Mimiviridae
| Mimiviridae | |
|---|---|
| File:Tupanvirus.jpeg | |
| Tupanvirus | |
| Virus classification Edit this classification | |
| (unranked): | Virus |
| Realm: | Varidnaviria |
| Kingdom: | Bamfordvirae |
| Phylum: | Nucleocytoviricota |
| Class: | Megaviricetes |
| Order: | Imitervirales |
| Family: | Mimiviridae |
| Subfamilies and genera | |
Mimiviridae is a family of viruses. Amoeba and other protists serve as natural hosts. The family contains three subfamilies that contain nine genera.[1][2][3][4] Viruses in this family belong to the nucleocytoplasmic large DNA virus clade (NCLDV), also referred to as giant viruses.
History
[edit | edit source]The first member of this family, Mimivirus, was discovered in 2003,[5] and the first complete genome sequence was published in 2004.[6] However, the mimivirus Cafeteria roenbergensis virus[7] was isolated and partially characterized in 1995,[8] although the host was misidentified at the time, and the virus was designated BV-PW1.[7]
Taxonomy
[edit | edit source]The family contains the following subfamilies and genera (-virinae denotes subfamily and -virus denotes genus):[2]
Structure
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Viruses in Mimiviridae have icosahedral and round geometries, with between T=972 and T=1141, or T=1200 symmetry. The diameter is around 400 nm, with a length of 125 nm. Genomes are linear and non-segmented, around 1200kb in length. The genome has 911 open reading frames.[1]
Life cycle
[edit | edit source]Replication follows the DNA strand displacement model. DNA-templated transcription is the method of transcription. Amoeba serve as the natural host.[1]
Molecular biology
[edit | edit source]Three putative DNA base excision repair enzymes were characterized from Mimivirus.[10] The base excision repair (BER) pathway was experimentally reconstituted using the purified recombinant proteins uracil-DNA glycosylase (mvUDG), AP endonuclease (mvAPE), and DNA polymerase X protein (mvPolX).[10] When reconstituted in vitro mvUDG, mvAPE and mvPolX function cohesively to repair uracil-containing DNA predominantly by long patch base excision repair, and thus these processes likely participate in the BER pathway early in the Mimivirus life cycle.[10]
Clinical
[edit | edit source]Mimiviruses have been associated with pneumonia but their significance is currently unknown.[11] The only virus of this family isolated from a human to date is LBA 111.[12] At the Pasteur Institute of Iran (Tehran), researchers identified mimivirus DNA in bronchoalveolar lavage (BAL) and sputum samples of a child patient, utilizing real-time PCR (2018). Analysis reported 99% homology of LBA111, lineage C of the Megavirus chilensis.[13] With only a few reported cases previous to this finding, the legitimacy of the mimivirus as an emerging infectious disease in humans remains controversial.[14][15]
Mimivirus has also been implicated in rheumatoid arthritis.[16]
See also
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References
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- ^ Lua error in Module:Citation/CS1/Configuration at line 2172: attempt to index field '?' (a nil value)., UCPMS ID: 1889607, PDF
- ^ Lua error in Module:Citation/CS1/Configuration at line 2172: attempt to index field '?' (a nil value). Fig. 4 and §Discussion: "Considering that tupanviruses comprise a sister group to amoebal mimiviruses..."
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- ^ a b c Lad SB, Upadhyay M, Thorat P, Nair D, Moseley GW, Srivastava S, Pradeepkumar PI, Kondabagil K. Biochemical Reconstitution of the Mimiviral Base Excision Repair Pathway. J Mol Biol. 2023 Sep 1;435(17):168188. doi: 10.1016/j.jmb.2023.168188. Epub 2023 Jun 26. PMID 37380013
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External links
[edit | edit source]
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