HUMAN ROTA VIRU INFECTIONS
Worldwide, an estimated one million infants die each year as a result of rotavirus diarrhea. Currently, in the United States, the total annual deaths now are thought to be less than 100, but these viruses are still major causes of severe illness and hospitalization in early life. Vomiting, abdominal cramps, and low-grade fever, followed by watery stools that usually do not contain mucus, blood, or pus, are all characteristic of the acute phase of illness, and can also be seen with infections due to caliciviruses, astroviruses and adenoviruses.
Outbreaks of rotavirus infection are common, particularly during the cooler months, among infants and children 1 to 24 months of age. Older children and adults can also be affected, but attack rates are usually much lower. Outbreaks among elderly, institutional-ized patients have also been recognized.
Although newborn infants can be readily infected with the virus, such infections often result in little or no clinical illness. This finding is illustrated by reported infection rates of 32 to 49% in some neonatal nurseries, but mild illness in only 8 to 28% of the infants. It is unclear whether this transient resistance to disease is a result of host matu-ration factors or transplacentally conferred immunity. Seroepidemiologic studies have been useful in demonstrating the ubiquity of these viruses and, perhaps, help to explain the age-specific attack rates. By the age of 4 years, more than 90% of individuals have humoral antibodies, suggesting a high rate of virus infection early in life.
Rotaviruses appear to localize primarily in the duodenum and proximal jejunum, causing destruction of villous epithelial cells with blunting (shortening) of villi and variable, usually mild, infiltrates of mononuclear and a few polymorphonuclear inflammatory cells within the villi. The gastric and colonic mucosa are unaffected; however, for unknown reasons, gastric emptying time is markedly delayed. The primary pathophysiologic effects are a decrease in absorptive surface in the small intestine and decreased production of brush border enzymes, such as the disaccharidases. The net result is a transient malabsorptive state, with defective handling of fats and sugars. It may take as long as 3 to 8 weeks to restore the normal histologic and functional integrity of the damaged mucosa. While the specific gene product associated with virulence is not yet known, some evidence suggests that one nonstructural protein, NSP4, may behave as an enterotoxin in a manner similar to the heat-labile enterotoxin (LT) of Escherichia coli and cholera toxin. This may further explain the excess fluid and electrolyte secretion in the acute phase of illness. Viral excretion usually lasts 2 to 12 days but can be greatly prolonged in malnourished or immunodeficient patients, with persistent symptoms.
Patients with rotavirus infection respond with production of type-specific humoral anti-bodies that appear to last for years, perhaps a lifetime. In addition, type-specific secre-tory IgA (sIgA) antibodies are produced in the intestinal tract, and their presence seems to correlate best with immunity to reinfection. Breastfeeding also seems to play a protec-tive role against rotavirus disease in young infants. Secretory IgA antibodies to ro-taviruses appear in colostrum and continue to be secreted in breast milk for several months postpartum. Human breast milk mucin glycoproteins have also been shown to bind to rotaviruses, inhibiting their replication in vitro and in vivo.
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