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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, protecting against MuV infection had been developed. MuV was first recognized as a species in 1971, and it has been given the scientific name Orthorubulavirus parotitidis. It is assigned to the genus Orthorubulavirus in the subfamily Rubulavirinae, family Paramyxoviridae.
The SH protein is thought to be involved in blocking NF(α)-mediated apoptosis of the host cell, which is done as an antiviral response to suppress the spread of viruses, though SH is not necessary for replication since MuVs engineered without SH are still able to replicate. The V protein is also involved in evading host antiviral responses by means of inhibiting production and signalling of . Unlike the other proteins, the I protein's function is unknown.
Upon entering the host cell, the RdRp begins transcribing mRNA from the genome inside the RNP. Transcription starts at or near the 3'-end (usually pronounced "three prime end") at a promoter region and moves sequentially toward the 5'-end. One mRNA strand is transcribed for each gene, and it is necessary for all genes sequentially before a gene to be transcribed for that gene to be transcribed. Genes closer to the 3'-end are transcribed at the highest frequency, decreasing in frequency as RdRp approaches the 5'-end. RdRp synthesizes a five-prime cap of the mRNA and a Polyadenylation on the 3'-end consisting of hundreds of consecutive . Once a gene has been transcribed, RdRp releases it into the cytoplasm for subsequent translation of viral proteins by host ribosomes. The V and P proteins are encoded by the same gene, so while transcribing mRNA, RdRp RNA editing the mRNA by inserting two non-templated 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. Progeny genomes can be used for additional transcription or replication or may simply be packaged into progeny virions.
HN and F proteins are synthesized in the endoplasmic reticulum and travel through the Golgi complex to the cell membrane, whether they bind to the cell membrane and protrude from the surface of the cell. M proteins bind to the sites of the cell membrane where HN and F proteins are, doing so at the positions where their "tails" protrude into the inside of the cell membrane in the cytoplasm. M proteins then act as a signals to newly synthesized RNPs as to where virions are to be formed. The interaction of RNP and M proteins is then thought to trigger budding from the host cell.
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.
This system is used in sequential order. For example, MuVs/NewYork.USA/17.11B (VAC) is a vaccine-associated genotype B MuV derived from clinical material in New York City, and MuVi/London.GBR/3.12/2G is a genotype G MuV derived from cell culture in London.
Initial vaccines contained inactivated virus particles and provided short-term protection against mumps. In the 1960s, Maurice Hilleman developed a more effective mumps vaccine using live virus particles that were taken from his then five-year-old infected daughter, Jeryl Lynn. This vaccine was approved for use in 1967 and recommended in 1977, replacing prior vaccines that were less effective. Hilleman would also work to develop the MMR vaccine in 1971, effective against measles, mumps, and rubella. The "Jeryl Lynn" strain of the mumps virus, which belongs to genotype A, continues to be used in vaccines against mumps.
Mumps virus was recognized as a species in 1971 by the International Committee on Taxonomy of Viruses (ICTV), which oversees virus taxonomy, when it was assigned to the genus Paramyxovirus. Since then, it has undergone numerous taxonomic changes and changes to its scientific name:
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