Despite causing severe, potentially life‐threatening diarrhea, most enteric viruses only infect a small percent of intestinal epithelial cells. Thus, the induction of paracrine signaling pathways to dysregulate both infected and neighboring uninfected cell remains a major premise of enteric virus pathogenesis. However, virus‐induced paracrine signaling has never been directly observed and therefore the mechanisms have yet to be defined. Rotavirus (RV) remains a major cause of severe diarrhea in children worldwide. A hallmark of RV infection is the activation of aberrant calcium (Ca 2+ ) signaling, which is necessary for replication and activation of secretory pathways in GI epithelium. We sought to characterize RV‐induced calcium signaling dynamics and identify paracrine signaling pathways responsible for infected‐to‐uninfected cell signaling. We conducted live‐cell Ca 2+ imaging throughout the entire infection using cell lines and human intestinal enteroids (HIEs) engineered to stably express the genetically‐encoded Ca 2+ indicator GCaMP. We found that rotavirus significantly increases both steady‐state and transient Ca 2+ signaling mediated by RV nonstructural protein 4 (NSP4) and mutation of the NSP4 ion channel domain altered the RV‐induced Ca 2+ signaling pattern observed, particularly low amplitude Ca 2+ puffs observed early in infected cells. Further, isolated rotavirus‐infected cells generated multiple intercellular calcium waves (ICWs), which was the most prominent p

Human norovirus (HuNoV) accounts for over 700 million cases of gastroenteritis annually. Episodes of HuNoV disease are characterized by vomiting and diarrhea as the two most prominent symptoms. Despite its prevalence, our understanding of the pathophysiological mechanisms triggered upon HuNoV infection is limited, mainly due to a lack of suitable animal models. Our aim was to use the recent HuNoV zebrafish larvae model to study the effect of HuNoV infection on intestinal motility and investigate whether one viral protein could act as an enterotoxin, as seen with rotavirus. We studied whether H

Irritable bowel syndrome (IBS) and small intestinal bacterial overgrowth (SIBO) share symptoms such as abdominal pain, bloating, and altered bowel habits. Both are linked to dysbiosis and gut-brain axis dysfunction. IBS is a multifactorial disorder characterized by abnormal motility, visceral hypersensitivity, low-grade inflammation, and alterations in the microbiota. In contrast, SIBO is defined by excessive bacterial colonization of the small intestine that can mimic or worsen IBS symptoms. Gut microbes and their metabolites influence motility, immune activation, barrier integrity, and gas production; methanogen overgrowth is associated with constipation-predominant presentations, while hydrogen- and hydrogen sulfide-related pathways may contribute to diarrhea and bloating. Because recurrent or empiric antibiotic use is common-particularly in suspected SIBO-yet carries risks of resistance, microbiome disruption, and relapse, there is a strong rationale to prioritize effective non-antibiotic strategies. Accordingly, this review synthesizes current evidence on IBS/SIBO pathophysiology and microbiota interactions. It evaluates non-pharmacological interventions including dietary approaches, probiotics/prebiotics, herbal therapies, and mind-body treatments (e.g., cognitive behavioral therapy and gut-directed hypnotherapy). We emphasize an integrative framework that supports symptom control and quality of life while helping reduce unnecessary antibiotic exposure.