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Results for “Genome, Viral”

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At least 19 recordsLinked to original sources

PubMed2026

The SARS-CoV-2 Integrated Genomic Epidemiology Database (IGED): Linking viral genomes with patient-level metadata to advance statewide genomic surveillance in California.

In July 2021, the California Code of Regulations Title 17 required all laboratories performing SARS‑CoV‑2 whole genome sequencing (WGS) to report their sequencing results to the California Department of Public Health (CDPH). These viral genomic data and patient metadata were compiled into the Integrated Genomic Epidemiology Database (IGED). Linking anonymized viral sequences with patient‑level information enabled monitoring of infectiousness, pathogenicity, transmission dynamics, evolution, and vaccine evasion among emerging SARS‑CoV‑2 lineages. Laboratories performing SARS-CoV-2 WGS transmitted sequencing results to CDPH through Electronic Laboratory Reporting (ELR) and non-ELR pathways. CDPH applied uniform reporting requirements but allowed flexibility in specific data formats to accommodate diverse data systems. To preserve data quality and interoperability across heterogeneous sources, CDPH implemented standardization, validation, and deduplication protocols. Snowflake, a cloud‑based data storage and analytics platform, and Posit Connect, a cloud deployment and automation platform, supported the management, processing, and integration of data within the IGED. The IGED established links between SARS‑CoV‑2 WGS data and epidemiologic metadata for 801,418 sequences, representing 81.7% of all sequences reported in California. Lineages reported to the IGED showed strong concordance with lineage proportions in GISAID. Sequences reported to the IGED had average turnaround times longer than one month, and the majority of sequencing was performed in Southern California and Los Angeles. The IGED enhanced genomic surveillance through predictive modeling and monitoring concerning evolutionary trends such as recombination and saltations in persistent infections. Development of the IGED highlighted the need for standardized data requirements, sustained funding for sequencing, incentives for data submission, and interdisciplinary collaboration to build an effective genomic surveillance system. This framework for linking genomic and epidemiologic data has not only generated critical insights for SARS‑CoV‑2 but also provided the foundation for CDPH and other public health organizations to develop similar IGED‑like systems for other priority pathogens as genomic surveillance expands.

Journal Article↗

PubMed2012

Limitations of encapsidation of recombinant self-complementary adeno-associated viral genomes in different serotype capsids and their quantitation.

We previously reported that self-complementary adeno-associated virus (scAAV) type 2 genomes of up to 3.3 kb can be successfully encapsidated into AAV2 serotype capsids. Here we report that such oversized AAV2 genomes fail to undergo packaging in other AAV serotype capsids, such as AAV1, AAV3, AAV6, and AAV8, as determined by Southern blot analyses of the vector genomes, although hybridization signals on quantitative DNA slot-blots could still be obtained. Recently, it has been reported that quantitative real-time PCR assays may result in substantial differences in determining titers of scAAV vectors depending on the distance between the primer sets and the terminal hairpin structure in the scAAV genomes. We also observed that the vector titers determined by the standard DNA slot-blot assays were highly dependent on the specific probe being used, with probes hybridizing to the ends of viral genomes being significantly overrepresented compared with the probes hybridizing close to the middle of the viral genomes. These differences among various probes were not observed using Southern blot assays. This overestimation of titer is a systemic error during scAAV genome quantification, regardless of viral genome sequences and capsid serotypes. Furthermore, different serotypes capsid and modification of capsid sequence may affect the ability of packaging intact, full-length AAV genomes. Although the discrepancy is modest with wild-type serotype capsid and short viral genomes, the measured titer could be as much as fivefold different with capsid mutant vectors and large genomes. Thus, based on our data, we suggest that Southern blot analyses should be performed routinely to more accurately determine the titers of recombinant AAV vectors. At the very least, the use of probes/primers hybridizing close to the mutant inverted terminal repeat in scAAV genomes is recommended to avoid possible overestimation of vector titers.

Blotting, Southern↗

PubMed2026

VirBinn improves viral genome binning from metagenomic Hi-C through graph diffusion.

MOTIVATION: Metagenomic Hi-C provides in situ proximity signals that can improve genome binning and enable virus-host-association analysis. However, viral genome recovery remains difficult because virus-virus Hi-C contact matrices are extremely sparse. Viral genomes are small, often low-abundance, and frequently assemble into short contigs, leaving many true within-genome links unobserved and causing viral bins to fragment. RESULTS: We present VirBinn, a graph-diffusion framework for viral binning from metagenomic Hi-C. VirBinn enhances virus-virus connectivity through two complementary mechanisms: random-walk-with-restart enhancement on the sparse virus-virus contact graph and host-guided diffusion that propagates viral seeds through the host network to infer indirect virus-virus associations. The enhanced views are integrated and clustered using Leiden community detection to produce viral metagenome-assembled genomes (vMAGs). On dataset-specific simulation benchmarks with ground truth, VirBinn consistently recovers more high-quality vMAGs than Hi-C-based and shotgun-based baselines and substantially increases the number of near-complete genomes. On four real metagenomic Hi-C datasets spanning human gut, pig gut, sheep gut (long-read assembly), and wastewater, VirBinn yields more high-completeness vMAGs under CheckV and produces bins with strong within-cluster contact support. Finally, host linkage analysis using reconstructed host MAGs reveals habitat-specific host-association patterns and plausible host taxonomic profiles. AVAILABILITY AND IMPLEMENTATION: VirBinn is available at https://github.com/dyxstat/VirBinn. The scripts to reproduce the results and figures in this article are available at https://github.com/dyxstat/Reproduce_VirBinn.

Genome, Viral↗

PubMed2026

Longitudinal analysis of high-risk HPV infections reveals within-host viral genome changes over time.

Persistent infection with high-risk (HR)-HPV causes cervical cancer, however, it is unclear why most infections resolve while a minority progress. We deep sequenced the HPV genomes of 1,228 HR-HPV-positive serial samples from 351 women with persistent infections (2-10 serial samples per woman over 1-8 years), including 279 controls and 72 precancer/cancer cases, to assess HR-HPV genome changes during infection and relation to infection outcomes. Seventy-seven percent of persistent infections (45-97% by HPV type) were infections with the same exact viral genome isolate; for HPV16, only 52% were persistent with the same isolate. This may suggest some infections include a type-specific isolate switch or new isolate infection during persistence. We additionally observed within-host change to the HPV genome estimated as gradual changes to intrahost single nucleotide variant (iSNV) frequency, and changes varied by HPV type, with HPV33 infections showing the most iSNV changes. Cases exhibited fewer viral genome changes during infection compared to controls (OR = 0.31, 95% CI = 0.1 - 0.86, p = 0.019), suggesting a more stable and clonal viral genome in cases. By viral gene, E7 had fewer nonsynonymous mutations in the cases compared to controls that cleared within 2 years of infection (p = 0.012), which confirms the importance of E7 conservation and suggests mutations to E7 reduce persistence associated with progression. There was a similar pattern in E4 (p = 0.013), while E5 had more changes in the cases (p = 0.008). A subset of 28 infections had an intervening HPV-negative sample between HPV-positive visits; 93% of these infections had the same exact viral genome isolate in the samples before and after the negative, consistent with subclinical persistence and subsequent re-detection. Our data suggests that HR-HPV type-persistence can include a collection of viral isolates, and viral mutations during infection, particularly in E7, reduce HR-HPV persistence and thus carcinogenic potential.

Humans↗

PubMed2026

A unified benchmark of supervised and retrieval-based methods for viral genomic sequence classification.

The rapid growth of genomic sequencing demands fast, accurate, and scalable analysis methods. In viral genomic classification, expanding labeled reference collections can make supervised models costly to update and dependent on fixed label sets, motivating retrieval-based genomic classification as a simpler, more flexible alternative. We present a unified benchmark of supervised and retrieval-based methods for viral genomic sequence classification across three viral classification tasks: hepatitis C virus (HCV) genotyping, COVID-19 discrimination, and human papillomavirus (HPV) genotyping. We compare standard sequence encodings (one-hot, k-mers, FCGR) with dense embeddings (dna2vec, DNABERT). For each representation, we evaluate supervised classifiers (Random Forest, Decision Tree, XGBoost) and retrieval-based classification, where sequence vectors are indexed with FAISS and labels are assigned via similarity-weighted k-NN. Furthermore, we benchmark multiple FAISS index types (Flat, IVF, HNSW, IVFPQ, OPQ) to characterize accuracy-speed-memory trade-offs at scale. The results show that XGBoost and retrieval using Flat or IVF indexes achieve strong classification performance under different computational profiles. Compressed indexes such as IVFPQ and OPQ substantially reduce memory usage, although their accuracy loss depends on the dataset and representation. Overall, supervised XGBoost provides a favorable accuracy-size trade-off, while retrieval-based classification remains competitive and allows labeled reference sequences to be incorporated without retraining a global classifier. This benchmark provides practical guidance for selecting sequence representations, classifiers, and vector-search indexes under different accuracy, memory, and update requirements.

Genome, Viral↗

PubMed2026

AI-enabled viral genomics: from virus discovery to host prediction and emerging variant forecasting.

The rapid expansion of metagenomic sequencing has generated vast repositories of viral sequence data that far outpace our capacity to interpret them using conventional approaches. Highly divergent sequences, sparse functional annotation, and taxonomically uneven sampling present fundamental challenges for reference-dependent methods, which lose sensitivity precisely for novel and understudied viruses with high public health relevance. Artificial intelligence (AI) provides a new avenue to address these challenges by enabling predictive inference from viral genomes and proteins while reducing dependence on sequence similarity. In this Review, we discuss representative advances in AI for virus discovery, taxonomic classification and functional annotation, prediction of host range and zoonotic potential, and efforts toward forecasting emerging variants. These advances are transforming viral genomics from a largely descriptive discipline into one with increasing predictive capability. We also critically assess the major challenges that constrain current approaches, including the availability of high-quality and representative datasets, rigorous model evaluation, biological interpretability and responsible governance for increasingly capable AI models.

Artificial Intelligence↗

PubMed2025

ELViS: an R package for estimating copy number levels of viral genomic segments at base-resolution.

MOTIVATION: Tumor viruses account for ∼10% of cancer diagnoses. Virally induced tumorigenesis is understood as direct signaling through oncogenes such as E6 and E7 genes in the case of human papillomavirus. Furthermore, pathogen characteristics such as viral oncogene dose may impact the disease course. To our knowledge, no tool has been proposed to assess the intra-viral copy number alterations that define the gene dose of viral oncogenes and associated suppressive pathways native to the pathogen's normal life cycle. RESULTS: We propose an R package, "ELViS," that analyzes viral copy number changes from DNA sequencing of whole viral genomes. The method adjusts for viral load with 2D transformation and segmentation to offer the relative viral gene doses. AVAILABILITY AND IMPLEMENTATION: The ELViS R package is available from https://bioconductor.org/packages/ELViS. This article used controlled access data from dbGaP (phs001713.v1.p1).

Software↗

PubMed2025

A Respiratory Syncytial Virus trailer sequence modulates viral replication and copy-back defective viral genome generation and propagation kinetics.

Copy-back defective viral genomes (cbDVGs) are key inducers of antiviral responses during negative-sense RNA virus infection. Once considered byproducts of in vitro viral replication, cbDVGs have since been detected in clinical specimens and implicated in affecting infection outcomes. The molecular mechanism of cbDVG generation remains unclear, thereby hindering our ability to manipulate cbDVG production during infection for therapeutic gain. Previous work showed that respiratory syncytial virus (RSV) cbDVG re-initiation sites cluster in trailer-end hotspots R1, R2, and R3, and that a poly-U mutation in R1 selectively reduced cbDVG formation at the mutated region. Here, we reported that a 10U mutation in R2 drastically reduced cbDVGs in this region in both minigenome and recombinant virus systems. Furthermore, during high-MOI passaging of the R2-10U virus, we observed delayed detection of cbDVGs with re-initiation sites in R1-R3 (trailer cbDVGs) compared to WT, while no differences in virus titers were observed. Interestingly, we observed the rapid emergence and accumulation of a viral variant bearing a 2-ribonucleotide deletion (R2-8U) within the R2-10U mutation sequence as early as P0. Compared to R2-10U, the R2-8U virus was stable, displayed faster generation and accumulation of trailer cbDVGs, restored cbDVGs with R2 re-initiation sites, and exhibited enhanced genomic replication. Overall, our data identify a sequence in the RSV trailer whose mutation critically modulates both viral replication and the generation/propagation of trailer cbDVGs. Our data also suggest that cbDVG generation, particularly near the trailer, may be an evolutionary tradeoff for more rapid virus genomic replication.

defective viral genome generation and accumulation↗

PubMed2025

Epstein-barr virus (EBV) in cervical carcinoma detected by in situ hybridization targeting ebers and the viral genome.

Epstein-Barr virus (EBV) infection has been suggested as a potential cofactor for the development and progression of cervical cancer, collaborating with high-risk Human Papillomavirus (HR-HPV). In situ hybridization (ISH) has been considered the gold standard in the investigation of EBV in neoplasms. This study aimed to detect EBV in cervical carcinoma samples using ISH targeting EBERs (EBER-ISH) and the BamHI-W region of the viral genome (BamHI-W-ISH), and compare the results of both targets. Of the 88 cases collected, 9 were EBER-ISH positive (10.2%), while 33 (37.5%) cases were positive for EBV by BamHI-W-ISH, all showing staining in the nuclei of the malignant cells. No statistically significant results were found between the presence of EBV and carcinoma type, differentiation grade or tumor staging. The kappa agreement index between the two targets was 0.092. Only 4 cases were EBER-ISH(+) and BamHI-W-ISH(-). On the other hand, 28 cases were BamHI-W-ISH(+) and EBER-ISH(-). Altogether, 37/88 (42%) cases were EBV-positive by one or both targets. Infected lymphocytes were verified in 9 (10.2%) and 34 (38.6%) cases, by EBER-ISH and BamHI-W-ISH, respectively. The slight agreement demonstrated between the targets may be due to the lack of expression of EBERs, suggesting that EBV may present a distinct latency pattern in the cervical mucosa, or that it has entered the replicative cycle in some of these tumors, in both cases, explaining the low positivity rate verified through EBER-ISH, while calling into question the latter's gold standard status in the detection of EBV in malignancies. Our findings also indicate that the chosen viral genomic target may represent a suitable candidate for EBV detection by ISH.

Humans↗

PubMed2026

hnRNPC facilitates coronavirus replication by directly binding the frameshift-stimulatory element of viral genomic RNA.

Translation of key viral replicative proteins in coronaviruses requires a programmed -1 ribosomal frameshifting (-1 PRF) event controlled by the viral frameshift-stimulatory element (FSE). Although previous studies have analyzed host factor dependencies of coronaviruses, how host cellular factors alter -1 PRF efficiency and affect viral replication remains poorly understood. Here, using RNA pull-down combined with LC-MS/MS analysis, we identified heterogeneous nuclear ribonucleoprotein C (hnRNPC) as a major interacting protein of FSE RNA. Coronavirus infection triggers hnRNPC mRNA decay, alters hnRNPC protein levels, and induces its cytoplasmic relocalization, where it appears to bind directly to FSE RNA through residues Asn7 and Asn83. This binding is associated with increased -1 PRF efficiency and may facilitate coronavirus replication. Deletion mapping analysis shows that hnRNPC preferentially binds U-rich regions of the FSE RNA. Finally, we demonstrated that the small molecule Elbasvir directly binds hnRNPC, disrupting the interaction between hnRNPC and FSE RNA and inhibiting coronavirus replication by decreasing -1 PRF efficiency. Collectively, our study identifies hnRNPC as a key host cofactor for coronaviruses and provides a novel target for broad-spectrum antiviral drug development.

RNA, Viral↗

PubMed2024

In vitro one-pot construction of influenza viral genomes for virus particle synthesis based on reverse genetics system.

The reverse genetics system, which allows the generation of influenza viruses from plasmids encoding viral genome, is a powerful tool for basic research on viral infection mechanisms and application research such as vaccine development. However, conventional plasmid construction using Escherichia coli (E.coli) cloning is time-consuming and has difficulties handling DNA encoding genes toxic for E.coli or highly repeated sequences. These limitations hamper rapid virus synthesis. In this study, we establish a very rapid in vitro one-pot plasmid construction (IVOC) based virus synthesis. This method dramatically reduced the time for genome plasmid construction, which was used for virus synthesis, from several days or more to about 8 hours. Moreover, infectious viruses could be synthesized with a similar yield to the conventional E.coli cloning-based method with high accuracy. The applicability of this method was also demonstrated by the generation of recombinant viruses carrying reporter genes from the IVOC products. This method enables the pathogenicity analysis and vaccine development using genetically modified viruses, and it is expected to allow for faster analysis of newly emerging variants than ever before. Furthermore, its application to other RNA viruses is also expected.

Genome, Viral↗

PubMed2021

Presence of complete murine viral genome sequences in patient-derived xenografts.

Patient-derived xenografts are crucial for drug development but their use is challenged by issues such as murine viral infection. We evaluate the scope of viral infection and its impact on patient-derived xenografts by taking an unbiased data-driven approach to analyze unmapped RNA-Seq reads from 184 experiments. We find and experimentally validate the extensive presence of murine viral sequence reads covering entire viral genomes in patient-derived xenografts. The existence of viral sequences inside tumor cells is further confirmed by single cell sequencing data. Extensive chimeric reads containing both viral and human sequences are also observed. Furthermore, we find significantly changed expression levels of many cancer-, immune-, and drug metabolism-related genes in samples with high virus load. Our analyses indicate a need to carefully evaluate the impact of viral infection on patient-derived xenografts for drug development. They also point to a need for attention to quality control of patient-derived xenograft experiments.

Animals↗

PubMed2025

Modeling airborne transmission of viral genome using computational fluid dynamics simulation: A case study for SARS-CoV-2 virus.

Predicting indoor air quality during infectious disease conditions relies on models simulating particle materials (PM)/bioaerosols distribution. Understanding the thermo-fluid properties of exhaled air is crucial for comprehending disease transmission dynamics. This study employs a computational fluid dynamics (CFD) model to simulate cough-induced particle dispersion in a closed space. Furthermore, the number of released particles and the presence of SARS-CoV-2 viral genomes by a cough were assessed (in eight COVID-19 patients). According to the CFD model, in the first 30 s of cough, the vertical height and lateral breadth of the particles' dispersion were up to 138cm and 92cm, respectively. As the distance from the patient's respiratory zone increased, the lateral distribution width of particles expanded, reaching 1.3 m at 2.4 m away. Larger droplets (> 62.5µ) were deposited at shorter distances, while smaller particles remained airborne longer. The comparison of experimental and simulated results focused on particle dispersion at specific distances from the patient, particularly in the 2.5µ range. The distribution pattern of PM2.5 and PM10 at a distance of 1 and 2 m for women, not men, is similar to the distribution pattern of PM in CFD modeling. Viral genome detection was more prevalent in particles near the left side of the body, especially within the first 20 min post-cough, exhibiting a correlation with CFD predictions.

Airborne transmission↗

PubMed2026

Next-Generation Sequencing Methods for Sensitive Hepatitis B Viral Genome Analysis: A European Study.

This multicentre study investigated the utility of next-generation sequencing (NGS) to detect and generate hepatitis B virus (HBV) genomes in samples of low viral load (from 0.2 to 6207 IU/mL). 23 HBV DNA-positive plasma samples of genotypes A-E and one HBV-negative control sample were assayed blindly via 9 established NGS methods from 6 European laboratories. Methods included untargeted metagenomics, pre-enrichment by probe-capture followed by Illumina sequencing, and HBV-specific PCR pre-amplification followed by sequencing with Nanopore or Illumina. Full HBV genomes were obtained only from samples with viral loads > 1000 IU/mL using probe-capture methods, > 200 IU/mL using PCR-Illumina methods, > 10 IU/mL using PCR-Nanopore methods, and in no samples using metagenomic methods. Contamination was observed in the negative control and samples with very low viral loads in PCR-based methods. Probe-capture and metagenomic methods detected additional viruses not routinely screened in blood donations, including polyomaviruses and herpesviruses; positive results were confirmed by PCR. In conclusion, NGS may delineate whole-genome sequences at low viral loads if supported by a PCR pre-amplification step. Probe-capture methods also reliably detect HBV without pre-amplification but show limited genome coverage for samples with low viral loads; they may additionally detect a wide range of blood-borne viruses.

Humans↗

PubMed2025

Viral genome sequence datasets display pervasive evidence of strand-specific substitution biases that are best described using non-reversible nucleotide substitution models.

Most phylogenetic trees are inferred using time-reversible evolutionary models that assume that the relative rates of substitution for any given pair of nucleotides are the same regardless of the direction of the substitutions. However, there is no reason to assume that the underlying biochemical mutational processes that cause substitutions are similarly symmetrical. We consider two non-reversible nucleotide substitution models: (1) a 6-rate non-reversible model (NREV6) that is applicable to analyzing mutational processes in double-stranded genomes in that complementary substitutions occur at identical rates; and (2) a 12-rate non-reversible model (NREV12) that is applicable to analyzing mutational processes in single-stranded (ss) genomes in that all substitution types are free to occur at different rates. Using likelihood ratio and Akaike Information Criterion-based model tests, we show that, surprisingly, NREV12 provided a significantly better fit than the General Time Reversible (GTR) and NREV6 models to 21/31 dsRNA and 20/30 dsDNA datasets. As expected, however, NREV12 provided a significantly better fit to 24/33 ssDNA and 40/47 ssRNA datasets. We tested how non-reversibility impacts the accuracy with which phylogenetic trees are inferred. As simulated degrees of non-reversibility (DNR) increased, the tree topology inferences using both NREV12 and GTR became more accurate, whereas inferred tree branch lengths became less accurate. We conclude that while non-reversible models should be helpful in the analysis of mutational processes in most virus species, there is no pressing need to use these models for routine phylogenetic inference.

Models of evolution↗

PubMed2026

Acrocomia aculeata (Mbokaja) Kernel Oil Inhibits Herpes Simplex Virus 1 Replication and Promotes Cutaneous Wound Healing in Infected Mice.

Background/Objectives: Herpes simplex virus type 1 (HSV-1) is a global and prevalent pathogen, presenting significant clinical challenges because of its recurring infections, the development of drug resistance and severe clinical complications. This study evaluated the antiviral efficacy against HSV-1 of Acrocomia aculeata (A. aculeata) kernel oil, a Neotropical palm native to the Americas. Methods: The chemical profile of A. aculeata kernel oil was determined by gas chromatography with flame ionization detection (GC-FID). Antiviral activity was assessed using dose-response curves, time-of-addition assays, and quantification of intracellular viral genomes, viral gene transcripts, and IL-6 expression. A. aculeata kernel oil's antiviral effect was also evaluated using an in vivo HSV-1 cutaneous infection model. Results: GC-FID analysis revealed lauric, oleic, and myristic acids as predominant components in the kernel oil. A. aculeata kernel oil exhibited potent antiviral activity against HSV-1. The oil inhibited HSV-1 early step post-entry, reducing the mRNA levels of the immediate-early genes ICP4 and ICP22, leading to the downregulation of early and late viral gene expression and intracellular viral genome. Furthermore, the oil suppressed IL-6 expression in infected cells. Importantly, A. aculeata kernel oil promoted the healing of cutaneous lesions in HSV-1-infected mice. Conclusions: These findings demonstrate that A. aculeata kernel oil is a promising candidate for developing novel antiviral and topical therapies against HSV-1.

Animals↗

PubMed2025

Amplification of Filovirus Genomes from Clinical Samples for Next Generation Sequencing.

Viral genome sequencing has become a critical tool in outbreak mitigation. Due to their small size relative to the host genome, viral genomes comprise a small fraction of next generation sequencing reads in clinical samples when using unbiased sequencing approaches. Long-range polymerase chain reaction facilitates the amplification of viral genomes from clinical and environmental samples with minimal primer sites, allowing researchers to target regions of the genome that are conserved across available variants. Here, we describe the amplification and sequencing of the Ebola virus genome from tissue samples collected from infected nonhuman primates. This protocol facilitates full viral genome recovery from as low as 103 median tissue culture infectious doses per milliliter.

High-Throughput Nucleotide Sequencing↗

PubMed2026

Nuclear body assembly by a viral repeat RNA promotes Kaposi's sarcoma-associated herpesvirus gene expression.

Kaposin is the most abundantly expressed viral RNA in tumors caused by the oncogenic virus Kaposi's sarcoma-associated herpesvirus (KSHV); however, its role in viral replication is not understood. Here, we show that kaposin, previously viewed as a protein-coding transcript, exists primarily as a nuclear viral long non-coding RNA (lncRNA) that rebuilds cellular nuclear speckles (NSs) adjacent to the viral genome to enhance viral gene expression. Kaposin is both necessary and sufficient to drive substantial NS remodeling, and this effect depends on repetitive elements within the RNA. Absence of kaposin-mediated NS remodeling, depletion of the essential NS protein, serine/arginine repetitive matrix 2 (SRRM2), or steric blocking of the kaposin repetitive elements impair viral gene expression. This work defines kaposin as a viral architectural RNA that drives nuclear speckle seeding beside the viral genome and reframes our understanding of lncRNA function and the spatial organization of transcription in the infected cell nucleus.

Kaposi's sarcoma-associated herpesvirus↗