Rotaviruses, found in many mammalian species, often have a fairly broad host range. Rotaviruses have a characteristic morphology that distinguishes them from other reoviruses: Namely, they have the appearance of wheels with spokes radiating from the center and a smooth outer rim (Figure 1). The particles also have a large number of channels connecting the outer surface of the virion to the inner core. It has been postulated that these channels are involved in the import of substrates needed for RNA transcription and the extrusion of newly synthesized RNA transcripts. These channels are necessary because viral replication in the cytoplasm occurs without complete uncoating of the virion particle.

Fig1. Structure of rotavirus. A. Electron micrograph. B. Schematic drawing.

A. Epidemiology

Rotaviruses are divided into seven serogroups (A through G) of which group A is the most important cause of outbreaks of disease in humans. Transmission of rotaviruses is via the fecal–oral route. Marked seasonal incidence is associated with rotavirus infections, with the peak months in the United States being January through March. Because infectious particles are relatively stable, they can survive for extended periods on various surfaces. Rotavirus infections account for about 50 percent of cases of severe diarrhea in infants and young children (up to age 2 years).

B. Viral replication

 After attachment to and uptake by the host cell, rotaviruses become partially uncoated in a lysosome. The rotavirus genome has 11 segments of linear, dsRNA, each of which codes for a single protein. Reassortment of the RNA segments can occur when a cell is infected with two different rotaviruses. The viral particles contain enzymes (such as RNA-dependent RNA polymerase) that are needed to synthesize positive-sense RNA transcripts with a 5' cap. These positive RNA strands function not only as mRNA but also as templates for the synthesis of negative-strand RNA. After the negative-strand RNA is made, it stays associated with its positive-strand template, giving rise to a dsRNA segment that is packaged in the virion. Rotaviruses are released following cell lysis rather than by budding through the membrane, thus accounting for the lack of a viral envelope. Figure 2 illustrates additional details of rotavirus replication.

Fig2. Replication of rotavirus.

C. Clinical significance

Following ingestion, rotaviruses infect the epithelial cells of the small intestine, primarily the jejunum (Figure 3). Rotaviruses are able to reach the small intestine because they are resistant to the acid pH of the stomach. The incubation period is usually 48 hours or less. Infection can be subclinical or may result in symptoms ranging from mild diarrhea and vomiting to severe, nonbloody, watery diarrhea with dehydration and loss of electrolytes. Although rotavirus infections are probably equally widespread around the world, the outcomes of infection vary significantly in different regions, and malnutrition dramatically increases the severity of the infection. For example, more than 90 percent of children in the United States may have antibodies to rotaviruses by age 3 or 4 years, and mortality in younger children is low because patients who are severely ill are generally hospitalized, with fluid and electrolyte losses rapidly corrected. Infection results in some degree of lifelong immunity with reinfected adults suffering a much milder illness. Infants who are breastfed also suffer milder disease manifestations. However, in developing countries and areas where medical facilities or personnel may be lacking, the mortality is significant: An estimated 1 million deaths per year worldwide result from rotavirus infection.

Fig3. Mechanism of rotavirus diarrhea.

D. Laboratory identification

 Severe diarrhea, dehydration, and electrolyte loss can be due to a variety of causes. Accordingly, a definitive diagnosis cannot be made on clinical grounds alone. As with many other viral infections, identification can be made by detection of viral capsid antigens in stool samples using enzyme-linked immunosorbent assay. An increase in the titer of antiviral antibody in a patient’s serum can also be diagnostic. Electron microscopy of stool specimens, although not a routine diagnostic measure, can aid in the identification of the virus because rotaviruses have a distinctive appearance (see Figure 1).

E. Treatment and prevention

 There is no specific antiviral drug appropriate for treatment of rotavirus infections. The most important clinical intervention is the rapid and efficient replacement of fluids and electrolytes, usually intravenously. Formulations are also being produced that can be used in developing countries so that fluids and electrolytes can be replaced orally. Two oral vaccines using weakened live virus have been shown to be highly efficacious in protecting infants against severe rotavirus gastroenteritis and not associated with increased risk of intussusception (telescoping of one portion of the intestine into another). Prevention of rotavirus infections requires improved sanitation measures.

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