Aetiology
A large number of viruses are found in the human intestine. These include viruses that infect bacteria (bacteriophages), viruses that use the intestines just as a portal of entry (e.g., poliovirus, enterovirus, hepatovirus, and some adenoviruses), and viruses that cause gastrointestinal infection. The final group of viruses causes damage to the gastrointestinal tract, resulting in vomiting, diarrhoea, or both. Rotaviruses, caliciviruses, astroviruses, coronaviruses, noroviruses, and enteric adenoviruses are the primary pathogens causing gastroenteritis in humans. HIV, cytomegalovirus, and herpes simplex virus mainly cause opportunistic infections in immunocompromised hosts.[4][5]
Pathophysiology
The pathogenesis of rotavirus infection is well studied. Rotavirus spreads from person to person, mainly by the faecal-oral route. Noroviruses may also be transmitted by the airborne route. Incubation period is 1 to 3 days but the symptoms can appear as early as 12 hours after exposure.[6][7]
The mechanism of diarrhoea is thought to be impaired fluid absorption due to cell damage. After ingestion (an infectious dose is approximately 100 virus particles), rotavirus infects the mature enterocytes. The rate of death of rotavirus-infected mature villous enterocytes exceeds the rate of production of new enterocytes in crypts. This imbalance causes structural damage to the small bowel mucosa, including villous shortening, crypt hyperplasia, and a mononuclear inflammatory infiltrate in the lamina propria. Immature enterocytes are secretory in nature, and there is loss of absorptive surface. Rotavirus damages the villous brush border, causing osmotic diarrhoea, and also produces an enterotoxin (NSP4) that causes calcium-mediated secretory diarrhoea.[8] The loss of brush-border enzymes can cause osmotic diarrhoea, and the permeable mucosa can cause food intolerance, which may exacerbate and prolong the diarrhoea.
In general, an infection with rotavirus confers high protection against symptomatic reinfection, but in developing countries where exposure is high, the protection is less. The major correlate of protective immunity seems to be antirotavirus immunoglobulin A coproantibodies.
Noroviruses particularly cause severe disease in young children, older people, and people with chronic diseases. Noroviruses also cause persistent infection in immunosuppressed patients. Host susceptibility factors for noroviruses have been identified and include histo-blood group antigens that probably function as initial receptors for some noroviruses. Noroviruses are resistant to commonly used disinfectants, and infected people can shed the virus for prolonged periods even after the illness stops. Genetic variability of noroviruses also counteracts immunity.
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