Background: Seagull as a migratory wild bird has become most popular species in southwest China since 1980s. Previously, we analyzed the gut microbiota and intestinal pathogenic bacteria configuration for this species by using 16S rRNA sequencing and culture methods. To continue in-depth research on the gut microbiome of migratory seagulls, the metagenomics, DNA virome and RNA virome were both investigated for their gut microbial communities of abundance and diversity in this study. Results: The metagenomics results showed 99.72% of total species was bacteria, followed by viruses, fungi, archaea and eukaryota. In particular, Shigella sonnei, Escherichia albertii, Klebsiella pneumonia, Salmonella enterica and Shigella flexneri were the top distributed taxa at species level. PCoA, NMDS, and statistics indicated some drug resistant genes, such as adeL, evgS, tetA, PmrF, and evgA accumulated as time went by from November to January of the next year, and most of these genes were antibiotic efflux. DNA virome composition demonstrated that Caudovirales was the most abundance virus, followed by Cirlivirales, Geplafuvirales, Petitvirales and Piccovirales. Most of these phages corresponded to Enterobacteriaceae and Campylobacteriaceae bacterial hosts respectively. Caliciviridae, Coronaviridae and Picornaviridae were the top distributed RNA virome at family level of this migratory animal. Phylogenetic analysis indicated the sequences of contigs of Gammacoronavirus and Deltacoronavirus had highly similarity with some coronavirus references. Conclusions: In general, the characteristics of gut microbiome of migratory seagulls were closely related to human activities, and multiomics still revealed the potential public risk to human health.

The epidemic of COVID-19 is mainly manifested by respiratory symptoms caused by SARS-CoV-2 infection. Recently, reports of central nervous system diseases caused or aggravated by SARS-CoV-2 infection are also increasing. Thus, the COVID-19 pandemic poses an unprecedented challenge to the diagnosis and management of neurological disorders, especially to those diseases which have overlapping clinical and radiologic features with each other. In this study, a 31-year-old female patient had been diagnosed with relapsing–remitting multiple sclerosis (RRMS) initially and subsequently developed tumefactive demyelinating lesions (TDLs) following an infection with SARS-CoV-2. After immunotherapy (glucocorticoid pulses), a significant improvement was observed in her both clinical and radiological characteristics. The patient was started on disease-modifying therapy (DMT) with teriflunomide after cessation of oral glucocorticoids. Following two months of DMT treatment, the imaging follow-up revealed that the patient’s condition continued to deteriorate. This case was characterized by the transformation of a multiple sclerosis patient (MS) infected with SARS-CoV-2 into TDLs and the ineffectiveness of DMT treatment, which added complexity to its diagnosis and treatment. The case also gave us a hint that SARS-CoV-2 has a potential contributory role in inducing or exacerbating demyelinating diseases of the central nervous system that warrants further investigation.

Mutations in myelin regulatory factor (MYRF) are linked to demyelinating disorders. We report a 38‐year‐old male who developed acute symmetric leukoencephalopathy mimicking a stroke following an influenza A virus infection. While clinical symptoms markedly improved with corticosteroids, MRI revealed persistent white matter lesions, contrasting with the known phenotype of MYRF‐related mild encephalopathy with reversible myelin vacuolization (MMERV). Genetic analysis identified a novel MYRF variant (c.2204G>A, p.Gly735Asp) in its C‐terminal domain, with familial cosegregation confirming autosomal dominant inheritance. This case demonstrates that viral infections can trigger severe MYRF‐related pathology and establishes persistent leukoencephalopathy as a novel clinical phenotype within the MYRF disease spectrum.

Progressive Multiple Sclerosis (PMS) remains a major cause of irreversible disability in Multiple Sclerosis (MS), yet current disease-modifying therapies incompletely address the compartmentalized Central Nervous System (CNS) inflammation, sustained microglial activation, chronic demyelination, and axonal degeneration that characterize progression. This topic is timely because the evidence linking Epstein–Barr Virus (EBV) to MS susceptibility, the recognition of B cell–myeloid interactions within the CNS, and the clinical development of CNS-penetrant Bruton’s Tyrosine Kinase inhibitors (BTKi) now converge on a common translational question: whether a connected EBV– B cell–microglia–BTK axis can explain part of progression independent of relapse activity and inform therapy for PMS. EBV establishes lifelong latency in memory B cells and may contribute to MS through molecular mimicry, aberrant antigen presentation, and persistent pro-inflammatory signaling. In progressive disease, B cells can interact with microglia and macrophages to sustain compartmentalized inflammation, while BTK links B-cell receptor and myeloid Fc receptor signaling. This review synthesizes EBV-associated B-cell dysregulation, B cell–microglia crosstalk, BTK biology, BTKi trial evidence, biomarkers, and safety considerations in an evidence-stratified framework. Rather than presenting a linear causal model, we distinguish established observations from emerging mechanisms and speculative hypotheses. We propose that this integrated pathophysiological framework may help clarify patient stratification, CNS target engagement, and rational therapeutic development for PMS while defining the limits that future studies must address.

Phthalates (PAEs) are widely used plasticizers that are increasingly linked to tumorigenesis. In this study, we integrated network toxicology and machine learning to elucidate the potential mechanisms of PAEs in lung squamous cell carcinoma (LUSC). By integrating multi-database target prediction, The Cancer Genome Atlas Program (TCGA) transcriptomic analysis, and algorithmic screening, four key genes, ANXA5, CDK4, MMP1, and SRD5A1, were identified as major targets of PAEs. Molecular docking and dynamics simulations indicated stable binding of butyl benzyl phthalate (BBP) to ANXA5, and SRD5A1. In vitro validation using H226 and NCI-H1703 cells confirmed these predictions. BBP at non-cytotoxic concentrations (0.1-10 μM) altered cell behavior: 0.1 μM BBP promoted migration and upregulated SRD5A1 and ANXA5, whereas 10 μM BBP downregulated ANXA5, showing a non-monotonic "low-dose activation-high-dose inhibition" pattern typical of endocrine disruptors. Collectively, these results indicate that BBP interferes with LUSC progression through multiple target and multipathway mechanisms, including direct binding to key proteins, disturbance of steroid metabolism, and modulation of membrane signaling. This integrative study links environmental phthalate exposure with lung cancer pathogenesis and provides a hypothesis worthy of further investigation for risk assessment and targeted prevention.