Since the emergence of the SARS-CoV-2 virus in 2019, nearly 700 million COVID-19 cases and 7 million deaths have been reported globally. Despite most individuals recovering within four weeks, the Center for Disease Control (CDC) estimates that 7.5% to 41% develop post-acute infection syndrome (PAIS), known as ‘Long COVID’. This review provides current statistics on Long COVID’s prevalence, explores hypotheses concerning epidemiological factors, such as age, gender, comorbidities, initial COVID-19 severity, and vaccine interactions, and delves into potential mechanisms, including immune responses, viral persistence, and gut dysbiosis. Moreover, we conclude that women, advanced age, comorbidities, non-vaccination, and low socioeconomic status all appear to be risk factors. The reasons for these differences are still not fully understood and likely involve a complex relationship between social, genetic, hormonal, and other factors. Furthermore, individuals with Long COVID-19 seem more likely to endure economic hardship due to persistent symptoms. In summary, our findings further illustrate the multifaceted nature of Long COVID and underscore the importance of understanding the epidemiological factors and potential mechanisms needed to develop effective therapeutic strategies and interventions.

Peanut allergy is a prevalent and potentially life-threatening condition affecting millions of people worldwide, necessitating strict dietary vigilance. Despite its widespread impact, current treatment options are predominantly limited to allergen avoidance and emergency management of allergic reactions. This review explores contemporary immunotherapeutic strategies aimed at achieving long-term relief for individuals with peanut allergy. We conducted a comprehensive literature review to discuss different treatment approaches, such as subcutaneous immunotherapy (SCIT), epicutaneous immunotherapy (EPIT), oral immunotherapy (OIT), and sublingual immunotherapy (SLIT), focusing on their mechanisms, efficacy, and safety profiles. Additionally, the review delves into novel approaches such as monoclonal antibodies targeting IgE and other critical immune pathways, adjuvanted therapies utilizing nanoparticles and gut microbiota, and advances in adoptive cell therapy including CAR-T cells and regulatory T cells. Furthermore, we highlight some clinical trials that test the efficacy and safety of these novel immunotherapeutic approaches in patients with peanut allergy. Collectively, we provide an overview of advancements in immunotherapeutic interventions for peanut allergy and recommendations for personalized immunotherapy regimens, ultimately paving the way for more effective treatment strategies.

Background: Influenza, a primarily respiratory illness, frequently manifests with gastrointestinal (GI) symptoms including nausea, vomiting, diarrhea, and abdominal pain. In this review, we analyze mechanisms describing GI infiltration and subsequent involvement of the GI system during influenza infection. Direct mechanisms involve the presence of viral particles in the GI tract and binding to sialic acid receptor, α2,3 and α2,6 linkages. The influenza virus may gain access to gut tissue via swallowing of respiratory secretions, hematogenous spread, or lymphocytic migration via the lung–gut axis. Indirect mechanisms involve immune system dysregulation via cytokine, interferon, and leukotriene flux, upregulation of consequential apoptotic pathways, or gut microbiome dysbiosis. Together, they promote secondary GI opportunistic infections. These findings improve our knowledge of GI infiltration during influenza infection which may aid in effective clinical diagnosis and treatment, ultimately improving patient outcomes.

Background/Objectives: Substance use behaviors share a complex, overlapping polygenic architecture, yet translating genome-wide association study (GWAS) findings into actionable biological mechanisms remains challenging. This study aimed to characterize the genetic architecture of five substance use traits (alcohol consumption, alcohol dependence, nicotine use, illicit drug use, and behavioral disinhibition) and identify shared and distinct gene expression signatures within the neural circuits governing addiction. Methods: We reanalyzed 7188 individuals from the Minnesota Center for Twin and Family Research (MCTFR) cohort utilizing longitudinal composite phenotypes spanning five substance-use domains and general behavioral disinhibition. Post-QC, 6874 individuals were retained for downstream analysis. Following genomic imputation and linear mixed model GWAS (GEMMA), we utilized the SNipar framework to partition polygenic risk scores (PRS) into direct and indirect genetic effects, investigating intergenerational shifts in genetic penetrance and effects of assortative mating. Finally, we integrated our summary statistics with brain tissue reference panels to perform a transcriptome-wide association study (TWAS) modeling genetically regulated gene expression within neural circuits relevant to addiction. Results: Partitioning of polygenic risk revealed that while surface-level parental DNA correlations were modest (r = 0.08), underlying latent genetic correlations approached unity (R_δ ≈ 0.99), indicating that addiction risk clustering in families is driven by intense assortive mating and concentrated biological inheritance. Multi-phenotype TWAS identified several significant gene–phenotype associations—notably ADAM32 and SLC9A3, which demonstrated pleiotropic effects across multiple substance use categories. Crucially, these significant TWAS signals were enriched in striatal structures (caudate, putamen, substantia nigra) and frontal cortical regions. Conclusions: Our findings support a model of shared genetic liability across diverse substance use behaviors, mediated by specific gene expression patterns in the mesolimbic dopamine system and frontal cortex. By integrating multi-phenotype GWAS and TWAS, this study highlights pleiotropic candidate genes and provides critical insights into the tissue-specific neurobiological pathways underlying addiction vulnerability.

Binge-eating disorder (BED), defined as recurrent episodes of consuming large amounts of food in a short period of time while experiencing a loss of control, remains difficult to manage. Although several pharmacological options are available, they often provide limited long-term benefit and may cause adverse effects. Emerging evidence suggests that gut microbiota dysbiosis contributes to BED pathophysiology. Cytokine infiltration of the gut barrier ultimately causes neuroinflammation, highlighting the gut–brain axis as a potential therapeutic target. This systematic review and meta-analysis evaluated the effectiveness and safety of central nervous system-targeting pharmacotherapies and psychobiotics for BED. Cochrane Library, PubMed, and the Virtual Health Library were searched for randomized controlled trials published from January 2000 to January 2026. Eligible studies evaluated monotherapy with a central nervous system-acting drug or psychobiotics in clinically diagnosed BED populations. Twenty pharmacological trials (n = 2154) and five psychobiotic trials (n = 304) met the inclusion criteria. Risk of bias was assessed using the Cochrane RoB 2 tool, and pooled estimates were calculated using random-effects models. Pharmacological interventions showed a significant pooled effect versus placebo (Standard Mean Difference (SMD) = 0.307, 95% Confidence Interval (CI): 0.103–0.511, p = 0.003), although heterogeneity warrants cautious interpretation. Psychobiotics showed a moderate and significant effect (SMD = 0.680, 95% CI: 0.448–0.913; I² (heterogeneity index) = 0%) and no reported adverse events. Overall, our study implies that psychobiotics may be a safe and potentially effective adjunctive approach for BED, but larger, well-designed trials are needed.