Mumps is an acute, systemic viral infection classically associated with swelling of one or both parotid glands.
Mumps is caused by a paramyxovirus with a negative-strand nonsegmented RNA genome of 15,384 bases encoding nine proteins. The nucleoprotein, phosphoprotein, and polymerase protein participate in viral replication and, together with genomic RNA, form the ribonucleocapsid. The ribonucleocapsid is surrounded by a host-derived lipid bilayer envelope containing the viral hemagglutinin-neuraminidase (HN) and fusion (F) proteins, which are responsible for cell binding by and entry of the virus and are major targets of virus-neutralizing antibodies. The functions of the other virus proteins (small-hydrophobic, matrix, V, and I) are less well understood. The small-hydrophobic gene sequence is highly variable and forms the basis for the 13 genotypes (A through M) used mainly for molecular epidemiologic purposes.
Mumps is endemic worldwide, with epidemics occurring every 3–5 years in unvaccinated populations. The estimated annual global incidence is 100–1000 cases per 100,000 population in countries without national mumps vaccination programs, where virtually the entire population has been infected by adulthood. Following the 1967 introduction of mumps vaccine in the United States, the reported number of cases declined; by 2001, this number had decreased from >150,000 to <300—a 99.8% reduction from prevaccine levels. In 2006, the United States experienced its largest mumps outbreak in more than 20 years, with 6584 reported cases. This outbreak was preceded by outbreaks in the United Kingdom (2004–2005) and followed by outbreaks in Canada. Compelling epidemiologic evidence links the genotype G virus to the outbreaks in all three countries. The majority of cases occurred in college students 18–23 years of age, most of whom had been vaccinated in early childhood. These outbreaks are probably the result of several coincident circumstances, including (1) situations promoting the spread of respiratory viruses among young adults (e.g., residence in college dormitories), (2) waning of vaccine immunity with time, (3) lack of endemically circulating wild-type virus to periodically boost vaccine-induced immune responses, and (4) continuing global epidemics of mumps (due either to lack of mumps vaccination programs or to low rates of mumps vaccination where such programs do exist). Whereas in the pre- and early postvaccine era mumps was historically a disease of childhood, the majority of U.S. cases now occur in previously vaccinated young adults.
Humans are the only natural hosts for mumps virus infection. The incubation period of mumps is ∼19 days (range, 7–23 days). The virus is transmitted by the respiratory route via droplets, saliva, and fomites. Mumps virus is typically shed from 1 week before to 1 week after symptom onset, although this window appears to be narrower in vaccinated individuals. Persons are most contagious 1–2 days before onset of clinical symptoms. Primary replication occurs in the nasal mucosa or upper respiratory mucosal epithelium. Mononuclear cells and cells within regional lymph nodes can become infected; such infection facilitates the development of viremia and poses a risk ...