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Results for “host-virus associations”

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PubMed2026

Tracing the evolution and diversity of human parvovirus B19 across human history.

Human parvovirus B19 (B19V) is an ubiquitously spread, exclusively human pathogen, mainly posing risks to children, as well as pregnant and immunocompromised individuals. Despite evidence of B19V infection of human populations as far back as 7,000 years, the evolutionary history of B19V remains poorly understood. In this study, we present B19V genomic data from the remains of 53 globally distributed individuals spanning more than 8,000 years, including 7 children. Our findings suggest that the most recent common ancestor of all present B19V lineages existed around 12,000 years ago, at the end of the last Ice Age. Additionally, we identified an extinct Eurasian clade that participated in the recombination event that led to the emergence of B19V genotype 2 (GT-2). We date this event to ∼3,200-1,800 BP, potentially in the greater Mediterranean area. Our study shows aspects of how ancient parvovirus variants arose, disseminated, and impacted human health through time.

ancient DNA↗

PubMed2024

Infection kinetics, syncytia formation, and inflammatory biomarkers as predictive indicators for the pathogenicity of SARS-CoV-2 Variants of Concern in Calu-3 cells.

The ongoing COVID-19 pandemic has led to the emergence of new SARS-CoV-2 variants as a result of continued host-virus interaction and viral genome mutations. These variants have been associated with varying levels of transmissibility and disease severity. We investigated the phenotypic profiles of six SARS-CoV-2 variants (WT, D614G, Alpha, Beta, Delta, and Omicron) in Calu-3 cells, a human lung epithelial cell line. In our model demonstrated that all variants, except for Omicron, had higher efficiency in virus entry compared to the wild-type. The Delta variant had the greatest phenotypic advantage in terms of early infection kinetics and marked syncytia formation, which could facilitate cell-to-cell spreading, while the Omicron variant displayed slower replication and fewer syncytia formation. We also identified the Delta variant as the strongest inducer of inflammatory biomarkers, including pro-inflammatory cytokines/chemokines (IP-10/CXCL10, TNF-α, and IL-6), anti-inflammatory cytokine (IL-1RA), and growth factors (FGF-2 and VEGF-A), while these inflammatory mediators were not significantly elevated with Omicron infection. These findings are consistent with the observations that there was a generally more pronounced inflammatory response and angiogenesis activity within the lungs of COVID-19 patients as well as more severe symptoms and higher mortality rate during the Delta wave, as compared to less severe symptoms and lower mortality observed during the current Omicron wave in Thailand. Our findings suggest that early infectivity kinetics, enhanced syncytia formation, and specific inflammatory mediator production may serve as predictive indicators for the virulence potential of future SARS-CoV-2 variants.

Humans↗

PubMed2025

Aberrant DNA methylation of genes regulating CD4+ T cell HIV-1 reservoir in women with HIV.

BACKGROUND: The HIV-1 reservoir in CD4+ T cells (HRCD4) pose a major challenge to curing HIV, with many of its mechanisms still unclear. HIV-1 DNA integration and immune responses may alter the host's epigenetic landscape, potentially silencing HIV-1 replication. METHODS: This study used bisulphite capture DNA methylation sequencing in CD4+ T cells from the blood of 427 virally suppressed women with HIV to identify differentially methylated sites and regions associated with HRCD4. RESULTS: The average total HRCD4 size was 1409 copies per million cells, with most proviruses defective and only a small proportion intact. The study identified 245 differentially methylated CpG sites and 85 regions linked to HRCD4 size, with 52% of significant sites in intronic regions. Genes associated with HRCD4 were involved in viral replication, HIV-1 latency and cell growth and apoptosis. HRCD4 size was inversely related to DNA methylation of interferon signalling genes and positively associated with methylation at known HIV-1 integration sites. HRCD4-associated genes were enriched on the pathways related to immune defence, transcription repression and host-virus interactions. CONCLUSIONS: These findings suggest that HIV-1 reservoir is linked to aberrant DNA methylation in CD4+ T cells, offering new insights into epigenetic mechanisms of HIV-1 latency and potential molecular targets for eradication strategies. KEY POINTS: Study involved 427 women with HIV. Identified 245 aberrant DNA methylation sites and 85 methylation regions in CD4+ T cells linked to the HIV-1 reservoir. Highlighted genes are involved in viral replication, immune defence, and host genome integration. Findings suggest potential molecular targets for eradication strategies.

Humans↗

PubMed2026

Differentiation-independent activation of HPV genome replication by the lncRNA DINO.

Human papillomaviruses (HPVs) rely on multiple host cell factors to replicate the viral genome, yet the contribution of host long non-coding RNAs (lncRNAs) to viral genome maintenance and amplification in the productive life cycle remains poorly understood. In this study, we show that the lncRNA damage-induced long non-coding RNA (DINO) is a driver of HPV DNA replication. DINO levels increase during keratinocyte differentiation, and ectopic expression of DINO promotes both HPV genome replication and the formation of replication foci, and this is independent of keratinocyte differentiation signals. Ectopic DINO expression increases select early viral transcript levels, including E1^E4, E1, and E2. Notably, DINO's subcellular localization is also context-dependent: during DNA damage, DINO is predominantly cytoplasmic, but during keratinocyte differentiation, nuclear retention is observed. This differential localization suggests that DINO has distinct functional roles in keratinocyte differentiation and HPV biology. Our findings highlight DINO as a lncRNA that promotes HPV genome replication and suggest that lncRNAs may play underappreciated roles in host-virus interactions. This work provides a foundation for further exploration of lncRNAs as potential therapeutic targets in HPV-associated diseases.IMPORTANCEHuman papillomaviruses (HPVs) are the causative agents of many anogenital tract and oral cancers, yet the host factors that trigger and support viral genome replication during the productive life cycle are incompletely understood. This study identifies the long non-coding RNA DINO as a host regulator that promotes HPV DNA replication, replication focus formation, and early viral gene expression independently of keratinocyte differentiation. We further show that DINO exhibits context-dependent subcellular localization, suggesting distinct functional roles in cellular stress responses and HPV biology. These findings reveal an underappreciated role for host lncRNAs in virus-host interactions and provide new insight into cellular pathways that support HPV genome replication.

Virus Replication↗

PubMed2026

Differentiation-independent Activation of HPV Genome Replication by the lncRNA DINO.

Human papillomaviruses (HPV) rely on multiple host cell factors to replicate the viral genome, yet the contribution of host long noncoding RNAs (lncRNAs) to viral genome maintenance and amplification in the productive life cycle remains poorly understood. In this study, we show that the lncRNA DINO is a driver of HPV DNA replication. DINO levels increase during keratinocyte differentiation and ectopic expression of DINO promotes both HPV genome replication and the formation of replication foci, and this is independent of keratinocyte differentiation signals. Ectopic DINO expression increases select early viral transcript levels including E1^4, E1, and E2. Notably, DINO's subcellular localization is also context-dependent: during DNA damage DINO is predominantly cytoplasmic, but during keratinocyte differentiation nuclear retention is observed. This differential localization suggests that DINO has distinct functional roles in keratinocyte differentiation and HPV biology. Our findings highlight DINO as a lncRNA that promotes HPV genome replication and suggest that lncRNAs may play underappreciated roles in host-virus interactions. This work provides a foundation for further exploration of lncRNAs as potential therapeutic targets in HPV-associated diseases.

Journal Article↗

PubMed2026

Spontaneous lytic reactivation drives a persistent B cell-vector pathway for epithelial dissemination of the Epstein-Barr virus.

The Epstein-Barr virus (EBV) establishes lifelong B cell infection via oral transmission; however, it paradoxically drives carcinomas in anatomically distant organs with striking geographic disparities. While genomic studies frequently link specific EBV variants to these epithelial cancers, the mechanisms bridging ubiquitous infection to distant, strain-dependent malignancies remain largely unresolved. Using an induction-free primary B cell system, we identify a circulating B cell-vector pathway driving immortalized epithelial dissemination. We demonstrate that B cells infected with carcinoma-associated strains exhibit markedly higher epithelial transmission compared with those carrying lymphoid strains. This contact-dependent process requires spontaneous lytic reactivation, viral DNA replication, and de novo virion production. Crucially, those infected B cells retain their transmission capacity for months, supporting sustained epithelial seeding. Mechanistically, entry requires gH/gL engagement of EphA2/desmocollin-2 (DSC2), with actin- and PI3K-dependent endocytosis. These findings define a lytic-coupled, receptor-dependent pathway by which the EBV exploits B cells to access the epithelium, offering a mechanistic framework for understanding strain tropism and host-virus interactions.

B cell vector↗

PubMed2026

Conserved host-exclusive oligonucleotide motifs enriched in pathogenic genes of human oncogenic viruses.

Comparative viral genomics can reveal sequence-level constraints influencing virus-host interactions. Relative minimal absent words (rMAWs) are short oligonucleotide motifs present in viral genomes but completely absent from the host, potentially reflecting selective pressures related to host adaptation and immune evasion. Using the EAGLE algorithm and the GRCh38 human reference genome, we systematically screened for prevalent rMAWs (prMAWs) across six major human oncogenic viruses: Epstein-Barr virus (EBV), hepatitis B virus (HBV), hepatitis C virus (HCV), human papillomavirus (HPV), human T-cell leukemia virus type 1 (HTLV-1), and human herpesvirus 8/Kaposi's sarcoma-associated herpesvirus (HHV-8/KSHV). highly conserved 11- and 12-bp prMAWs were identified in EBV, HBV, HTLV-1, and HHV-8/KSHV, with sequence prevalences ranging from 91.5% to 97.9%. Conversely, no short prMAWs were detected in HCV or HPV, likely reflecting differences in genome architecture, mutation rates, and long-term host adaptation to the human host. Importantly, the identified host-exclusive motifs exhibited non-random genomic distribution and were preferentially embedded within viral genes central to replication, persistence, immune modulation, and oncogenesis, including EBNA-1 (EBV), HBx (HBV), Tax-associated regions (HTLV-1), and lytic replication genes of HHV-8/KSHV. Notably, all detected prMAWs were enriched in GC nucleotides and exhibited marked CpG over-representation, suggesting sequence constraints associated with epigenetic regulation and viral persistence. Collectively, these highly conserved, host-exclusive signatures offer promising, candidates for sequence-directed approaches in the diagnosis, monitoring, and investigation of virus-associated cancers.

Humans↗

PubMed2026

Host-virus dynamics in anaerobic digesters facing abiotic inhibition.

Viruses play a major role in controlling the structure and dynamics of microbial communities in anaerobic digesters, ecosystems sensitive to disturbances that inhibit methane production. Here, we studied the interplay between abiotic disturbances, microbiome and virome composition, and process performance, to assess whether provirus induction can be triggered by abiotic stresses known to inhibit anaerobic digestion (ammonium, phenol and sodium chloride). We monitored viral dynamics in batch mesophilic anaerobic digesters fed with biowaste through shotgun metavirome sequencing. The diversity of both prokaryotes and viruses was high, with Clostridiales dominating the prokaryotic community and Caudoviricetes dominating the viromes. We identified 132 viral contigs and 19 host genera that were differentially abundant under disturbed conditions. No significant impact of the tested abiotic stresses on provirus induction was observed under the current experimental and analytical framework. The results were consistent with viruses exerting steady, background-level predation through a putative combination of kill-the-winner dynamics at the sub-genus level and piggyback-the-winner dynamics, rather than stress-triggered, synchronous lytic bursts. A few auxiliary metabolic genes were detected, potentially targeting carbon, sulfur and cofactor metabolism in anaerobic digestion. Temperate viruses were dominant, representing up to 71% of the viral genomes confirmed as complete across all conditions. Electron microscopy analysis revealed diverse virus-like particles, including head-tailed particles typical of Caudoviricetes, but also spherical, rod-shaped and spindle-shaped particles typical of archaeal viruses. Notably, we present a new virus family, Eurekaviridae, of spindle-shaped viruses associated with methanogenic archaea.

Anaerobiosis↗

PubMed2026

Selective Enrichment of Newly Synthesized Proteins Using Phos-Tag Click Tip Enables Nascent Proteome Analysis in Influenza A Virus Infection.

Profiling of newly synthesized proteins (NSPs) provides access to dynamic changes in protein production that accompany acute cellular responses. Bioorthogonal noncanonical amino acid tagging (BONCAT)-based approaches enable selective labeling of NSPs; however, their broader application remains constrained by labor-intensive enrichment workflows and limited sensitivity for direct peptide-level analysis. Here, we developed a workflow termed "Phos-tag Click Tip" by integrating a phosphorylated variant of bicyclononyne (pBCN) with Phos-tag affinity purification to selectively capture azidohomoalanine (AHA)-labeled peptides for newly synthesized proteome analysis (NSProteomics). This approach overcomes key limitations of conventional proteomics and BONCAT-based strategies by enabling efficient enrichment and sensitive detection of NSP-derived peptides. Using this workflow, we performed comprehensive NSP profiling of host cells during influenza A virus infection. We identified dynamic changes in distinct NSP profiles associated with viral replication, host restriction, and immune responses, many of which were not readily detected with conventional whole-cell- or phospho-proteomic analyses. Overall, the Phos-tag Click Tip workflow provides a complementary approach for stimulus-responsive NSP profiling, offering functionally relevant insights into host-virus interactions and cellular response mechanisms.

Proteome↗

PubMed1976

The role of circulating interferon in the modifications of immune responsiveness by mouse hepatitis virus (MHV-3).

MHV-3 modifies the humoral immune response to SRBC. During acute infections timing was critical: infecting mice before antigen administration led to immunodepression. Simultaneous injection with virus and SRBC resulted in immunostimulation. Persistent MHV-3 infections were associated with a chronic immunodepression. The presence of circulating interferon (IF) was well correlated with these modifications. IF peaking before antigen was associated with immunodepression whereas IF secretion after antigen was associated with immunostimulation. Low, permanent levels of IF were associated with chronic immunodepression. Since IF is, up to now, the only product of activated lymphocytes that has been shown to modulate immune responses, our results suggest that induction of IF by MHV-3 may be the main mechanism by which this virus modifies immune responsiveness. Moreover, we have shown that MHV-3 infection in susceptible mice diminishes the secretion of lymphocyte IF in response to Sendai virus. In these animals, the thymus cortex was profoundly depleted although the thymus medulla remained unchanged. The MHV-3 infection may, therefore, interfere with a subpopulation of IF-secreting lymphocytes. The possible physiologic role of such lymphocyte subpopulation in terms of host-virus relationships is discussed.

Animals↗