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The species Lloviu cuevavirus ( ) is the taxonomic home of a virus that forms filamentous virion, Lloviu virus (LLOV). The species is included in the genus Cuevavirus. LLOV is a distant relative of the commonly known Ebola virus and Marburg virus.
In 2010, the species and the genus cuevavirus were proposed as independent species and genus. In July 2013, 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.
Lloviu virus ( ; LLOV) is a virus distantly related to the well-known pathogens Ebola virus and Marburg 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 Capitalization (because "Lloviu" is a proper noun), but is never Italic type, and may be Abbreviation (with LLOV being the official abbreviation).
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.
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. Updated genome data was obtained from the Hungarian samples in 2020, using the Nanopore sequencing technique. The infectious virus was isolated from Schreibers's long-fingered bat in Hungary, making it only the third filovirus along with Marburg virus and Ravn virus viruses ever isolated from bats.
Species inclusion criteria
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.
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. It has not yet been proven that the virus is the Etiology 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 for certain bats. Autopsy of dead bats did not reveal macroscopic pathology, but microscopic examination suggested viral pneumonia. No information is available about whether or not LLOV infects humans. However, Cueva del Lloviu is frequented by Tourism and no human infections or disease has yet been observed, suggesting that it is possible that LLOV might be the second Filoviridae that is not pathogenic for humans (the first one being Reston virus).
Virology
Genome
Although LLOV was isolated in tissue culture, yet its genome has been determined in its entirety with exception of the 3' and 5' UTRs. Like all Mononegavirales, LLOV virions contain a non-infectious, linear nonsegmented, single-stranded RNA genome of negative polarity that most likely possesses inverse-complementary 3' and 5' termini, does not possess a 5' cap, is not Polyadenylation, and is not Covalent bond linked to a protein. The LLOV genome is probably approximately 19 base pair long and contains seven in the order 3'-UTR- NP- VP35- VP40- GP- VP30- VP24- L-5'-UTR. In contrast to and , which synthesize seven mRNAs to express the seven structural proteins, LLOV seems to produce only six Messenger RNA, i.e. one mRNA ( VP24/ L) is thought to be Cistron. LLOV genomic transcriptional termination sites are identical to those of ebolavirus genomes but different from those of Marburgvirus genomes. LLOV transcriptional initiation sites are unique.
Replication
The LLOV life cycle is hypothesized to begin with virion attachment to specific cell-surface receptors, followed by internalization, fusion of the virion envelope with Endosome membranes and the concomitant release of the virus nucleocapsid into the cytosol. LLOV glycoprotein (GP) is cleaved by endosomal cysteine proteases () and the cleaved glycoprotein interacts with the intracellular entry receptor, Niemann-Pick C1 (NPC1). The virus RdRp would partially uncoat the nucleocapsid and transcribe the genes into positive-stranded , which would then be translated into structural and nonstructural proteins. LLOV L would bind to a single 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 Budding 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.
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