| Lloviu cuevavirus | |
|---|---|
Virus classification | |
| (unranked): | Virus |
| Realm: | Riboviria |
| Kingdom: | Orthornavirae |
| Phylum: | Negarnaviricota |
| Class: | Monjiviricetes |
| Order: | Mononegavirales |
| Family: | Filoviridae |
| Genus: | Cuevavirus |
| Species: | Lloviu cuevavirus |
| Member virus | |
Lloviu virus (LLOV) | |
The speciesLloviu cuevavirus (/ˈjɒvjuːˌkwɛvəˈvaɪrəs/YOV-ewKWEV-ə-VY-rəs) is thetaxonomic home of a virus that forms filamentous virion,Lloviu virus (LLOV). The species is included in the genusCuevavirus.[1][2] LLOV is a distant relative of the commonly knownEbola virus andMarburg virus.
ThespeciesLloviu cuevavirus is avirological taxon (i.e. a man-madeconcept) included in the genusCuevavirus, familyFiloviridae, orderMononegavirales.[1] The species has a singlevirus member, Lloviu virus.[1] Lloviu virus is the sole member of the speciesLloviu cuevavirus, which is included genusCuevavirus,familyFiloviridae,orderMononegavirales.[1][2] The name Lloviu virus is derived fromCueva del Lloviu (the name of aSpanishcave in which it was first discovered[1]) and thetaxonomicsuffixvirus (which denotes a virus species).[1]
In 2010, the species and the genuscuevavirus were proposed as independent species and genus.[1] In July 2013, the species and the genuscuevavirus were ratified by theInternational Committee on Taxonomy of Viruses (ICTV) to be included in its report, therefore the name is now to be italicized.[3]
A virus that fulfills the criteria for being a member of the genus "Cuevavirus" is a member of the species "Lloviu cuevavirus" if it has the properties of "cuevaviruses" (because there is currently only "cuevavirus" species) and if its genome differs from that of Lloviu virus (variant Bat86) by <30% at the nucleotide level.[1]
Lloviu virus (/ˈjɒvjuː/YOV-yoo;[1]LLOV) is a virus distantly related to the well-known pathogensEbola virus andMarburg virus.[1][2]
LLOV was discovered in 2011 inSchreibers's long-fingered bats (speciesMiniopterus schreibersii) that were found dead in Cueva del Lloviu in 2002,Asturias,Spain, as well as in caves in SpanishCantabria and in caves inFrance andPortugal.[2] It has not yet been proven that the virus is theetiological agent of a novel bat disease, but healthy Schreibers' long-fingered bats were not found to contain traces of the viruses, thereby at least suggesting that the virus may bepathogenic for certain bats.Necropsies of dead bats did not revealmacroscopicpathology, butmicroscopic examination suggestedviral pneumonia.[2] No information is available about whether or not LLOV infects humans.[4]
Seroreactivity of additionalSchreibers's long-fingered bats were reported from North Spain from 2015, suggesting the circulation of the virus among those bat colonies. HoweverPCR positive animals were not found.[5]
AdditionalSchreibers's long-fingered bat die-off events were reported fromHungary in 2013, 2016 and 2017. The presence of LLOV was confirmed in bat carcasses from 2016, presenting hemorrhagic symptoms.[6] Updated genome data was obtained from the Hungarian samples in 2020, using theNanopore sequencing technique.[7] The infectious virus was isolated fromSchreibers's long-fingered bat in Hungary, making it only the third filovirus along withMarburg andRavn viruses ever isolated from bats.[8]
Although LLOV was isolated intissue culture, yet its genome has been determined in its entirety with exception of the3' and5' UTRs.[2][8] Like allmononegaviruses, LLOV virions contain a non-infectious, linear nonsegmented, single-strandedRNAgenome of negative polarity that most likely possesses inverse-complementary 3' and 5' termini, does not possess a5' cap, is notpolyadenylated, and is notcovalently linked to aprotein.[9] The LLOV genome is probably approximately 19kb long and contains sevengenes in the order3'-UTR-NP-VP35-VP40-GP-VP30-VP24-L-5'-UTR. In contrast toebolaviruses andMarburgviruses, which synthesize seven mRNAs to express the seven structural proteins, LLOV seems to produce only sixmRNAs, i.e. one mRNA (VP24/L) is thought to bebicistronic. LLOV genomictranscriptional termination sites are identical to those ofebolavirus genomes but different from those ofMarburgvirus genomes. LLOVtranscriptional initiation sites are unique.[2]
The LLOVlife cycle is hypothesized to begin with virion attachment to specific cell-surfacereceptors, followed by internalization,fusion of the virion envelope withendosomal membranes and the concomitant release of the virusnucleocapsid into thecytosol. LLOV glycoprotein (GP) is cleaved by endosomal cysteine proteases (cathepsins) and the cleaved glycoprotein interacts with the intracellular entry receptor, Niemann-Pick C1 (NPC1).[10] The virus RdRp would partially uncoat the nucleocapsid andtranscribe thegenes into positive-strandedmRNAs, which would then betranslated into structural and nonstructuralproteins. LLOV L would bind to a singlepromoter located at the 3' end of the genome. Transcription would either terminate after a gene or continue to the next gene downstream. This means that genes close to the 3' end of the genome would be transcribed in the greatest abundance, whereas those toward the 5' end would be least likely to be transcribed. The gene order would therefore be a simple but effective form of transcriptional regulation. The most abundant protein produced would be thenucleoprotein, whoseconcentration in the cell would determine when L switches from gene transcription to genome replication. Replication would result in full-length, positive-stranded antigenomes that would in turn be transcribed into negative-stranded virus progeny genome copies. Newly synthesized structural proteins and genomes would self-assemble and accumulate near the inside of thecell membrane. Virions wouldbud off from the cell, gaining their envelopes from the cellular membrane they bud from. The mature progeny particles would then infect other cells to repeat the cycle.[9]
| Ebolavirus |
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| Marburgvirus | |||||||||||||||
| Cuevavirus |
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| Dianlovirus |
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| Striavirus |
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| Thamnovirus |
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