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Pathogenesis

Many aspects of the pathogenesis of mumps are poorly understood and are inferred from clinical observations and experimental infections in laboratory animals. These animal studies may be unreliable due to unnatural methods of inoculation. Following exposure, the virus infects epithelial cells in the upper respiratory tract that express sialic acid receptors on their surface. After infection, the virus spreads to the parotid glands, causing the signature parotitis. It is thought that shortly after infection the virus spreads to lymph nodes, in particular T-cells and viruses in the blood, called viremia. Viremia lasts for 7–10 days, during which MuV spreads throughout the body.

In mumps orchitis, infection leads to: parenchymal edema; congestion, or separation, of the seminiferous tubules; and perivascular infiltration by lymphocytes. The tunica albuginea forms a barrier against edema, causing an increase in intratesticular pressure that causes necrosis of the seminiferous tubules. The seminiferous tubules also experience hyalinization, i.e. degeneration into a translucent glass-like substance, which can cause fibrosis and atrophy of the testes.

In up to half of cases, MuV infiltrates the central nervous system (CNS), where it may cause meningitis, encephalitis, or hydrocephalus. Mumps is rarely fatal, so few post-mortem analyses have been done to analyze CNS involvement. Of these, fluid buildup, congestion, and hemorrhaging in the brain, white blood cell infiltration in the perivascular spaces in the brain, reactive changes to glial cells and damage to the myelin sheaths surrounding neurons were observed. Neurons appear to be relatively unaffected.

In laboratory tests on rodents, MuV appears to enter the CNS first through cerebrospinal fluid (CSF), then spreading to the ventricular system. There, MuV replicates in ependymal cells that line the ventricles, which allows the virus to enter the brain parenchyma. This often leads to MuV infecting pyramidal cells in the cerebral cortex and hippocampus. Infected ependymal cells become inflamed, lose their cilia, and collapse into CSF, which may be the cause of the narrowing of the cerebral aqueduct thought to cause mumps hydrocephalus.

In humans, mumps hydrocephalus may be due to obstruction of the cerebral aqueduct with dilatation of the lateral and third ventricles, obstruction of the interventricular foramina, or obstruction of the median and lateral apertures. Ependymal cells have been isolated from CSF of mumps patients, suggesting that animals and humans share hydrocephalus pathogenesis. Hydrocephalus has also been observed in the absence of canal obstruction, however, indicating that obstruction may be a result of external compression by edematous tissue and not related to hydrocephalus.

Deafness from mumps may be caused by MuV infection in CSF, which has contact with the perilymph of the inner ear, possibly leading to infection of the cochlea, or it may occur as a result of inner ear infection via viremia that leads to inflammation in the endolymph. Hearing loss may also be caused indirectly by the immune response. In animal studies, MuV has been isolated from the vestibular ganglion, which may explain vestibular symptoms such as vertigo that often co-occur with deafness.