Lloviu virus

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Lloviu cuevavirus
Virus classification Edit this 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 species Lloviu cuevavirus (

Ebola virus and Marburg virus
.

Use of term

The

Cuevavirus, family Filoviridae, order Mononegavirales.[1][2] The name Lloviu virus is derived from Cueva del Lloviu (the name of a Spanish cave in which it was first discovered[1]) and the taxonomic suffix virus (which denotes a virus species).[1]

In 2010, the species and the genus

cuevavirus were ratified by the International Committee on Taxonomy of Viruses (ICTV) to be included in its report, therefore the name is now to be italicized.[3]

Species inclusion criteria

A virus that fulfills the criteria for being a member of the genus "

cuevavirus" species) and if its genome differs from that of Lloviu virus (variant Bat86) by <30% at the nucleotide level.[1]

Lloviu virus (

According to the rules for taxon naming established by the International Committee on Taxonomy of Viruses (ICTV), the name Lloviu virus is always to be capitalized (because "Lloviu" is a proper noun), but is never italicized, and may be abbreviated (with LLOV being the official abbreviation).[citation needed]

History

LLOV was discovered in 2011 in Schreibers's long-fingered bats (species Miniopterus schreibersii) that were found dead in Cueva del Lloviu in 2002, Asturias, Spain, as well as in caves in Spanish Cantabria and in caves in France and Portugal.[2] It has not yet been proven that the virus is the etiological 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 be pathogenic for certain bats. Necropsies of dead bats did not reveal macroscopic pathology, but microscopic examination suggested viral pneumonia.[2] No information is available about whether or not LLOV infects humans.[4] However, Cueva del Lloviu is frequented by tourists and no human infections or disease has yet been observed, suggesting that it is possible that LLOV might be the second filovirus that is not pathogenic for humans (the first one being Reston virus (RESTV)). [citation needed]

Seroreactivity of additional Schreibers's long-fingered bats were reported from North Spain from 2015, suggesting the circulation of the virus among those bat colonies. However PCR positive animals were not found.[5]

Additional Schreibers's long-fingered bat die-off events were reported from Hungary 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 the Nanopore sequencing technique.[7] The infectious virus was isolated from Schreibers's long-fingered bat in Hungary, making it only the third filovirus along with Marburg and Ravn viruses ever isolated from bats.[8]

Virology

Genome

Although LLOV was isolated in

transcriptional initiation sites are unique.[2]

Structure

The structure of LLOV virions has not yet been described. Like all other

ribonucleocapsid, which would consist of the genomic RNA wrapped around a polymer of nucleoproteins (NP). Associated with the ribonucleoprotein would be the RNA-dependent RNA polymerase (L) with the polymerase cofactor (VP35) and a transcription activator (VP30). The ribonucleoprotein would be embedded in a matrix, formed by the major (VP40) and minor (VP24) matrix proteins. These particles would be surrounded by a lipid membrane derived from the host cell membrane. The membrane would anchor a glycoprotein (GP1,2) that projects 7 to 10 nm spikes away from its surface. While nearly identical to ebolavirions and marburgvirions in structure, lloviuvirions may be antigenically distinct from both (just as they are from each other).[original research?
]

Replication

The LLOV

promoter 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 the nucleoprotein, whose concentration 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 the cell membrane. Virions would bud 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]

References

External links