 CHB, 25 CHI, and 25 healthy controls. Serum Gal-3 levels were measured in all subjects, with liver biopsies performed in CHB patients. Gal-3 and HBV DNA levels were monitored at 0, 1, 3, 6, and 12 months during antiviral therapy in CHB patients. Serum Gal-3 levels were significantly higher in CHI (median: 422 U/L, interquartile range [IQR]: 144-900) and CHB (median: 567 U/L, IQR: 196-1093) patients than controls (median: 179 U/L, IQR: 79-350; < 0.001). Although Gal-3 levels were higher in CHB than CHI, the difference was not significant ( = 0.08). Median Gal-3 levels in CHB patients decreased from 567 U/L to 288 U/L after 12 months of antiviral therapy ( = 0.043 after excluding an outlier). Gal-3 levels showed weak correlations with HBV DNA (Spearman's rho = 0.32, = 0.12), ALT (rho = 0.28, = 0.17), and fibrosis scores (rho = 0.35, = 0.09). Elevated Gal-3 levels correlate with HBeAg-negative CHB and CHI, with a significant decline posttreatment in CHB. If validated, Gal-3 could serve as a noninvasive marker for fibrosis and treatment response.

To assess the dynamics of humoral immune responses to inactivated SARS-CoV-2 vaccines across populations with and without prior COVID-19 infection, a longitudinal cohort study was conducted. A total of 38 COVID-19-recovered individuals and 165 naïve participants (without prior COVID-19 infection) were enrolled, all of whom completed a two-dose vaccination regimen. Levels of anti-spike (anti-S) and anti-nucleocapsid (anti-N) antibodies were analyzed at baseline and post-vaccination time points, including 6 weeks post-first dose, and 1 month and 6 months post-second dose. Among naïve participants, the seropositivity rate for anti-S antibodies increased to 96.23% at 1 month after the second dose with anti-S titers peaking at a median of 54.59 U/mL ( < 0.0001). Conversely, COVID-19-recovered participants exhibited significantly elevated anti-S levels after the first dose (median titer: 637.70 U/mL, < 0.0001), with no notable changes following the second dose. Anti-S levels in both groups declined by 6 months post-second dose. The dynamic pattern of anti-N antibodies was comparable to that of anti-S, albeit with weaker vaccine-induced responses. Notably, levels of both anti-S and anti-N antibodies decreased with advancing age ( < 0.001). Males demonstrated lower anti-N antibody levels compared with females ( = 0.038), while the presence of underlying diseases was associated with higher anti-S antibody levels ( = 0.030). In conclusion, two doses effectively augmented antibody levels in naïve individuals, whereas a single dose may suffice to confer immune protection in COVID-19-recovered individuals. Antibody levels wane over time, necessitating further investigations into the durability of vaccine-mediated immune protection, evidence-based recommendations for preventive vaccination, and the formulation of immunization strategies tailored to distinct populations.

In a subgroup of patients, coronavirus disease (COVID)-19 is a severe illness with high mortality due to hyperinflammation, development of acute respiratory distress syndrome, and multiorgan dysfunction syndrome. Complement system activation plays a critical role in the pathogenesis and severity of COVID-19 disease. This cross-sectional, single-center study aimed to investigate the correlation between serum C3 and C4 levels and COVID-19 severity. We included 125 patients hospitalized between December 2020 and March 2021. Patients were stratified into three groups based on the level of respiratory support needed to maintain adequate oxygenation (PaO ≥ 60 mmHg): 51 patients requiring oxygen supplementation up to 15 L/min, 51 patients requiring high-flow oxygen therapy, and 23 patients requiring mechanical ventilation (MV). We analyzed the blood counts and serum levels of C3, C4, C-reactive protein (CRP), IL-6, procalcitonin, d-dimers, high-sensitive troponin I (TnI), N-terminal pro-brain natriuretic peptide (NT-proBNP), IgA, IgG, IgM, C3, C4, rheumatoid factor, and anticitrullinated peptide antibodies. Patients on MV had significantly lower levels of C3 and C4 (0.98 ± 0.24 g/L for C3 and 0.21 ± 013 g/L for C4) compared with patients with less severe disease ( < 0.001 for C3, < 0.001 for C4). Serum C3 and C4 levels were lower in patients requiring high-flow oxygen therapy than in those requiring oxygen supplementation, however, the difference was not statistically significant. In addition, higher neutrophil counts were observed in patients on MV or high-flow oxygen therapy than in those on oxygen supplementation, and higher CRP, procalcitonin, and NT-proBNP levels were observed only in patients on MV. The levels of IL-6, d-dimers, and high-sensitive TnI were positively correlated with disease severity, whereas lymphocyte counts showed a negative correlation, and these differences were statistically significant among all three groups. The determination of serum levels of C3 and C4, along with other known laboratory risk factors, may contribute to the detection of patients at an increased risk for severe COVID-19.

Analysis of the viral load in respiratory syncytial virus (RSV) infection has focused on the nasopharyngeal site (NPS) near the lower respiratory tract, which is the primary lesion site, and the viral load in the anterior nasal site (ANS) near the nostrils has not been clarified in adults or children. The study evaluated the nasal distribution of RSV. A total of 49 patients, with 0 months to 71 years of age, participated in the study. A total of 774 specimens were collected from the ANS and NPS. In the pediatric group, the highest viral load in the NPS was 1.1 × 10 copies/mL on day 1 of onset, and the highest in the ANS was 4.1 × 10 copies/mL on day 2. Thereafter, the viral load at both sites decreased gradually over time. The adult group showed a peak viral load on the onset day, with 1.5 × 10 copies/mL in the NPS and 8.4 × 10 copies/mL in the ANS. By day 7 of onset, the viral load was 3.9 × 10 copies/mL in the NPS and 1.3 × 10 copies/mL in the ANS, indicating that the viral load at both sites remained parallel. We demonstrated that the RSV load was present in the ANS and NPS of children and adults from the date of onset. The ANS is closer to the nostrils and is a more promising specimen collection site than the NPS at all ages but has a lower viral load than the NPS.

Cell senescence, induced by various internal and external stresses, plays a significant role in the development of various diseases such as cancer, neurodegeneration, and infections. Viral infections can also induce cellular senescence, known as virus-induced senescence (VIS), which occurs in close correlation with the severity of the viral infections. However, due to the unclear mechanisms underlying VIS, the effective inhibition of VIS during viral infections is challenging, leading to rapid disease progression. This study utilized the widely used vesicular stomatitis virus (VSV) model virus to simulate RNA virus infections for exploring the mechanisms by which RNA viruses induce cellular senescence. The results indicated that VSV infection, both and , could significantly induce the upregulation of senescence-associated markers and the secretion of the senescence-associated secretory phenotype (SASP), promoting the senescence process. Further research found that the activation of the NF-κB pathway played a crucial role in VSV-induced cellular senescence. Targeted inhibition of the NF-κB pathway could reduce the level of organ senescence induced by viral infections, decrease the expression of SASP inflammatory factors, and ameliorate tissue damage in mice. Overall, our findings reveal the mechanisms underlying RNA virus-associated VIS and provide potential targets for inhibiting the occurrence of VIS and preventing disease progression.

Human metapneumovirus (HMPV) is a prominent respiratory pathogen causing significant morbidity and mortality worldwide, mostly in young teenagers, the old, and immunocompromised individuals. Despite its clinical impact, no licensed vaccine is currently available, highlighting the urgent need for effective prophylactic strategies. This research aimed to design a multiepitope vaccine (MEV) targeting conserved and immunodominant regions of HMPV, leveraging immunoinformatics tools to ensure broad coverage and efficacy against the virus and its diverse sublineages. Glycoproteins from HMPV genotypes A2a, A2b, and A2c were analyzed to identify 18 highly antigenic and overlapping epitopes capable of eliciting robust B-cell, T-cell, and interferon-gamma (IFN-γ)-mediated immune responses. Toxicity and allergenicity studies confirmed the safety of particular epitopes, which were incorporated into two vaccine constructs using immunogenic linkers and adjuvants. The chimeric vaccines displayed high antigenicity, molecular stability, and nonallergenic properties. Structural refinement and Ramachandran plot analyses established the stability and accuracy of the 3D models. Molecular docking studies verified strong interactions with immune receptors, particularly toll-like receptor (TLR)2, TLR3, TLR4, TLR8, and human leukocyte antigen molecules, indicating robust immune stimulation potential. Molecular dynamics simulations further validated the vaccine's stability and interaction dynamics, with immune simulations predicting promising responses. The designed vaccine constructs were shown to be highly soluble, stable, and suitable for recombinant expression in , enabling further biochemical and immunoreactivity validation. These findings provide a foundation for next-generation vaccine development against HMPV, offering promising avenues for clinical application and future research. [Figure: see text].

The aim of this study was to compare immune response against SARS-CoV-2 in Balb/C mice when self-amplifying RNA lipid nanoparticles (saRNA LNPs) combined with TLR4 Agonist (monophosphoryl lipid A) as the adjuvant 1 and TLR9 Agonist (CpG) as the adjuvant 2. Here, we found that the size distribution of saRNA LNPs was 88-165 nm with a mean size of 126 nm. Although TLR4 Agonist (adjuvant 1) and TLR9 Agonist (adjuvant 2) could increase the expression of S-protein in HEK293T/17 cells compared with saRNA LNPs alone, the combination of both adjuvants had a significant effect on the expression of the S-protein. Moreover, combining TLR4 Agonist (adjuvant 1) and TLR9 Agonist (adjuvant 2) increased the antibody (IgG and IgA) titer. Here, the ratio of IgG2a/IgG1 showed a T helper type 1-biased response. ELISpot test showed the mice vaccinated with saRNA LNPs+ TLR4 Agonist and TLR9 Agonist had significantly more secreting cells compared with other vaccinated mice ( < 0.05). The secretion of interleukin (IL)-4 and interferons (IFN)-γ by re-stimulated splenocytes confirmed these data. Significant differences in concentration of IL-4 and IFN-γ produced by activated splenocytes were also seen in the mice vaccinated with saRNA LNPs+ TLR4 Agonist and microparticles compared with other groups ( < 0.05). The highest quantity of S-protein was detected in the blood, followed by the small intestine and spleen. The interesting thing was that no significant difference was seen between the amount of S-protein induced by different formulations and the type of adjuvant did not affect the biodistribution.

Evaluating the impact of cardiac surgery on humoral and cellular immunity in pediatric congenital heart disease patients with prior Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) infection or vaccination is crucial for postoperative care planning. This study enrolled 61 pediatric patients undergoing cardiac surgery with cardiopulmonary bypass at a single institution. Measurements were taken before the operation, immediately postoperation, and during the first follow-up examination at least 1 month later. The evaluations included SARS-CoV-2-specific immunoglobulin G (IgG) and neutralizing antibodies for humoral immunity assessment, as well as specific and nonspecific T-cell immune responses to gauge T-cellular immunity and functionality. The results demonstrated that the serum titers of IgG and neutralizing antibodies remained comparable postsurgery to preoperative levels. Nevertheless, significant decreases in specific and nonspecific T-cell immune responses, along with a decline in CD3 T-cell numbers, were observed immediately following surgery. This was followed by a gradual recovery of immune response to preoperative levels approximately 1 month later. These findings suggest that in the first month following cardiac surgery in pediatric patients, residual specific antibodies, potentially derived from the original production or plasma transfusion, may provide partial protection against COVID-19 infection. Subsequently, T-cellular immunity gradually recovers and resumes its protective role. The study provides important insights into the dynamics of immune recovery following cardiac surgery in this vulnerable patient population, which may be essential for optimizing postoperative management and reducing the risk of COVID-19 infection.

La Crosse virus (LACV), a constituent of the California serogroup (CSG) within the genus in the Peribunyaviridae family, is the causative agent of LACV encephalitis. This form of encephalitis stands as one of the most significant and burgeoning mosquito-borne diseases in the United States, ranking as the second most prevalent mosquito-borne illness following West Nile virus encephalitis. Predominantly identified in the Midwestern, Mid-Atlantic, and Southeastern regions of the United States, LACV primarily afflicts humans through the bites of mosquitoes. Its genome, divided into three segments, encodes proteins that not only facilitate efficient replication within hosts but also hinder host immune responses. Infections by LACV can lead to a spectrum of neurological outcomes, ranging from mild aseptic meningitis to severe encephalitis with the potential for long-lasting neurological deficits. Despite the availability of diagnostic tools, several challenges persist. Currently, the management of LACV infection remains supportive, underscoring the importance of preventative measures in substantially mitigating the infection's incidence and severity. Moreover, global warming elevates the risk of LACV spreading to new territories. This review delves into recent advancements concerning the transmission and pathogenesis of LACV, drawing upon current knowledge regarding its genetic framework, transmission modes, geographical spread, phylogenetic relationships, clinical presentations and neuropathogenic effects, diagnostic approaches, treatment modalities, and prevention strategies.

SARS-CoV-2 has evolved into several variants of concern, with Omicron and its subvariants currently being the most prevalent. Previously, we developed a mouse monoclonal antibody (m1E3H12 mAb) specific to the receptor binding domain of SARS-CoV-2 Omicron spike protein, and the mAb showed neutralizing activity against SARS-CoV-2 Omicron BA.1 and its subvariants BA.5, BQ.1.1, and XBB. Here, we showed that the mAb provided protection against SARS-CoV-2 Omicron infection in K18-hACE2 transgenic mice when administered intranasally. The mAb treatment reduced viral loads in both the brain and lungs. Additionally, the elevated levels of RANTES (CCL5) and MIP-3 alpha (CCL20) in the brain following SARS-CoV-2 Omicron infection showed a decreasing trend after mAb treatment. Therefore, we conclude that our mAb specific to SARS-CoV-2 Omicron spike protein has the potential to be applied as therapeutics against SARS-CoV-2 Omicron BA.1 and its subvariants BA.5, BQ.1.1, and XBB.

BK virus is a childhood virus that can reactivate in immunocompromised individuals, particularly organ transplant recipients, causing transplant rejection due to BK virus-associated nephropathy. The study aimed to assess the prevalence of BK virus infection in kidney transplant recipients, examine the relationship between demographic and laboratory factors and active infection, evaluate the impact of reducing immunosuppressive drug doses on BK virus reactivation, and explore the genotyping of BK virus strains in this population. This cross-sectional study utilized 245 serum samples from kidney transplant recipients. Viral DNA was extracted from these samples, and initially, Nested PCR was employed for screening to ensure accuracy, with primers targeting a segment of the VP1 gene used to detect the BK virus genome. Real-Time PCR was subsequently performed on positive samples to measure viral load more precisely. The prevalence of BK virus infection among kidney transplant recipients was 5.3%. Out of 245 kidney transplant recipients, 13 individuals were diagnosed with active BK virus infection. Genotype I was the most prevalent, accounting for 90% of the cases. The relationship between demographic factors (gender and age) and laboratory parameters (fasting blood glucose, creatinine, hemoglobin, and platelet count) was examined in both kidney transplant recipients with and without active BK virus infection. The results revealed that a reduction in immunosuppressive drug dosages, particularly tacrolimus, was associated with a decrease in BK viral load, potentially contributing to a lower incidence of active BK virus infections. Additionally, hematological analysis showed a significant decrease in hemoglobin levels in kidney transplant recipients with active BK virus infection, accompanied by a significant increase in serum creatinine levels. Balancing immunosuppressive therapy, especially reducing tacrolimus, helps control BK virus reactivation and preserve graft function. Regular monitoring of hematological parameters and viral load is crucial for optimal management in kidney transplant recipients.

Following reports of highly pathogenic avian influenza H5N1 infections of dairy cattle in the United States in March 2024, we established a Pan-Canadian Milk network to monitor retail milk in Canada. Milk samples from across Canada that had previously tested negative for influenza A virus (IAV) RNA were tested for the presence of anti-IAV nucleoprotein (NP) antibodies as an indicator of past infection of dairy cattle. None of the 109 milk samples tested had evidence of anti-IAV NP antibodies. This is consistent with previous findings from our academic group as well as others including federal testing initiatives that have not found any IAV RNA in milk. Although not surprising given that no cases of H5N1 in cattle have been reported in Canada to date, this work further supports that the extensive outbreak in dairy cattle in the United States has not extended northward into Canada, and the integrity of the Canadian milk supply remains intact.

This study aimed to generate a monoclonal antibody (mAb) against feline coronavirus (FCoV) spike (S) protein and to develop a colloidal gold immunochromatographic strip for the rapid and accurate FCoV detection. BALB/c mice were immunized with the purified protein, and hybridoma technology was employed to produce highly effective mAb. A positive hybridoma cell line (E5) was identified, which stably secreted mAb with a high titer of 1:256000 against the FCoV S recombinant protein. Western blot analysis confirmed the mAb E5's specificity. The established test strip can detect FCoV specifically and detect the antigen concentrations as low as 1.2 × 10 mg/mL. The diagnostic sensitivity and specificity of the FCoV detection strip for feline coronavirus infections were 94.2% and 100%, respectively, as confirmed by reverse transcription polymerase chain reaction (RT-PCR). The detection strip demonstrated no cross-reactivity with other feline pathogens and showed consistent results in reproducibility tests. The developed colloidal gold test strip offers a highly sensitive and specific tool for rapid FCoV detection, contributing to improved real-time epidemic monitoring.