Alongshan virus in Russia

Kholodilov, I. S.; Litov, A. G.; Klimentov, A. S.; Belova, O. A.; Polienko, A. E.; Nikitin, N. A.; Shchetinin, A. M.; Ivannikova, A. Y.; Bell-Sakyi, L.; Yakovlev, A. S.; Bugmyrin, S. V.; Bespyatova, L. A.; Gmyl, L. V.; Luchinina, S. V.; Gmyl, A. P.; Gushchin, V. A.; Karganova, G. G.

doi:10.1101/862573

bioRxiv · 10.1101/862573

Alongshan virus in Russia

Kholodilov, I. S.·Litov, A. G.·Klimentov, A. S.·Belova, O. A.·Polienko, A. E.·Nikitin, N. A.·Shchetinin, A. M.·Ivannikova, A. Y.·Bell-Sakyi, L.·Yakovlev, A. S.·Bugmyrin, S. V.·Bespyatova, L. A.·Gmyl, L. V.·Luchinina, S. V.·Gmyl, A. P.·Gushchin, V. A.·Karganova, G. G.

View original source ↗Export metadata ↓

Abstract

In recent decades, many new flavi-like viruses have been discovered predominantly in different invertebrates and, as was recently shown, some of them may cause disease in humans. The Jingmen tick virus (JMTV) group holds a special place among flavi-like viruses because, in contrast to the "classic" flaviviruses and other flavi-like viruses, they have a segmented ssRNA(+) genome. Two segments of the JMTV genome have homology with regions of the flavivirus genome encoding polymerase and helicase-protease proteins. JMTVs have several open reading frames (ORF) in segments encoding glycoprotein(s) and capsid protein and these ORF are specific only to them. JMTVs greatly differ in virion size. We isolated three strains of Alongshan virus (ALSV), which is a representative of the JMTV group, from adult Ixodes persulcatus ticks collected in two geographically-separated Russian regions in the tick cell line IRE/CTVM19. One of the strains persisted in the IRE/CTVM19 cells without cytopathic effect for three years. Most virions purified from tick cells were spherical with a diameter of approximately 40.5 nm. In addition, we found smaller particles of approximately 13.1 nm in diameter. We obtained full genome sequences of all four segments of two of the isolated ALSV strains, and partial sequences of one segment from the third strain. Phylogenetic analysis on genome segment 2 of the JMTV group clustered our novel strains with other ALSV strains. We found evidence for the existence of a novel upstream ORF in the glycoprotein-coding segment of ALSV and other members of the JMTV group. Significance StatementWe isolated three strains of Alongshan virus (ALSV) from adult Ixodes persulcatus ticks from two geographically separate areas of Russia in the Ixodes ricinus tick cell line IRE/CTVM19. One of the strains persisted in the IRE/CTVM19 cells without cytopathic effect for three years. Our study confirmed the value of tick cell lines in virus isolation and maintenance of persistent infection. The majority of virions of the ALSV strain Miass527 were enveloped spherical particles with a diameter of 40.5{+/-}3.7 nm. We found evidence for the existence of a novel upstream ORF in the glycoprotein-coding segment of ALSV and other members of the Jingmen tick virus group.

Source connections

Published article ↗

Explore related subjects

molecular biology Preprint

Keep this discovery

Explore connections, maps & timelines

BibTeX RIS

Kholodilov, I. S., Litov, A. G., Klimentov, A. S., Belova, O. A., Polienko, A. E., Nikitin, N. A., Shchetinin, A. M., Ivannikova, A. Y., Bell-Sakyi, L., Yakovlev, A. S., Bugmyrin, S. V., Bespyatova, L. A., Gmyl, L. V., Luchinina, S. V., Gmyl, A. P., Gushchin, V. A., Karganova, G. G.. 2019-12-03. Alongshan virus in Russia. https://doi.org/10.1101/862573

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related preprints

bioRxiv2026

Genomic features and instability of linezolid resistance in vancomycin-resistant Enterococcus faecalis ST525

This study investigated the mechanisms of oxazolidinone resistance and genomic background in clinical ST525 Enterococcus faecalis isolates, a poorly characterized lineage reported in Brazilian hospitals as either vancomycin-resistant (VRE) or linezolid- and vancomycin-resistant (LVRE). Five LVREfs from intensive care unit patients (linezolid MICs, 8-32 mg/L; vancomycin MICs, >256 mg/L) carried only G2576T and G2505A (in three of four rrl copies) as known linezolid resistance determinants, despite variable linezolid MICs. During serial in vitro passages without antibiotic pressure, isolates with initial MICs of 8-16 mg/L exhibited progressive MIC reductions accompanied by reversion of mutant to wild-type rrl copies, whereas the isolate with an initial MIC of 32 mg/L maintained high-level resistance without reversion. Additional domain V substitutions emerged during MIC decline, while growth kinetics remained broadly similar. Whole-genome sequencing of a representative isolate (LVREfs L7) revealed a ~2.8-Mb chromosome enriched in mobile genetic elements (~8.6%), lacking a functional CRISPR-Cas system. A plasmid-borne prototype Tn1546 carrying vanA, devoid of internal insertion sequences, was found inserted into a Tn3-family transposase gene, a platform not typically associated with vanA mobilization. Together, these findings indicate that ST525 LVREfs, whose genomic features are consistent with long-term persistence in hospitals, may pose a challenge to routine susceptibility testing. A single mutational mechanism can yield variable linezolid MICs, and the ratio of mutated vs wild-type rrl copies can become heterogeneous in the absence of antibiotic pressure, without correlating directly with these values, contrary to the well-documented copy number-MIC correlation.

molecular biology↗

bioRxiv2026

Global repression of mesenchymal genes in epithelial cells by the histone demethylase LSD1

Epithelial-mesenchymal transition (EMT) is an essential process in development, tissue repair, and tumour metastasis, and is triggered by SNAI, ZEB and TWIST transcription factors, that recruit lysine-specific demethylase 1 (LSD1) to repress epithelial genes such as E-cadherin. In mesenchymal cells, LSD1 inhibition restores E-cadherin expression and reduces migration and invasion, consistent with LSD1 inhibition reverting EMT, and offering a therapeutic modality for EMT-associated disease. Recent data, however, suggest context-dependent roles for LSD1, as its inhibition in epithelial cells increases mesenchymal marker expression, potentially promoting EMT. To investigate this discrepancy, we mapped genome-wide binding of LSD1 in HCT116 epithelial cells and used rapid degron-mediated ablation of endogenous LSD1 to measure changes in nascent and steady-state transcription and chromatin accessibility. In epithelial cells, LSD1 binds constitutively-accessible, primed mesenchymal promoters. These are rapidly derepressed after LSD1 ablation, with activation of SNAI2 and ZEB1, which repress epithelial hallmarks such as E-cadherin. Re-introduction of LSD1 downregulates SNAI2 and ZEB1 but, surprisingly, further represses E-cadherin, indicating sustained loss of epithelial characteristics. Collectively, our results show that LSD1 maintains epithelial identity by repressing mesenchymal genes, questioning the therapeutic utility of LSD1 inhibition for EMT control.

molecular biology↗

bioRxiv2026

The long noncoding RNA FOSIL shapes the dynamics of FOS induction

Immediate-early genes require rapid, transient, and precisely tuned transcriptional activation in response to extracellular signals, yet how this kinetic precision is achieved remains poorly understood. We characterize FOSIL (LINC01220), an inducible lncRNA locus downstream of FOS. Depleting FOSIL RNA delays heregulin (HRG)-induced FOS mRNA and protein accumulation and prolongs the response, indicating that FOSIL sharpens both the onset and the shutoff of the induction wave. Capture Micro-C maps show that FOSIL depletion weakens the chromatin boundary between FOS and FOSIL and increases local compaction across the pre-assembled FOS-FOSIL neighborhood during serum starvation, demonstrating that basal FOSIL production maintains a locally insulated, poised conformation prior to signal arrival. Upon HRG stimulation, FOSIL depletion blunts the rapid movement of the locus toward nuclear speckles, diminishes early speckle-proximal FOS transcription, and extends late firing at speckle-distant alleles. At single transcription active sites, nascent FOSIL activity correlates with closer speckle proximity and higher FOS output, and activating the endogenous FOSIL promoter by CRISPRa, but not supplying FOSIL RNA in trans, enhances both speckle association and FOS induction. Together, these findings support a mechanism where endogenous FOSIL activity coordinates pre-stimulus chromatin folding with dynamic nuclear speckle positioning to fine-tune the onset, amplitude, and resolution of immediate-early gene expression.

molecular biology↗