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Rotaviruses cause enteric disease with symptoms characterized by diarrhea, vomiting, abdominal discomfort, and fever, or any combination. The virus affects mainly infants and young children. Diarrhea ranges from mild to severe and can cause fatal dehydration.
The 70-nm-diameter wheel-shaped particles consist of a double-layered icosahedral capsid enclosing a core particle that contains 11 segments of double-stranded RNA, each segment representing one gene.
Rotavirus is a genus in the family Reoviridae. Rotaviruses have three important antigenic specificities: group, subgroup, and serotype. Group A rotaviruses are major pathogens in humans and animals. Ten serotypes of human group A rotaviruses are defined by neutralization of one (VP7) of the two outer capsid proteins. Of the non-group A rotaviruses (groups B through G), only groups B and C have been detected in humans; they are not an important cause of disease in infants and young children.
The virus enters the cell by endocytosis or by direct membrane penetration if activated by protease. Replication occurs in the cytoplasm. Removal of the outer shell of the capsid in lysosomes activates the viral RNA polymerase. Newly assembled subviral particles acquire the outer capsid proteins by budding through the endoplasmic reticulum, and are released by cell lysis.
Transmission is by the fecal-oral route (and possibly the respiratory route). Reversible damage to the proximal small intestine appears as shortened villi and as sparse, irregular microvilli with a patchy, irregular but predominantly intact mucosa and as mononuclear cell infiltration of the lamina propria.
The mechanism of immunity is not firmly established. In animals, antibody in the intestinal lumen is crucial. In humans, studies of the role of serum antibodies with protection have yielded conflicting results.
Group A rotaviruses are ubiquitous and infect most individuals by the third year of life. They are the single most important cause of severe diarrhea in infants and young children worldwide, accounting for about 30 to 50 percent of cases requiring hospitalization or treatment. In temperate climates, incidence peaks in the winter; in the tropics, the disease occurs year-round.
Clinical findings are nonspecific. Diagnosis depends on detecting virus in feces (e.g., by immunoassay) or on demonstrating a serum antibody response.
Dehydration is treated by fluid and electrolyte replacement. Vaccine development is under way and appears promising.
Reovirus infections occur frequently, but most are mild or subclinical. The role of these viruses in human disease is not clear, but they are not considered to be important agents of human disease.
Four human orbiviruses or coltiviruses cause fevers. The most important is Colorado tick fever, a diphasic fever with headache, severe muscle pain, and arthralgia. Children may develop hemorrhage or encephalitis.
The spherical virions (diameter, 60 to 80 nm) are similar to those of rotaviruses except that the genome contains 10 or (in Coltivirus) 12 RNA segments.
The genera Orbivirus and Coltivirus contain 109 serotypes in 13 serogroups; four serotypes cause human disease.
Multiplication is as for rotaviruses and takes place in both the arthropod vector and the vertebrate host. Gene segment reassortment occurs among closely related serotypes.
Colorado tick fever coltivirus chronically infects the tick Dermacentor andersoni, which transmits it to humans. The virus infects bone marrow cells, arresting development of several blood cell types and sometimes causing thrombocytopenia. In young children, the virus may invade the central nervous system and cause encephalitis.
Colorado tick fever elicits interferon and humoral antibody; the role of these and other defenses is not known.
The distribution of Colorado tick fever, in the Rocky Mountains and western United States, matches that of its tick vector. The virus propagates in a rodent-tick cycle, with humans as secondary hosts.
Diagnosis depends on isolation of virus from erythrocytes or detection of viral antigen on erythrocytes by immunofluorescence. Antibody appears in convalescent-phase serum.
Control is by avoidance of tick bites.
