Pathogenesis of gut virus infection

Abstract

In summary, the pathogenesis of many gut virus infections remains uncertain. However, human and animal studies indicate that the majority of gut viruses infect villous enterocytes. Viruses appear to have different affinities for enterocytes at different sites on the villus. Infection of enterocytes leads to cell death, extrusion into the lumen, and villous atrophy when the rate of cell production in the crypts cannot keep pace with the rate of enterocyte loss. This results in a reduced surface area as well as impairment of digestive and absorptive functions. This may also result in a net secretory state. All these changes, along with others such as reduced enzymatic activity and reduced epithelial integrity, may contribute to the induction of an acute but transient malabsorptive diarrhoea which may persist until the digestive/absorptive functions of the enterocyte are restored. However, if colonic compensation is sufficient to handle the increased fluid load, diarrhoea may not be evident. The roles of villous ischaemia, altered countercurrent exchanger of altered immune responses still remain uncertain and require further investigation.

Rotavirus Enterotoxin NSP4 Binds to the Extracellular Matrix Proteins Laminin-β3 and Fibronectin

“…Rotavirus-induced disease is thought to be caused by a combination of factors (70), including a reduction in epithelial surface area, replacement of mature enterocytes by immature (crypt-like) cells (10,60), an osmotic effect resulting from incomplete absorption of carbohydrates from the intestinal lumen in combination with bacterial fermentation of these nonabsorbed compounds, secretion of intestinal fluid and electrolytes through activation of the enteric nervous system (43), and the secretory effect of NSP4, which is thought to act as a viral enterotoxin (3). During rotavirus infection, there is an enhanced turnover of epithelial cells that is thought to result in the presence of immature cells on the villi (10,60).…”

Changes in Small Intestinal Homeostasis, Morphology,and Gene Expression during Rotavirus Infection of InfantMice

“…Rotavirus-induced diarrhea is thought to be caused by a combination of factors (55), which include a reduction in epithelial surface area, replacement of mature enterocytes by immature (crypt-like) cells (43), an osmotic effect resulting from incomplete absorption of carbohydrates from the intestinal lumen in combination with bacterial fermentation of these nonabsorbed compounds, secretion of intestinal fluid and electrolytes through activation of the enteric nervous system (37), and the effect of the rotavirus nonstructural protein 4 (NSP4), which is thought to act as a viral enterotoxin (1).…”

Lactic Acid Bacteria: Genetics, Metabolism and Applications

“…Rotavirus invades and replicate in the differentiated absorptive columnar cells of the small intestinal epithelium. This results in partial disruption of the intestinal mucosa with loss of microvilli, a decrease in the villus/crypt ratio and an increased intestinal permeability (Salim et al 1990). Several studies have shown that selected probiotics, such as L. rhamnosus GG, L. reuteri, L. casei Shirota and B. lactis Bb12, can shorten the duration of rotavirus diarrhoea by approximately 1 day (Kaila et al 1992;Saavedra et al 1994;Sugita & Togawa 1994;Shomikova et al 1997).…”