Etiology
The mumps virus is a single-stranded RNA virus and a member of the Paramyxovirus genus. It is an enveloped virus composed of a matrix protein and 2 surface glycoproteins. The glycoproteins, known as hemagglutinin-neuraminidase and fusion protein, enable viral absorption, and fusion of the virion membrane with the host cell membrane, respectively.[11] The envelope is composed of a lipid bilayer membrane, making the virus susceptible to ether and alcoholic disinfectants.[2]
Twelve mumps virus genotypes have been described, designated A to N (E has been included in C and M in K). Their prevalence varies by geographic location.[11] Humans are the only natural host for mumps.[2]
Pathophysiology
Spread occurs via respiratory droplets, direct contact, or contaminated fomites. The incubation period typically ranges from 14-18 days, with peak contagion manifesting 1-2 days before symptom onset. Viral shedding has been detected in saliva as early as 7 days before and until 9 days after the emergence of clinical symptoms. Vaccination status appears not to influence the duration of viral shedding.[2]
The primary site of viral replication is the epithelium of the upper respiratory tract; occasionally, the infection remains localized to the respiratory tract. Typically, the virus rapidly disseminates to local lymphoid tissue, leading viremia and enabling the virus to travel to distant parts of the body. Infected mononuclear cells also facilitate virus spread.[2] Mumps virus has an affinity for glandular epithelium; virus replication often occurs in the parotid gland ductal epithelium, causing interstitial edema, local inflammation, and painful swelling of the gland.[2]
Generally, a mumps infection confers life-long immunity, although 1% to 2% of cases are thought to be reinfections.
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