Mumps

==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.<ref name=rubin /> 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.<ref name=junghanss /> It is thought that shortly after infection the virus spreads to [[lymph node]]s, in particular T-cells and viruses in the blood, called viremia.<ref name=su /><ref name=rubin /> Viremia lasts for 7–10 days, during which MuV spreads throughout the body.<ref name=davis />

In mumps orchitis, infection leads to: parenchymal edema; congestion, or separation, of the [[seminiferous tubules]]; and perivascular infiltration by lymphocytes. The [[Tunica albuginea of testis|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 [[Hyaline|hyalinization]], i.e. degeneration into a translucent glass-like substance, which can cause [[fibrosis]] and atrophy of the testes.<ref name=davis /><ref name=masarani />

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, [[Gliosis|reactive changes to glial cells]] and [[Demyelinating disease|damage to the myelin sheaths surrounding neurons]] were observed. [[Neuron]]s appear to be relatively unaffected.<ref name=rubin />

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 cell]]s that line the ventricles, which allows the virus to enter the brain [[parenchyma]]. This often leads to MuV infecting [[pyramidal cell]]s 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 [[Stenosis|narrowing]] of the [[cerebral aqueduct]] thought to cause mumps hydrocephalus.<ref name=rubin />

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 (neuroanatomy)|interventricular foramina]], or obstruction of the [[Median aperture|median]] and [[Lateral aperture|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 [[edema]]tous tissue and not related to hydrocephalus.<ref name=rubin />

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.<ref name=rubin />