Materiały źródłowe

• #1 Viral Gastroenteritis – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK518995/

  Viral gastroenteritis is a widespread infectious illness caused by various viruses, including rotavirus, norovirus, adenovirus, and astrovirus, characterized by nausea, vomiting, diarrhea, abdominal pain, fever, and dehydration. […] Transmission occurs primarily through the fecal-oral route via contaminated food, water, and surfaces, with outbreaks commonly occurring in close-contact settings such as daycare centers, nursing homes, and cruise ships. […] The clinical manifestations of viral gastroenteritis are due to the effects that the viruses, along with specific cytotoxins, have on the enterocytes of the intestine. The virus uses the enterocyte to replicate, leading to interference with brush border enzyme production, which leads to malabsorption and osmotic diarrhea. […] Additionally, viral toxins lead to direct damage and cell lysis of enterocytes and intestinal villi, causing a transudative fluid loss into the intestine.

• #2 Gastrointestinal tract and viral pathogens

  https://www.wjgnet.com/2220-3249/full/v12/i3/136.htm

  Viral gastroenteritis is the most common viral illness that affects the gastrointestinal (GI) tract, causing inflammation and irritation of the lining of the stomach and intestines. Common signs and symptoms associated with this condition include abdominal pain, diarrhea, and dehydration. The infections commonly involved in viral gastroenteritis are rotavirus, norovirus, and adenovirus, which spread through the fecal-oral and contact routes and cause non-bloody diarrhea. […] Since the pandemic in 2019, coronavirus gastroenteritis has increased in incidence and prevalence. Morbidity and mortality rates from viral gastroenteritis have declined significantly over the years due to early recognition, treatment with oral rehydration salts, and prompt vaccination. Improved sanitation measures have also played a key role in reducing the transmission of infection.

• #3 Overview of Gastroenteritis – Gastrointestinal Disorders – Merck Manual Professional Edition

  https://www.merckmanuals.com/professional/gastrointestinal-disorders/gastroenteritis/overview-of-gastroenteritis

  Viruses infect enterocytes in the villous epithelium of the small bowel. The result is transudation of fluid and electrolytes into the intestinal lumen; sometimes, unabsorbed carbohydrates resulting from malabsorption in the affected bowel subsequently worsen symptoms by causing osmotic diarrhea. Diarrhea is watery. Inflammatory diarrhea (dysentery), with fecal white blood cells (WBCs) and red blood cells (RBCs) or gross blood, is uncommon. […] In viral infections, watery diarrhea is the most common symptom; stools rarely contain mucus or blood. For manifestations specific to norovirus and rotavirus, see Norovirus Gastroenteritis and Rotavirus Gastroenteritis. […] The hallmark of adenovirus gastroenteritis is diarrhea lasting 1 to 2 weeks. Affected infants and children may have mild vomiting that typically starts 1 to 2 days after the onset of diarrhea. Low-grade fever occurs in about 50% of patients. Respiratory symptoms may be present. Symptoms are generally mild but can last longer than with other viral causes of gastroenteritis. […] Astrovirus causes a syndrome similar to mild rotavirus infection. […] Cytomegalovirus can cause bloody diarrhea in patients with immunocompromise.

• #4 Viral Gastroenteritis – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK518995/

  The loss of cell function can lead to electrolyte abnormalities caused by the loss of transporter functionality. That can lead to acid-base disturbances as well. The virus is then shed through feces and occasionally in the vomitus. Peak viral load within the stool is anywhere between 24 to 48 hours after symptomatology. Some studies show viral shedding lasting for several weeks past symptomatology. […] Rotavirus pathogenesis is complicated, with several possible mechanisms, including malabsorption from mucosal damage, viral enterotoxin secretion, and enteric secretions in response to the virus. Rotavirus increases electrolyte secretion from the small intestine and decreases the glucose cotransport of these electrolytes.

• #5 Viral Gastroenteritis: Background, Pathophysiology, Etiology

  https://emedicine.medscape.com/article/176515-overview

  Viral spread from person to person occurs by fecal-oral transmission of contaminated food and water. Some viruses, like noroviruses, may be transmitted by an airborne route. Clinical manifestations are related to intestinal infection, but the exact mechanism of the induction of diarrhea is not clear. […] The most extensive studies have been done with rotavirus. Rotaviruses attach and enter mature enterocytes at the tips of small intestinal villi. They cause structural changes to the small bowel mucosa, including villus shortening and mononuclear inflammatory infiltrate in the lamina propria. […] The current knowledge on the mechanisms leading to diarrheal disease by rotavirus is as follows: Rotavirus infections induce maldigestion of carbohydrates, and their accumulation in the intestinal lumen, as well as a malabsorption of nutrients and a concomitant inhibition of water reabsorption, can lead to a malabsorption component of diarrhea.

• #6 Viral gastroenteritis

  https://pmc.ncbi.nlm.nih.gov/articles/PMC8883799/

  Rotavirus infects intestinal villus enterocytes and enteroendocrine cells; crypt cells are spared. Rotavirus infection-associated diarrhoea is non-inflammatory and involves both malabsorptive and secretory mechanisms. Malabsorption occurs from virus-mediated destruction of absorptive enterocytes, downregulation of the expression of absorptive enzymes, and functional changes in tight junctions between enterocytes that lead to paracellular leakage. A secretory component of rotavirus infection-associated diarrhoea involves elevated intracellular Ca2+ concentration, which is important for the stimulation of Cl secretion. Rotavirus replication in enterocytes and enteroendocrine cells stimulates serotonin release from human enterochromaffin cells, and activates brain regions associated with nausea and vomiting. Altered plasma-protein function and decreased Na+ absorption by inhibition of sodiumhydrogen exchanger activity also contribute to diarrhoea.

• #7 Gastrointestinal tract and viral pathogens

  https://www.wjgnet.com/2220-3249/full/v12/i3/136.htm

  Norovirus is an RNA virus belonging to the Caliciviridae family and consists of forty-nine genotypes. According to Centers for Disease Control and Prevention (CDC), Norovirus is the leading cause of acute gastroenteritis among all age groups in the United States. […] On average, each year in the United States, Norovirus causes 109000 hospitalizations. Outbreaks usually occur in congregant environments like healthcare centers, cruise ships, and restaurants via fecal-oral transmission through food, water, or person-to-person contact. […] Rotavirus, an RNA virus, and a member of the Reoviridae family is the major cause of diarrhea in children younger than five years. […] Diarrhea caused by the virus is thought to be via two mechanisms: (1) Osmotic diarrhea due to malabsorption secondary to enterocyte damage; and (2) secretory diarrhea from activation of the enteric nervous system and non-structural protein-4.

• #8 Viral Gastroenteritis: Background, Pathophysiology, Etiology

  https://emedicine.medscape.com/article/176515-overview

  Rotavirus secretes an enterotoxin, NSP4, which leads to a Ca2+ -dependent Cl- secretory mechanism. Mobilization of intracellular calcium associated with NSP4 expressed endogenously or added exogenously is known to induce transient chloride secretion. […] Morphologic abnormalities can be minimal, and studies demonstrate that rotavirus can be released from infected epithelial cells without destroying them. Viral attachment and entry into the epithelial cell without cell death may be enough to initiate diarrhea. The epithelial cell synthesizes and secretes numerous cytokines and chemokines, which can direct the host immune response and potentially regulate cell morphology and function. Studies also suggest that one of the nonstructural viral proteins may act as an enterotoxin, promoting active chloride secretion mediated through increases in intracellular calcium concentration. Toxin-mediated diarrhea would explain the observation that villus injury is not necessarily linked to diarrhea. […] An animal study in zebrafish suggests that the viral capsid and possibly the minor capsid protein VP2 may have key roles in human norovirus symptomatology, perhaps behaving functionally as a viral enterotoxin.

• #9 Mechanism behind virally-caused vomiting identified | ScienceDaily

  https://www.sciencedaily.com/releases/2011/07/110718085218.htm

  What researchers have found is that the viral infection and the toxin excreted from infected cells stimulate a type of sensory cell called enterochromaffin cells in the walls of the digestive tract. These cells can communicate with the brain via the vagus nerve. […] „We have shown that the viral toxin stimulates the cells to release serotonin, a signalling substance that in turn activates the brain’s vomiting centre,” says Maria Hagbom, laboratory engineer in the Department of Molecular Virology at LiU and the chief author of the article in PLoS Pathogens. […] The pattern was studied both in cell cultures, where the researchers demonstrated that the viral toxin caused a release of serotonin, and in mice, where it was seen that a rotavirus infection in the intestines activated the areas in the brain where the vomiting centre is located. […] The researchers’ hypothesis is that the same medicine can relieve vomiting caused by rotavirus and norovirus. […] Through restricting vomiting with this medicine, many lives in developing countries could be saved.

• #10 Viral gastroenteritis

  https://pmc.ncbi.nlm.nih.gov/articles/PMC8883799/

  Information about norovirus pathogenesis, pathology, and immunity has been obtained primarily from volunteer studies, because human noroviruses remained non-cultivatable in intestinal epithelial cells until 2016, and no animal model fully recapitulates human disease after oral inoculation. Histological changes are present in jejunal biopsy samples. Symptomatic illness correlates with broadening and blunting of intestinal villi, crypt-cell hyperplasia, cytoplasmic vacuolisation, and infiltration of polymorphonuclear and mononuclear cells into the lamina propria, with the mucosa remaining intact. The extent of small intestinal involvement remains unknown. Intestinal biopsy samples from children chronically infected with norovirus after small intestinal transplants show increased enterocyte apoptosis and inflammation that is difficult to distinguish from allograft rejection. Additionally, human norovirus antigen has been detected in villus enterocytes but not crypt cells of immunocompromised patients with chronic norovirus infection who had undergone haematopoietic-stem-cell or small-bowel transplantation. Norovirus infection is also associated with epithelial barrier dysfunction.

• #11 Prevalence of gastrointestinal symptoms in patients with influenza, clinical significance, and pathophysiology of human influenza viruses in faecal samples: what do we know? | Virology Journal | Full Text

  https://virologyj.biomedcentral.com/articles/10.1186/s12985-015-0448-4

  Shu et al. found that receptors for influenza virus were abundantly expressed on GI epithelial cells, which are highly permissive of influenza virus replication in vitro. Human and avian influenza A viruses use different receptors for cell entry. Human-adapted influenza A viruses preferentially bind to humanlike sialic acid (SA)2,6galactose (Gal)-terminated saccharides, whereas avian influenza A viruses prefer receptors with avian-like 2,3 linkages. Examination of human colonic samples indicated that SA–2,6-Gal receptors are abundant on epithelial cells of the GI tract, and SA–2,3-Gal receptors can be found from the ileum to the rectum, with abundant expression of avian-like SA–2,3-Gal receptors in goblet cells being found mostly in the large intestine. Both types of SA receptors are expressed on the surface of in vitro differentiated intestinal epithelial cells, suggesting that both avian and human influenza viruses have the potential to infect and replicate in human intestinal epithelial cells. Indeed, influenza A(H5N1) virus can directly target human gut tissues. Intestinal epithelial cells are also susceptible to influenza A(H9N2) and A(H1N1)pdm09 viruses, and the infected cells become apoptotic with elevated pro-inflammatory responses.

• #12 Norovirus: Causes, symptoms and treatment | Live ScienceLive Science

  https://www.livescience.com/42944-what-is-norovirus.html

  Norovirus is a virus that causes vomiting and diarrhea in humans. It is the leading cause of gastrointestinal illness worldwide and across all age groups, according to a 2022 review in the journal Viruses. […] Norovirus is a very stable pathogen. It can survive for long periods of time on surfaces and in water, even in extremely harsh environments, Yuan said. „In addition, there is a lack of long-term immunity after norovirus infection,” she said. […] The mechanism of norovirus infection is not fully understood, according to a 2012 review published in The Journal of Infectious Diseases. Norovirus is a relatively simple pathogen — each viral particle carries just nine protein-coding genes. […] Human norovirus binds to human cells via several specific receptors, such as histo-blood group antigens (HBGA), according to a 2019 review published in the journal Viruses. […] In addition to humans, norovirus can infect a broad range of hosts including livestock, pets, and wild animals like marine mammals and bats. Norovirus may not be restricted to one host and might be able to jump the species barrier, according to a 2019 review published in the journal Viruses.

• #13 V. Background | Infection Control | CDC

  https://www.cdc.gov/infection-control/hcp/norovirus-guidelines/background.html

  Norovirus is the most common etiological agent of acute gastroenteritis and is often responsible for outbreaks in a wide spectrum of community and healthcare settings. […] The P2 subdomain of the viral capsid is the likely binding site of norovirus, and is the most variable region on the norovirus genome. […] The strength of the virus binding may be dependent on the human host HBGA receptor sites, as well as on the infecting strain of norovirus. […] Infection appears to involve the lamina propria of the proximal portion of the small intestine, yet the cascade of changes to the local environment is unknown.

• #14 Your blood type may influence your vulnerability to norovirus: BioNews: Spring 2020: Newsletters: News & Events: Department of Biology: Indiana University Bloomington

  https://biology.indiana.edu/news-events/newsletters/2020-spr-newsletter/norovirus.html

  In the last few [winter] months, schools all over the country have closed because of outbreaks of norovirus. Also known as stomach flu, norovirus infections cause watery diarrhea, low-grade fever and, most alarming of all, projectile vomiting, which is an extremely effective way of spreading the virus. […] Noroviruses are the most common cause of acute gastroenteritis (infection of the stomach and intestines) in the United States. […] When norovirus is ingested, it initially infects the cells that line the small intestine. Researchers dont know exactly how this infection then causes the symptoms of the disease. But a fascinating aspect of norovirus is that, after exposure, blood type determines, in a large part, whether a person gets sick. […] The same oligosaccharides on red blood cells also appear on the surface of cells that line the small intestine. Norovirus and a few other viruses use these oligosaccharides to grab onto and infect the intestinal cells. Its the specific structure of these oligosaccharides that determines whether a given strain of virus can attach and invade.

• #15 How highly contagious norovirus infection gets its start – WashU Medicine

  https://medicine.washu.edu/news/how-fast-spreading-norovirus-infection-gets-its-start/

  Norovirus – the highly contagious gastrointestinal illness best known for spreading rapidly on cruise chips, in nursing homes, schools and other densely populated spaces – kills an estimated 200,000 people annually, mostly in the developing world. […] Now, researchers at Washington University School of Medicine in St. Louis have shown, in mice, that the virus infects a rare type of intestinal cell called a tuft cell, so named because each cell sports a cluster of hairlike extensions on its surface. While tuft cells are few in number, the scientists’ findings indicate that once the virus strikes, such cells multiply the virus quickly and set off severe infections. […] The new study indicates that such infections in the mice cause the number of tuft cells to increase by five- to tenfold, leading the norovirus to replicate more efficiently.

• #16 How highly contagious norovirus infection gets its start – WashU Medicine

  https://medicine.washu.edu/news/how-fast-spreading-norovirus-infection-gets-its-start/

  The researchers, including Herbert W. “Skip” Virgin, MD, PhD, now at Vir Biotechnology, also noted that noroviruses tucked inside tuft cells are effectively hidden from the immune system, which could explain why some people continue to shed virus long after they are no longer sick. […] “This raises important questions about whether human norovirus infects tuft cells and whether people who have chronic norovirus infections and continue to shed the virus long after infection do so because the virus remains hidden in tuft cells,” Wilen said. “If that’s the case, targeting tuft cells may be an important strategy to eradicate the virus.”

• #17 Human norovirus targets enteroendocrine epithelial cells in the small intestine | Nature Communications

  https://www.nature.com/articles/s41467-020-16491-3

  Human noroviruses are a major cause of diarrheal illness, but pathogenesis is poorly understood. […] Investigation of the signaling pathways induced in EECs that mediate communication between the gut and brain may clarify mechanisms of pathogenesis and lead to the development of in vitro model systems in which to evaluate norovirus vaccines and treatment. […] The purpose of this study is to identify target cells in the human enteric tract that support active norovirus replication. […] Enteroendocrine cells (EECs), specialized epithelial cells in the intestine that secrete hormones and other signaling molecules integral to gut function, are identified as permissive target cells during acute and chronic infection in four immunocompromised patients. […] This opens avenues of investigation into the mechanisms of norovirus pathogenesis in diarrheal disease and in the development of optimized in vitro cell culture systems for the evaluation of vaccines and treatment.

• #18 Human norovirus targets enteroendocrine epithelial cells in the small intestine | Nature Communications

  https://www.nature.com/articles/s41467-020-16491-3

  The intensity of protein and RNA staining in intestinal tissue was reflected in the high number of viral genome copies in stool, allowing us to investigate the distribution and cellular tropism of norovirus in the likely absence of pre-existing immunity. […] Enteroendocrine cells were identified as an epithelial cell type associated with active norovirus replication. […] This discovery may offer insight into the pathogenesis of human norovirus, where symptoms often have an acute onset with explosive vomiting and diarrhea. […] Immune cell activation, coupled with a strong innate immune response and chemical signaling in specialized epithelial cells, including EECs, may contribute to the signs and symptoms of norovirus disease.

• #19 Mechanism behind virally-caused vomiting identified | ScienceDaily

  https://www.sciencedaily.com/releases/2011/07/110718085218.htm

  Every year, more than 800,000 children in impoverished countries die from diarrhea and vomiting caused by rotavirus and norovirus — 'winter vomiting disease’. […] Researchers at Linkping University and other institutions have now discovered how vomiting develops in viral infections and have found a way to quickly treat these children and others in the risk zone for dehydration. […] It is well known that viruses like rotavirus and norovirus are behind the majority of stomach infections. But it was unclear how vomiting developed, and the treatments available were oral fluid replacement and intravenous drips to prevent dehydration of the body. […] Now a research team, led by Professor Lennart Svensson at Linkping University, has produced results that show for the first time how the viruses give rise to vomiting.

• #20 Norovirus encounters in the gut: multifaceted interactions and disease outcomes | Mucosal Immunology

  https://www.nature.com/articles/s41385-019-0199-4

  Thus, both the host mutation, specifically in the intestinal epithelium, and viral infection are required for the Crohn’s disease-like phenotype, raising the possibility that enteric infections could contribute to IBD in humans. […] These studies have suggested that NoVs may serve as viral triggers for IBS or IBD in some environmental and genetic contexts, and also indicated that the microbiota may be important for NoV pathogenesis. […] The microbiota plays a fundamental role in the induction, training, and function of the host immune system, and the gut microbiota has an important role in maintaining intestinal homeostasis by preventing colonization by exogenous pathogens and potentially harmful indigenous microorganisms. […] Experimental alteration of the microbiota dramatically alters MNoV infection, as pretreatment of mice with an antibiotic cocktail prevents infection of the intestine by both acute strain MNV-1 and by persistent MNoV strains MNV-3 and CR6.

• #21 Prevalence of gastrointestinal symptoms in patients with influenza, clinical significance, and pathophysiology of human influenza viruses in faecal samples: what do we know? | Virology Journal | Full Text

  https://virologyj.biomedcentral.com/articles/10.1186/s12985-015-0448-4

  Influenza A virus significantly increases the adhesive properties of mucosa-associated E. coli strains, inducing the exposure of cellular receptors by intestinal cells. The expression of these cellular receptors increased after influenza virus infection of lung epithelial cells, and influenza virus was shown to replicate efficiently in human primary intestinal cells. These findings suggest that viral infection of intestinal epithelial cells alters the glycosylation pattern of mucosal proteins and thereby increases bacterial adhesiveness, increasing the number of E. coli, thereby causing vomiting and diarrhea. These data suggest an increased number of E. coli as a consequence of influenza virus infection is the primary cause of intestinal injury during influenza virus infection.

• #22 Gastrointestinal tract and viral pathogens

  https://www.wjgnet.com/2220-3249/full/v12/i3/136.htm

  Adenovirus is a double-stranded DNA virus belonging to the Adenoviridae family. HAdV-F40 and F41 are the enteric serotypes implicated in causing acute gastroenteritis. […] Symptoms of adenoviral gastroenteritis are like any other gastroenteritis including diarrhea, vomiting, and abdominal cramps. […] Human Coronaviruses are known to cause respiratory infections, but they also cause GI symptoms including diarrhea, nausea, vomiting, and abdominal pain. […] The majority of HCoV infections like diarrhea occur in neonates, infants, and children. […] SARS-CoV-2 causing COVID-19 also presents as diarrhea, nausea, vomiting, and abdominal pain along with respiratory symptoms and sometimes even in the absence of respiratory manifestations. […] Currently, no specific antivirals are indicated in SARS and MERS infections, whereas COVID-19 treatment entails various therapies like antivirals, steroids, biologics, etc.

• #23 Prevalence of gastrointestinal symptoms in patients with influenza, clinical significance, and pathophysiology of human influenza viruses in faecal samples: what do we know? | Virology Journal | Full Text

  https://virologyj.biomedcentral.com/articles/10.1186/s12985-015-0448-4

  While influenza virus is likely to spread to the GI tract of patients after a primary respiratory infection, the route of dissemination remains unknown. Current knowledge explains the detection of human influenza viruses in faeces because of: (i) swallowing of influenza viruses from the upper respiratory tract; (ii) remnants of infected submucosal intestinal antigen-presenting immune cells; and (iii) virus replication in intestinal cells. […] A low pH environment, such as in the stomach, should render most influenza viruses non-infectious by inducing an irreversible conformational change of the viral haemagglutinin. For this reason, influenza virus detection in stools has generally been attributed to swallowed respiratory secretions. However, in this case the acid lability of influenza viruses that destroys their infectivity when passing through the stomach could also result in viral RNA degradation. Therefore, in the hypothetical scenario of swallowed influenza viruses from the upper respiratory tract, the fact that influenza virus RNA and, in some cases, infectious influenza virus was detected and/or isolated from stools could indicate that the viruses were mixed with food and thus protected, or that the gastric acidity was reduced as a consequence of medical treatment, gastric disease, or mutations conferring resistance to low pH.

• #24 Prevalence of gastrointestinal symptoms in patients with influenza, clinical significance, and pathophysiology of human influenza viruses in faecal samples: what do we know? | Virology Journal | Full Text

  https://virologyj.biomedcentral.com/articles/10.1186/s12985-015-0448-4

  The faecal presence of influenza virus RNA may be related to the detection of human influenza viral RNA in remnants of infected intestinal antigen-presenting immune cells. Influenza virus could bind intestinal cells such as DC-SIGN+ CD68+ dendritic cells, which are localized in the small and large intestine. These intestinal DC-SIGN+ CD68+ cells act as antigen-presenting cells and participate in the stimulation of immunity through T-cell activation. Antigen-presenting cells of various origins are susceptible to infection by different influenza virus subtypes, and may act as vehicles for extrapulmonary dissemination of the virus. The shedding of viable influenza virus in stools in the absence of viraemia suggests that the virus does not disseminate to the GI tract haematogenously after a primary respiratory tract infection.

• #25 Viral gastroenteritis (stomach flu) – Symptoms & causes – Mayo Clinic

  https://www.mayoclinic.org/diseases-conditions/viral-gastroenteritis/symptoms-causes/syc-20378847

  Viral gastroenteritis is an intestinal infection that includes signs and symptoms such as watery diarrhea, stomach cramps, nausea or vomiting, and sometimes fever. […] The most common way to develop viral gastroenteritis — often called stomach flu — is through contact with an infected person or by consuming contaminated food or water. […] Viral gastroenteritis is an inflammation of these organs caused by a virus. […] Many viruses can cause gastroenteritis, including: Noroviruses. Both children and adults are affected by noroviruses, the most common cause of foodborne illness worldwide. […] In most cases, you pick up the virus from contaminated food or water. […] Rotavirus. Worldwide, this is the most common cause of viral gastroenteritis in children, who are usually infected when they put their fingers or other objects contaminated with the virus into their mouths. […] The main complication of viral gastroenteritis is dehydration — a severe loss of water and essential salts and minerals. […] If you’re healthy and drink enough to replace fluids you lose from vomiting and diarrhea, dehydration shouldn’t be a problem.

• #26 Viral Gastroenteritis (Stomach Flu) Symptoms & Treatment | Ada

  https://ada.com/conditions/viral-gastroenteritis/

  Most cases of viral gastroenteritis clear up without specific medical treatment. […] In most cases, an episode of viral gastroenteritis clears up completely, without causing any long-term problems or complications. However, in a few cases, there may be complications. The risk of developing complications from stomach flu is highest in very young children, elderly people, and people who have a chronic condition such as diabetes, or a weakened immune system. […] Dehydration is the most common complication of viral gastroenteritis (stomach flu).

• #27 Norovirus encounters in the gut: multifaceted interactions and disease outcomes | Mucosal Immunology

  https://www.nature.com/articles/s41385-019-0199-4

  An intact immune system is critical to effective control of NoV infection, and data from responses to both human and mouse NoV infection support important roles for both the innate and adaptive arms of immunity to keep NoVs in check. […] Although effective in inhibiting and regulating virus replication, endogenous IFN responses are counteracted by a number of viral evasion mechanisms. […] Collectively, as with other pathogens, an active virus-host interaction has evolved with the host reacting antivirally to infection and the virus avoiding these pathways through multiple mechanisms. […] HNoV infection is mostly acute with symptoms manifested after an incubation period of 12-48h. […] In addition to the acute symptomatic manifestations of NoV infection, there has been some evidence linking NoV infections to sequelae including post-infectious irritable bowel syndrome (IBS) and inflammatory bowel disease (IBD).

• #28 Gastroenteritis: What It Is, Symptoms, Causes & Treatment

  https://my.clevelandclinic.org/health/diseases/gastroenteritis

  Infectious diseases or toxic chemicals can trigger acute gastroenteritis. […] Chemicals can injure and inflame the lining of your stomach and intestines. Some chemicals do this even in small amounts. Others, like alcohol and certain medications, can cause gastroenteritis in larger doses. […] Gastrointestinal infections are most contagious during the period when you have symptoms, and for two days after. These last two days are when your body is shedding the infection through your poop. […] Most of the time, gastroenteritis is brief and ends by itself. When this is the case, the primary complication to look out for is dehydration. […] If gastroenteritis lasts a long time, it could begin to damage your stomach and intestines. For example, you might develop ulcers in your organs that bleed.

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