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Viral agent that causes mumps

The mumps virus (MuV) is the virus that causes mumps. MuV contains a single stranded, negative sense genome made of ribonucleic acid (RNA). Its genome is about 15,000 nucleotides in length and contains seven genes that encode nine proteins. The genome is encased by a capsid that is in turn surrounded by a viral envelope. MuV particles, called virions, are pleomorphic in shape and vary in size from 100 to 600 nanometers in diameter. One serotype and twelve genotypes that vary in their geographic distribution are recognized. Humans are the only natural host of the mumps virus. MuV replicates first by binding to the surface of cells, whereby its envelope merges with the host cell membrane to release the capsid inside of the cell. Once inside, the viral RNA dependent RNA polymerase transcribes messenger RNA (mRNA) from the genome and later replicates the genome. After translation of viral proteins, virions are formed adjacent to the cell membrane, where they then leave the cell by budding from its surface, using the cell membrane as the envelope. The mumps virus was first identified as the cause of mumps in 1934 and was first isolated in 1945. Within a few years after isolation, vaccines protecting against MuV infection had been developed. MuV was first recognized as a species in 1971, and it has been given the scientific name Mumps orthorubulavirus. It is assigned to the genus Orthorubulavirus in the subfamily Rubulavirinae, family Paramyxoviridae.

MuV first interacts with a host cell by binding to its surface via the HN protein's receptor, sialic acid, which binds to sialic acid receptors on the surface of host cells. Following attachment, the F protein is triggered and begins fusing the viral envelope with the host cell's membrane. The F protein does so by changing from a metastable state to refolding to a more stable hairpin structure, which allows the contents of the virion, including the RNP, to be released into the host cell's cytoplasm. The V and P proteins are encoded by the same gene, so while transcribing mRNA, RdRp edits the mRNA by inserting two non templated guanines into the mRNA to transcribes mRNA for the P protein. Later in the replication cycle, once a sufficient number of nucleoproteins are present after translation, RdRp switches functions to replicate the genome. This occurs in a two step process: first, a positive sense antigenome is synthesized by RdRp from the negative sense genome, and second, negative sense genomic RNA strands are in turn synthesized by RdRp from the antigenome. During this process, the antigenome and newly replicated genomes are encapsidated by the nucleoprotein at the same time as replication. Budding from the host cell begins once M proteins recruit host class E proteins that form endosomal sorting complex required for transport (ESCRT) structures at the site of budding. There, ESCRT proteins form into concentric spirals and push the contents of the virion outward from the cell in the form of a vesicle that protrudes from the cell. The ESCRT proteins then constrict the opening of the vesicle and terminate budding by cutting off the vesicle from the rest of the membrane, forming a complete virion that is released from the host cell. During this process, the neuraminidase of HN proteins aids in separation from the host membrane and prevents virion aggregation. The different genotypes vary in frequency from region to region. For example, genotypes C, D, H, and J are more common in the western hemisphere, whereas genotypes F, G, and I are more common in Asia, although genotype G is considered to be a global genotype. Genotypes A and B have not been observed in the wild since the 1990s. This diversity of MuV is not reflected in the antibody response since because there is only one serotype, antibodies to one genotype are also functional against all others.

The F, SH, HN genes, used to distinguish genotypes, are estimated to experience genetic mutations at a rate of 0.25 · 10^(−3) substitutions per site per year, which is considered to be a very low mutation rate for an RNA virus. Phylogenetic analysis of the entire SH gene indicates that genotypes A and J are related in one branch and split apart from the other genotypes. In that second branch, genotype I is a sister clade of the other genotypes, which cluster into five sequential sister clades: G and H; D and K; C; L; and B, F, and N. meningitis, orchitis, myocarditis, pancreatitis, nephritis, oophoritis, and mastitis. Mumps is usually not life threatening and typically resolves within a few weeks after the onset of symptoms, but long term complications such as paralysis, seizures, hydrocephalus, and deafness can occur. Treatment is supportive in nature, and infection is preventable via vaccination.

Mumps virus, scientific name Mumps orthorubulavirus, is assigned to the genus Orthorubulavirus, in the subfamily Rubulavirinae, family Paramyxoviridae. The mumps virus was isolated for the first time in 1945 and by 1948 the first mumps vaccine had been developed. In 1995, Mumps virus was established as the type species of the newly established genus Rubulavirus. In 2016, Mumps virus was renamed to Mumps rubulavirus. In 2018, Mumps rubulavirus was renamed to Mumps orthorubulavirus to accompany Rubulavirus being abolished and replaced with the subfamily Rubulavirinae bearing the same name and the newly established genus Orthorubulavirus. In 2020, type species in virus taxonomy were abolished, so Mumps orthorubulavirus was removed as the type species of Orthorubulavirus.

The word "mumps" is first attested circa 1600 and is the plural form of "mump", meaning "grimace", originally a verb meaning "to whine or mutter like a beggar". The disease was likely called mumps in reference to the swelling caused by mumps parotitis, reflecting its impact on facial expressions as well as its causing of painful, difficult swallowing. "Mumps" was also used starting from the 17th century to mean "a fit of melancholy, sullenness, silent displeasure".