Use of term
The International Committee on Taxonomy of Viruses, species ''Lloviu cuevavirus'' is a International Committee on Taxonomy of Viruses, virological taxon (i.e. a man-made concept) included in the genus ''Cuevavirus'', family ''Filoviridae'', order ''Mononegavirales''. The species has a single virus member, Lloviu virus. Lloviu virus is the sole member of the species ''Lloviu cuevavirus'', which is included genus ''Cuevavirus'', International Committee on Taxonomy of Viruses, family ''Filoviridae'', International Committee on Taxonomy of Viruses, order ''Mononegavirales''. The name Lloviu virus is derived from ''Cueva del Lloviu'' (the name of a Spain, Spanish cave in which it was first discovered) and the Taxonomy (biology), taxonomic suffix ''virus'' (which denotes a virus species). 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.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. 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, capitalized (because "Lloviu" is a proper noun), but is never Italic type, italicized, and may be Abbreviation, abbreviated (with LLOV being the official abbreviation).History
LLOV was discovered in 2011 in common bent-wing bat, Schreibers's long-fingered bats (species ''Miniopterus schreibersii'') that were found dead in Cueva del Lloviu back 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, 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. Autopsy, Necropsies of dead bats did not reveal Macroscopic scale, macroscopic pathology, but microscopic scale, microscopic examination suggested viral pneumonia. No information is available about whether or not LLOV infects humans. However, Cueva del Lloviu is frequented by Tourism, tourists and no human infections or disease has yet been observed, suggesting that it is possible that LLOV might be the second Filoviridae, filovirus that is not pathogenic for humans (the first one being Reston virus, Reston virus (RESTV)). Seroreactivity of additional common bent-wing bat, Schreibers's long-fingered bats were reported from North Spain from 2015, suggesting the circulation of the virus among those bat colonies. However Polymerase chain reaction, PCR positive animals were not found. Additional common bent-wing bat, 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 common bent-wing bat, Schreibers's long-fingered bat in Hungary, making it only the third filovirus along with Marburg virus, Marburg and Ravn virus, Ravn viruses ever isolated from bats.Virology
Genome
Although LLOV was isolated in tissue culture, yet its genome has been determined in its entirety with exception of the Three prime untranslated region, 3' and Five prime untranslated region, 5' UTRs. Like all Mononegavirales, mononegaviruses, 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, polyadenylated, and is not Covalent bond, covalently linked to a protein. The LLOV genome is probably approximately 19 base pair, kb long and contains seven genes in the order Three prime untranslated region, 3'-UTR-''NP''-''VP35''-''VP40''-''GP''-''VP30''-''VP24''-''L''-Five prime untranslated region, 5'-UTR. In contrast to ebolaviruses and Marburgviruses, which synthesize seven mRNAs to express the seven structural proteins, LLOV seems to produce only six Messenger RNA, mRNAs, i.e. one mRNA (''VP24''/''L'') is thought to be Cistron, bicistronic. LLOV genomic Transcription (genetics), transcriptional termination sites are identical to those of ebolavirus genomes but different from those of Marburgvirus genomes. LLOV Transcription (genetics), transcriptional initiation sites are unique.Structure
The structure of LLOV virions has not yet been described. Like all other Filoviridae, filoviruses, LLOV virions are expected to be filamentous particles that may appear in the shape of a shepherd's crook or in the shape of a "U" or a "6", and they may be coiled, toroid, or branched. Their diameter is expected to be 80 nm in width, but vary in length. The LLOV genome suggests that LLOV particles consist of seven structural proteins. At the center would be the Helix, helical ribonucleoprotein, 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 bilayer, 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).Replication
The LLOV Biological life cycle, life cycle is hypothesized to begin with virion attachment to specific cell-surface Receptor (biochemistry), receptors, followed by internalization, Lipid bilayer fusion, fusion of the virion envelope with Endosome, endosomal membranes and the concomitant release of the virus nucleocapsid into the cytosol. LLOV glycoprotein (GP) is cleaved by endosomal cysteine proteases (cathepsins) and the cleaved glycoprotein interacts with the intracellular entry receptor, Niemann-Pick C1 (NPC1). The virus RdRp would partially uncoat the nucleocapsid and Transcription (genetics), transcribe the genes into positive-stranded mRNAs, which would then be translation (biology), translated into structural and nonstructural proteins. LLOV L would bind to a single Promoter (biology), 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, 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.References
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