Viral immunology最新文献

The clinical features of viral respiratory infections in individuals with rheumatic immune diseases, renal diseases, hematological diseases, and healthy individuals were analyzed. Additionally, the impact of immunosuppressive therapy on the clinical manifestations of viral respiratory infections was explored. Patients attending the outpatient clinic of the Department of Rheumatology and Immunology at Suzhou Hospital of Traditional Chinese Medicine from October 1, 2023, to May 1, 2024, as well as healthy individuals undergoing physical examinations, were selected for the study. Data were collected through questionnaires, including information on viral respiratory infections, vaccination status, clinical symptoms, and medication use. A total of 425 questionnaires were collected. There were significant differences among groups in recovery time, disease classification, vaccination rates, and specific clinical symptoms (p < 0.05). Immunosuppressive therapy significantly reduced the incidence of runny nose (p = 0.046) and chills (p < 0.001) but was associated with a higher proportion of ordinary cases, suggesting that it may be associated with increased disease severity (p = 0.012). Multivariate logistic regression analysis showed that the use of glucocorticoids significantly prolonged both recovery time (p = 0.007) and duration of cough (p = 0.044). The rheumatology group experienced shorter recovery time (p = 0.016) and a lower risk of fever (38°C-39°C), whereas the hematology group had an increased risk of high fever (>39°C; p = 0.037). Vaccination significantly increased the likelihood of mild cases (p = 0.041), serving as an important protective factor. Additionally, younger patients and females tended to exhibit relatively more severe clinical manifestations. Significant differences between the groups existed in terms of symptomatology, clinical symptoms, and time to recovery, and the use of immunosuppressive therapy, especially glucocorticoids, may have exacerbated the patient's condition. Vaccination provided a protective effect for patients undergoing immunosuppressive therapy, mitigating the condition to a certain extent.

Human respiratory syncytial virus (hRSV) is a leading cause of respiratory infections in infants and older adults. The COVID-19 pandemic disrupted hRSV transmission due to non-pharmaceutical interventions (NPI), resulting in atypical circulation patterns, earlier seasonal peaks, and increased post-pandemic prevalence. Two key factors are proposed to underlie these changes: a reduced specific immune response due to decreased viral exposure and the emergence of novel hRSV variants. These factors contributed to a larger cohort of immunologically naïve children and lower levels of maternally derived antibodies, increasing susceptibility to severe hRSV disease, particularly in infants and children. Additionally, adults experienced waning immunity following prolonged periods of limited hRSV circulation. The post-pandemic resurgence was accompanied by the emergence of novel hRSV variants with altered transmissibility and virulence, such as GB5.0.6a in Europe and B.D.E.1 in China. These variants may reflect mutations driven by the reduced immunity, though further research is needed to assess their pathogenicity. Understanding the interplay between the reduced immunity due to NPI and virological factors is essential for addressing hRSV epidemiology. Enhanced molecular surveillance and immunological monitoring are crucial for guiding vaccination strategies and protecting vulnerable populations against future hRSV outbreaks.

Background: Several lines of evidence have shown high intraindividual and intraindividual variability in serum levels of IgM and IgG antibodies in response to severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2). The present study aimed to assess the levels of SARS-CoV-2-specific IgM and IgG antibodies in serum samples of laboratory-confirmed coronavirus disease 2019 (COVID-19) patients.

Methods: The study included 286 patients diagnosed with COVID-19, with 118 males and 168 females. Serum samples were taken from all subjects at two different time points, including 2 and 4 weeks after the onset of symptoms. Serological levels of SARS-CoV-2-specific IgM and IgG was assessed using the enzyme-linked immunosorbent assay technique. The Student's t-test were used to compare the mean levels of SARS-CoV-2-specific IgM and IgG between groups.

Results: We found that the mean serum levels of SARS-CoV-2-specific IgM and IgG in COVID-19 patients were increased in 4 weeks after symptom onset compared to 2 weeks earlier, but it was not statistically significant (p > 0.05). There was no significant sex-dependent difference in serological levels of SARS-CoV-2-specific IgM and IgG (p > 0.05).

Conclusion: Our findings suggest that the serum levels of SARS-CoV-2-specific IgM and IgG did not show significant differences depending on sex. Furthermore, serological levels of SARS-CoV-2-specific IgM and IgG did not significantly differ between 2- and 4-weeks following illness onset.

Vaccination is an effective way to prevent influenza virus infection. Currently, intramuscular vaccines are the most commonly used and can provide strong humoral immunity, but they may not induce the mucosal immune response well. A variety of pathogens gain access to the host via the respiratory tract, and the mucosa serves as the initial line of defense against bacterial invasions. Therefore, developing mucosal vaccines is a valuable strategy for preventing respiratory infectious diseases. The mucosal barrier hinders antigen delivery and immune activation, making efficient mucosal adjuvants crucial for vaccine advancement, though their use faces several obstacles. The main challenges faced by mucosal adjuvants are mucosal tolerance, delivery efficiency, and immune response balance. Future mucosal adjuvants will continue to focus on multitarget synergistic design and combination adjuvant application. The safety and efficacy of future influenza vaccines are contingent upon the judicious selection of suitable mucosal adjuvants. The creation of next-generation influenza vaccines will be made easier as our knowledge of adjuvants grows. In this review, we summarize the current progress and applications of mucosal adjuvants for influenza vaccines, with implications for the development of novel influenza vaccines and vaccines against other infectious diseases.

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 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 immunological properties of recombinant hepatitis B surface antigen (rHBsAg), prepared using yeast (Saccharomyces cerevisiae [SC]) and Chinese hamster ovary (CHO) cells, were evaluated through in vitro and in vivo assays to support the efficacy of recombinant hepatitis B vaccines. In vitro, antigenicity was assessed by measuring the affinity of rHBsAg to anti-HB antibodies using surface plasmon resonance. In vivo, 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. In vitro, the equilibrium dissociation constant (K_D) of rHBsAg from CHO cells was significantly lower than that from yeast cells, indicating stronger antibody affinity. In vivo, 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.

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 CD56⁺CD16^- 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.

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 in silico 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 (E. coli) system, followed by anti-HDAg antibodies production in rabbits. After determining and amplifying the antigenic region of HDAg of HDV, the fragment was cloned into the pET-28a vector and expressed in E. coli TOP10 cells. Following the successful expression of recombinant HDAg protein with a His-tag at its C-terminal end, we purified the HDAg 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 HDAg. 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.