Hypochlorous acid (HOCl), a naturally occurring antimicrobial agent produced by neutrophils during the respiratory burst, has emerged as a potential candidate for antiviral intervention. This perspective article explores its possible therapeutic application in human immunodeficiency virus (HIV) treatment, leveraging its well-documented oxidative properties. HOCl exerts its antiviral effects through targeted oxidative modifications of key viral components, including disulfide bonds in envelope glycoproteins (gp120 and gp41), thiol-dependent viral enzymes, and lipid membranes. These modifications disrupt viral entry, replication, and maturation, potentially limiting HIV infectivity. In addition, HOCl plays a pivotal role in modulating innate immune responses by enhancing phagocytic activity and cytokine signaling, which may contribute to immune-mediated viral suppression. While existing evidence suggests that HOCl could serve as a complementary or alternative approach to conventional antiretroviral therapy, its therapeutic application in HIV remains speculative. Critical aspects such as optimal dosing, delivery mechanisms, host specificity, and long-term safety require further investigation before clinical translation can be considered. This article provides a scientific perspective on HOCl’s antiviral potential, advocating for further research to assess its feasibility and efficacy in HIV treatment.

The coronavirus disease 2019 (COVID-19) pandemic magnified long-standing disparities in health care. Among the general population, racial/ethnic minorities often face disproportional barriers, such as poverty, reduced health literacy, a generational mistrust of health-care institutions, and limited access to health care, contributing to the disparities reported in severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection and outcomes. Racial/ethnic minorities in the military comprise nearly 43% of active-duty service members and face disproportionate health burdens influenced by systemic and individual factors. As a result, minority service members within the military health system had similar rates of SARS-CoV-2 testing compared to those of white service members. Reports have found that while the rates of testing are similar, SARS-CoV-2 infection remained disproportionately higher among Black and Hispanic service members. This perspective examines disparities in the United States military, focusing on the role of social determinants of health, comorbidities, risk factors, and access to care in shaping COVID-19 health outcomes.

Vagus nerve-related adverse events (AEs) can be triggered by gastrointestinal infections. This raises the question of whether AE data from live-attenuated virus vaccination can be leveraged to investigate potential vagus nerve involvement. In this study, data from the Vaccine AEs Reporting System were retrospectively analyzed for candidate vagus nerve-related AEs in infants aged 0 and 1. Live-attenuated rotavirus vaccinations were associated with elevated normalized frequencies across all 16 selected vagus nerve-related AEs in both age groups, with the majority showing higher normalized frequencies in infants aged 0 than in those aged 1. These findings suggest that oral, live-attenuated virus vaccination may provide valuable insights into vagus nerve-related AEs. Furthermore, the higher normalized frequencies of AEs observed in infants aged 0 could indicate that the administered dose or minimum infectious units may be excessive for a subset of younger infants.

African swine fever (ASF) is among the most devastating viral diseases of pigs. Despite nearly a century of research, there is still no safe and effective vaccine available. The current situation is that either vaccines are safe but not effective, or vice versa. The ASF vaccine prepared using the inactivation method with β-propiolactone provided 98.6% protection within 100 days after three intranasal immunizations spaced 7 days apart. In conclusion, an inactivated vaccine made from complete ASF virus particles using β-propiolactone can safely and effectively control ASF through mucosal immunity.

Pulmonary tuberculosis (PTB) caused by Mycobacterium tuberculosis (MTB), remains a major global health concern due to its high morbidity and mortality rates, especially in resource-limited settings. The pathophysiology of tuberculosis (TB) is characterized by complex interactions between the human host immune system and the pathogen. Alveolar macrophages are especially vulnerable targets of MTB, triggering a cascade of pro-inflammatory and anti-inflammatory responses that either contain the infection or facilitate progression to active disease. In addition, recent advances in immunopathology have highlighted the roles of cytokine networks, T-cell responses, and immune checkpoints in disease progression. A deeper understanding of TB pathophysiology has significant implications for clinical management and research. It aids in the development of novel diagnostic biomarkers, host-directed therapies, and more effective vaccine strategies. Emerging therapeutic approaches focus on modulating the immune response to enhance MTB clearance while minimizing tissue damage. Moreover, drug-resistant TB strains pose a growing challenge, necessitating research into host-pathogen interactions that could lead to more effective treatment strategies. This review provides a concise examination of the key mechanisms underlying PTB, emphasizing recent scientific advancements and their relevance for clinicians and researchers. By bridging the gap between basic science and clinical application, this work aims to contribute to the ongoing efforts to improve TB control and patient outcomes.

The Eph receptor-ephrin system is essential for embryonic, neural, and vascular development and contributes to tumor promotion or suppression. Ephrin type-A receptor 7 (EphA7) has been identified as a tumor suppressor often lost or downregulated in lymphomas. In contrast, EPHA7 mutations have been suggested as potential driver genes in other cancers. However, the detailed molecular function has not been clarified. Therefore, a monoclonal antibody (mAb) against EphA7 is essential for basic research and clinical applications. In this study, we developed a novel anti-human EphA7 mAb, Ea₇Mab-10, using the Cell-Based Immunization and Screening (CBIS) method. Ea₇Mab-10 reacted with EphA7-overexpressed Chinese hamster ovary-K1 (CHO/EphA7) and EphA7-overexpressed LN229 (LN229/EphA7) in flow cytometry. The binding affinities were determined as 3.1 × 10⁻⁹ M for CHO/EphA7 and 6.9 × 10⁻⁹ M for LN229/EphA7. Furthermore, Ea₇Mab-10 did not show cross-reactivity with other Eph family members and was suitable for Western blotting and immunohistochemistry. These results demonstrate that Ea₇Mab-10, developed using the CBIS method, supports basic research on EphA7 and could be used for mAb-based targeted therapies.

Colorectal cancer (CRC) remains one of the leading contributors to global cancer-associated deaths, with its development and progression closely influenced by the complex and evolving interplay between host and gut microbial communities. The gut fungal community has emerged as a crucial factor in the oncogenesis, progression, and treatment of CRC. Through multi-cohort fecal metagenomic analysis, it has been found that the gut fungal community structure of CRC patients undergoes significant changes, with pathogenic fungi becoming enriched and overall fungal diversity decreasing. In addition, fungal metabolites and other components are also associated with cancer development, including effects on cell proliferation, apoptosis, and immune responses. In terms of mechanisms, fungi may influence CRC progression by affecting intestinal immune responses, modulating inflammatory pathways, and interacting with bacteria. However, current research is mainly focused on correlation analysis, with causality remaining unclear. Moreover, the diversity of fungi across different populations limits their clinical application. This article examines the role of fungi in CRC onset and progression, summarizes current therapies, and outlines future research to support early diagnosis, precision treatment, and improved prognosis.

Long coronavirus disease (COVID) is defined as an infection-associated chronic condition that occurs after severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection and is present for at least 3 months as a continuous, relapsing, and remitting, or progressive disease state. While COVID-19 vaccines have been credited by public health officials with preventing COVID-associated morbidity and mortality, a portion of the population reports post-vaccination syndrome, often concerning long COVID. To investigate the association between post-vaccination syndrome and long COVID, we performed an observational cohort study at our outpatient clinical practice, evaluating SARS-CoV-2 semi-quantitative spike Ab in 100 consecutive patients (47% female and 53% male) with symptoms of long COVID. A total of 81 participants (46.9% female and 53.1% male) with post-vaccination syndrome and 19 unvaccinated participants (47.4% female and 52.6% male) with symptoms of long COVID were evaluated. SARS-CoV-2 Semi-Quant Spike Ab in the vaccinated cohort showed an average result of 11356.86 U/mL, whereas SARS-CoV-2 Semi-Quant Spike Ab in the unvaccinated cohort showed an average result of 1631.94 U/mL. The findings reveal potential immune differences in both individuals with long COVID and those with post-vaccination syndrome that merit further investigation to better understand these conditions and inform future research into diagnostic and therapeutic approaches.

The resurgence of mpox (formerly known as monkeypox), caused by the mpox virus, has emerged as a global health concern, extending beyond its endemic regions and affecting countries such as India since 2022. Although less severe than smallpox, mpox shares clinical similarities with smallpox, complicating clinical diagnosis and reporting. Its rapid transmission, coupled with the absence of targeted vaccines and antiviral therapies, underscores the urgent need for focused research and public health preparedness. This review synthesizes findings from over 350 publications originating from Indian institutions, highlighting progress in epidemiology, clinical characterization, genomic analysis, vaccine development, and public health strategies. It discusses breakthroughs in diagnostics, molecular studies, and therapeutic approaches, while identifying key challenges and future priorities. The World Health Organization’s declaration of mpox as a public health emergency of international concern in 2022 has catalyzed research efforts in India. Indian scientists have responded with a surge in publications, exploring viral pathogenesis, host interactions, and the development of novel diagnostic tools and vaccines. The review also emphasizes the role of computational biology, artificial intelligence, and traditional medicine in shaping India’s response. India has made significant progress in mpox-related research, particularly in diagnostics, clinical management, and epidemiology. However, the absence of specific vaccines and antiviral treatments remains a critical gap. Continued investment in research, international collaboration, and policy innovation will be essential for developing effective containment and treatment strategies. With sustained efforts, India is well-positioned to make a meaningful contribution to global mpox control and preparedness.

Infectious bursal disease (IBD) outbreaks significantly undermine chicken production. Syndromic surveillance based on lesion indicators is an established tool for monitoring the disease following reports of morbidity and mortality. This study aimed to develop an epidemiological profile of the IBD burden, including syndromic outbreak prevalence rates, yearly trends, mortality rates, and lesion patterns, used for surveillance. Records of IBD outbreaks from two veterinary hospitals in Maiduguri, Nigeria, were extracted from all reported disease outbreaks in chicken flocks between 2008 and 2018. IBD outbreaks accounted for 493 cases (7.6%; 95% confidence interval [CI]: 7.0-8.3%) of 6,486 recorded disease outbreaks. Annual prevalence ranged from 1.6% (95% CI: 0.9-2.3%) to 17.3% (95% CI: 12.9-21.7%) and showed a linear trend (r = −0.73; p < 0.01), with a significant association across years (p < 0.001). Prevalence varied significantly with chicken type (p < 0.05), with the highest rate observed in Noilers (25.0%), followed by cockerels (17.5%), local chickens (9.1%), broilers (7.2%), and layers (7.1%). Affected chickens were aged 2-27 weeks, with a modal age of 4-5 weeks and a mean age of 5.0 ± 1.7 weeks. The overall mortality rate was 12.6% (95% CI: 12.3-12.9) based on a total flock size of 38,485 from 2015 to 2018, the period for which flock size and mortality records were available. Key lesions used for syndromic detection of acute IBD included inflammatory swelling of the bursa of Fabricius (90.9%), hemorrhages in thigh, leg, and/or breast muscles (72.2%), mucosal hemorrhages at the proventriculus-ventriculus junction, with and without enteritis (24.9%), and kidney lesions (7.7%). This syndromic surveillance system enables outbreak monitoring and can inform the planning of control measures to reduce disease-associated production losses.

The tumor-associated microbiome has emerged as a novel hallmark of cancer. Gastric cancer (GC) serves as a paradigm for microbiome-associated carcinogenesis, with well-established roles for specific pathogens such as Helicobacter pylori and Epstein-Barr virus. However, the detailed molecular and cellular mechanisms by which microbial communities drive gastric tumorigenesis remain incompletely understood. Recent technological advancements have unveiled a broader spectrum of microorganisms implicated in GC, highlighting the emerging roles of the mycobiome (fungal microbiome) and bacterial-fungal interactions in shaping the tumor microenvironment. This review comprehensively summarizes recent progress in GC-associated pathogens, with a particular emphasis on how bacteria and fungi contribute to GC through direct carcinogenic effects, modulation of host immune responses, and influencing the efficacy of immune checkpoint inhibitors. We critically analyze the “double-edged sword” nature of the microbiome in GC and discuss the potential of multi-omics approaches to unravel complex microbe-host interactions. Finally, we explore the frontier of leveraging synthetic biology to develop engineered microbes (including bacteria and oncolytic viruses) as novel anticancer therapeutics, while addressing the challenges in translating these strategies into clinical practice. A deeper understanding of the gastric microbiome, particularly the multi-kingdom microbial network, is poised to open new avenues for microbiome-based precision diagnosis and innovative therapies for GC management.

Marine ecosystems are prolific sources of structurally diverse bioactives—including polysaccharides (e.g., alginate, fucoidan, laminarin, and carrageenan), peptides/proteins, ω-3 long-chain polyunsaturated fatty acids, carotenoids (e.g., astaxanthin and fucoxanthin), steroids, macrolides, and alkaloids—that modulate innate and adaptive immunity through convergent pathways. Evidence across algae, fish, shellfish, microbes, and sponges shows these molecules regulate toll-like receptor signaling, nuclear factor κB/mitogen-activated protein kinase axes, cyclooxygenase/lipoxygenase-derived eicosanoids, complement activation, and redox tone; rebalance cytokine profiles (↓ tumor necrosis factor-α/interleukin (IL)-1β/IL-6; ↑ IL-10); and influence effector functions of macrophages, natural killer and T cells. Marine peptides and protein hydrolysates, often generated through enzymatic hydrolysis or fermentation and purified by membrane fractionation and chromatography, display antioxidant, antimicrobial, antihypertensive, antihyperlipidemic, anti-inflammatory, immunostimulatory, and anticancer activities in vitro and in vivo. Polysaccharide structure (e.g., molecular weight, linkage, and sulfation) and peptide sequence/composition drive bioactivity, whereas ω-3-derived specialized pro-resolving mediators contribute to inflammation resolution. Beyond direct immune effects, several marine bioactives exert prebiotic-like actions that reshape gut microbiota and mucosal defenses. Advances in extraction, stabilization, and delivery are accelerating incorporation into functional foods, nutraceuticals, cosmeceuticals, and medical nutrition. Key translation barriers remain—heterogeneity of sources, batch-to-batch variability, processing stability, bioavailability and pharmacokinetics, allergenicity, and limited standardized immune endpoints and human trials. This review synthesizes mechanistic and application-oriented evidence for marine-derived immunomodulators, outlines safety and regulatory considerations, and prioritizes research needed to enable evidence-based deployment in food and health.

Hepatitis E virus (HEV) is a major zoonotic pathogen, and pigs are an important reservoir. Serology for anti-HEV antibodies poorly reflects active infection, while reverse transcription polymerase chain reaction (RT-PCR) is sensitive but not always feasible for large-scale surveillance. This study aimed to develop an immunoglobulin Y (IgY)-based sandwich enzyme-linked immunosorbent assay (ELISA) for direct detection of HEV antigen (HEV-Ag). An antigenic epitope from the HEV open reading frame 2 capsid protein was identified in silico, synthesized, and used to immunize laying hens; IgY was purified from egg yolk and characterized by sodium dodecyl sulfate-polyacrylamide gel electrophoresis. An in-house sandwich ELISA was subsequently developed using the anti-HEV IgY antibodies. Its diagnostic performance was evaluated against RT-PCR using 350 field-collected pig serum samples and compared with commercial anti-HEV IgG and IgM ELISA kits. Immunization yielded high-purity IgY antibodies, with antigen-specific antibody kinetics showing a significant increase in specific immunoreactivity from week 4 onward and peak sensitivity at weeks 6-8 post-immunization. The anti-HEV IgY showed high specificity, with no cross-reactivity observed against a heterologous antigen (HBsAg). The optimized sandwich ELISA detected HEV-Ag with a sensitivity of 95.4% and a specificity of 100% relative to RT-PCR. The prevalence of HEV-Ag was 17.7% (62/350), which was not significantly different from RT-PCR (18.6%, 65/350; p=0.250). In contrast, commercial IgG and IgM ELISAs showed high seroprevalence rates (34.9% and 28.3%, respectively) but exhibited significant discrepancies with RT-PCR (p<0.0001), indicating limited utility for identifying active infection. Overall, the developed IgY-based sandwich ELISA demonstrated high diagnostic performance for detecting active HEV infection. This assay represents a viable alternative to RT-PCR for large-scale surveillance, particularly in resource-constrained settings, and may contribute to improved control of zoonotic HEV transmission.

The human gut microbiome plays a critical role in maintaining immune homeostasis and metabolic health. Aging is accompanied by significant shifts in microbial composition—termed dysbiosis—which contribute to a proinflammatory state known as “inflammaging.” This chronic, low-grade inflammation underlies numerous age-associated diseases, including atherosclerosis, neurodegeneration, and metabolic syndrome. This review aims to explore the mechanisms through which age-related microbial dysbiosis contributes to chronic inflammation and to examine current therapeutic strategies targeting the microbiome to mitigate inflammaging. A comprehensive literature review was conducted using PubMed-indexed articles from 2000 to 2025. Studies addressing microbiome composition in aging, microbial metabolite pathways, immune modulation, and interventions including probiotics, dietary modifications, and fecal microbiota transplantation (FMT) were included. Aging is associated with reduced microbial diversity, a decline in beneficial taxa such as Faecalibacterium prausnitzii, and enrichment of proinflammatory taxa like Proteobacteria. This dysbiosis impairs gut barrier function, promoting systemic translocation of microbial products such as lipopolysaccharide (LPS). Metabolites like short-chain fatty acids (SCFAs) are diminished, leading to decreased regulatory T cell (Treg) function and epithelial integrity. Conversely, elevated levels of trimethylamine N-oxide (TMAO) and LPS activate pattern recognition receptors, triggering innate immune pathways (e.g., NF-κB, NLRP3 inflammasome) that perpetuate chronic inflammation. Interventions such as probiotic supplementation and FMT from young donors show promise in reversing dysbiosis, restoring microbial metabolites, and attenuating inflammatory responses in both animal models and early human trials. Understanding the gut-immune-metabolite axis offers new opportunities to intervene in age-related diseases through targeted microbiome modulation.

Fusobacterium nucleatum (FN) is an opportunistic pathogen associated with several diseases, including periodontitis, cardiovascular disease, and colorectal cancer. Owing to genetic variation, FN strains may display distinct epitope profiles to the host immune system. Likewise, the human leukocyte antigen allele repertoire is highly polymorphic and varies across ethnic groups. This study examines how these variations influence immune recognition of FN among different ethnicities and evaluates the potential for autoimmune responses arising from cross-reactivity with the FN proteome. A set of 140 experimentally verified epitopes and their variants was analyzed for binding affinities to major histocompatibility complex Class-I and Class-II molecules. Using the prevalence of these molecules across ethnicities and their affinity for FN epitopes, a new metric—pathogen detection capacity (PDC)—was formulated. PDC enabled comparison of FN recognition across populations. Additionally, the FN proteome was assessed for similarity to human epitopes implicated in autoimmune disorders. Results showed that European, South Asian, and Amerindian populations had a greater potential to detect FN, whereas Oceanian groups exhibited comparatively lower PDC values. Within super-populations, ethnicities that migrated from their ancestral homelands displayed altered PDC profiles relative to non-migrating groups. The analysis also identified four previously unreported FN peptide fragments with potential antigenic properties. Overall, this study provides a foundational framework for understanding FN immunogenicity and its variation across ethnicities. The findings highlight that disease pathophysiology can differ meaningfully among populations and that ethnicity-specific medical strategies may contribute to improved therapeutic outcomes.

Ulcerative colitis (UC) is a chronic inflammatory bowel disease characterized by recurrent inflammation of the colon. The absence of simple, noninvasive, and early biomarkers for disease onset and progression remains a major clinical challenge. This study aimed to evaluate the potential of pH values in biological samples as noninvasive indicators for the early disease-related changes in an experimental rat model of UC. Experimental colitis was induced in rats by administering dextran sulfate sodium, and the results were compared to those of healthy controls. Disease progression was monitored by evaluating disease severity scores and histopathological changes. Throughout the experimental period, stool and urinary pH were measured daily, while colonic and serum pH were assessed post-mortem. As the experiment progressed, the colitic rats exhibited marked weight loss and severe inflammatory changes in the colon. Despite the worsening disease, no significant alterations were observed in colonic or serum pH. In contrast, both stool and urinary pH values significantly decreased during the early phase of experimental colitis. However, these pH fluctuations did not consistently correlate with UC severity. In conclusion, our findings suggest that stool and urinary pH represent promising, noninvasive biomarkers for the early detection and monitoring of disease activity in UC.

Gastric adenocarcinoma (GAC) remains one of the deadliest malignancies worldwide, and the identification of molecular biomarkers is essential to improve prognostic stratification and guide therapeutic strategies. Cancer-testis antigens (CTAs) represent promising targets for immunotherapy, yet their expression landscape in GAC remains limited, especially when considering comprehensive and updated gene lists. In this study, we analyzed 389 samples, including tumor, peritumoral, metaplastic, and normal tissues, using RNA sequencing data to characterize the transcriptional profile of CTAs in GAC. We identified 104 CTAs differentially expressed among groups, with a predominance of upregulated genes in tumors compared with other tissues. The expression of several CTAs, such as MAGEA2, MAGEA3, MAGEA6, MAGEA12, CTCFL, IGF2BP1, and GAST, showed significant associations with clinically relevant variables, including tumor-node-metastasis staging, lymph node involvement, metastasis, histological subtype, and therapeutic management. Survival analysis revealed 17 CTA genes associated with overall survival, of which 14 correlated with poor prognosis, whereas PIK3R3, SYCE1L, and ZNF683 demonstrated a protective effect. Co-expression analysis identified five well-defined functional modules, reflecting coordinated CTA signatures related to germline reprogramming, proliferation, and immune remodeling within the tumor microenvironment. Collectively, our results provide the most comprehensive characterization of CTAs in GAC to date, highlighting genes with clinical relevance, prognostic value, and translational potential as candidates for future personalized immunotherapeutic approaches.

Marine ecosystems, particularly corals and their microbiomes, are recognized as prolific sources of unique natural products with diverse bioactivities. Despite the evident paucity of literature on microbial compounds associated with Fijian corals, this study aims to explore and elucidate the potential of actinomycetes associated with Fijian hard corals as sources of bioactive compounds. To highlight, actinomycete strains were isolated from five hard coral genera using three distinct isolation media. Among these, all 41 strains are facultative salt-tolerant, with 16 demonstrating biological activity by inhibiting the growth of three or more test pathogen strains. Interestingly, all ethyl acetate extracts of putative strains exhibited varying degrees of antimicrobial activity, with isolates FJC 16, 28, 33, and 41 being the most active. Moreover, the brine shrimp lethality test confirmed that actinomycete strain FJC 16 exhibited the highest toxicity toward brine shrimps with a lethal concentration of 37.50 μg/mL for 50% of the test population. The International Streptomyces Project medium-2 demonstrated high efficiency in isolating total actinomycetes. With a focus on cultivation techniques, the applications of pretreatment practices contributed to a successive recovery of actinomycetes. The current study serves as a foundational effort to evaluate the biosynthetic capabilities of Fijian hard corals, aiming to advance the current frontier of microbial natural product research within coral-associated microbiomes. Overall, as the footprint of microbial metabolites grows, Fijian hard corals represent a valuable prospect for further advanced studies of microbial designer molecules or analogs.