Viral-associated cancers and disorders

Neutralizing vaccination against viral interleukin-6 from a primate rhadinovirus

This study explores using viral IL-6 as a vaccine antigen against primate rhadinoviruses, showing that a vIL-6-Fc fusion protein elicits high-titer neutralizing antibodies.

Kinetochore Proteins CENPB and LIC2 are critical for Episome Persistence and Replication of Kaposis's Sarcoma-Associated Herpesvirus

This study identifies CENPB and LIC2 as critical kinetochore proteins required for KSHV episome persistence and replication through a shRNA-based screen of kinetochore-associated genes.

Divide and conquer: a viral bifunctional RNA utilizes both RNA and protein to modulate pro-tumourigenic pathways

This study uncouples the effects of kaposin RNA and KapB protein from Kaposi's sarcoma-associated herpesvirus, showing they have distinct and opposing effects on cellular growth and inflammatory pathways.

Kaposi sarcoma herpesvirus vFLIP induces lipid droplet formation in Tert-immortalized microvascular endothelial cells via NF-κB activation

This study shows that KSHV vFLIP induces lipid droplet formation in TIME cells via NF-κB activation and ACSL activity.

Epstein-Barr Virus in HIV-Associated Conjunctival Squamous Cell Carcinoma and Transcriptional Reprogramming of Conjunctival Epithelial Cells

This study identifies Epstein-Barr virus (EBV) in a subset of HIV-associated conjunctival squamous cell carcinomas and establishes an epithelial model to study host responses to EBV infection.

Tissue-resident memory T cells are diminished in the Kaposi sarcoma tumor microenvironment of people living with HIV

This study identifies reduced tissue-resident memory T cells and increased PD-1 expression in the KS tumor microenvironment of HIV-positive individuals, suggesting impaired antitumor immunity and potential for immune checkpoint therapy.

A Human Genome-wide CRISPR-Cas9 Screen Reveals Host Factors That Support Epstein-Barr Virus B cell infection

This study uses a genome-wide CRISPR-Cas9 screen to identify host factors essential for EBV B cell infection, revealing new pathways and potential therapeutic targets.

HIGH DOSE GAMMAHERPESVIRUS INFECTION IN MACROPHAGES RESULTS IN INFLAMMATORY MULTIMODAL CELL DEATH

This study shows high-dose MHV68 infection of macrophages causes inflammatory cell death independent of lytic replication, involving autophagy and pyroptosis.

Cytokine signaling regulates multiple stages of gammaherpesvirus infection in myeloid cells

This study shows that IFNγ and IL-4 regulate lytic infection in myeloid cells via JAK/STAT signaling, with IFNγ restricting lytic replication through multiple mechanisms.

Kaposi's sarcoma-associated herpesvirus forms and maintains R-loops at origins of lytic replication

This study investigates how KSHV maintains R-loops at replication origins by inhibiting RNaseH1, a key R-loop resolver, through RTA-mediated degradation.

KLHL9 acts as a KSHV vBcl-2-interacting host factor that supports lytic replication

This study identifies KLHL9 as a host factor that interacts with KSHV vBcl-2 and supports lytic replication by facilitating its mitochondrial localization and function.

Targeting soluble immunoglobulins ameliorates idiopathic multicentric Castleman disease in a mouse model

This paper develops a mouse model of idiopathic multicentric Castleman disease (iMCD) by targeting IL-6 to Foxp3+ Treg cells, showing that reducing soluble immunoglobulin production alleviates disease symptoms and improves survival.

Transcriptome Profiling Identifies a Natural Antisense Transcript of IRF4 Associated with EBV Latency

The paper identifies IRF4-AS1, a natural antisense transcript of IRF4, as upregulated in EBV Type III latency and functionally linked to IRF4 expression.

Epstein Barr virus exploits ER stress and TMX4 dependent nuclear envelope remodeling to enable capsid egress

This study shows EBV uses ER stress and TMX4 to remodel the nuclear envelope, enabling capsid egress during viral maturation.

A novel wild-derived MHC-linked locus regulates host immunity to gammaherpesvirus infection

This study identifies a novel MHC-linked locus in mice that enhances resistance to gammaherpesvirus infection without relying on NK cells or large cytotoxic T cell expansion.

Kaposi Sarcoma herpesvirus reactivation and replication are dispensable for cell-lineage specific tumorigenesis in whole genome transgenic mice

This study shows that KSHV tumorigenesis can occur without viral reactivation or replication in a whole-genome transgenic mouse model.

Cytotoxic T cells targeting lytic KSHV gene products infiltrate Kaposi sarcoma tumors

The paper identifies KSHV-specific T-cell receptors in KS tumors, showing they recognize lytic KSHV gene products and could inform immunotherapies.

OGG1-Binding to Oxidized Guanine Base in Viral DNA Overcomes Epstein-Barr Virus Latency

This study shows that OGG1 binding to oxidized guanine in EBV DNA promotes reactivation by activating lytic genes, suggesting OGG1 as a therapeutic target.

Nucleolar Targeting and ROS-dependent inhibition of rRNA synthesis by Epstein-Barr Virus Nuclear Antigen 1

This paper identifies a bipartite nucleolar localization signal in EBNA-1 and shows it induces ROS-dependent rRNA suppression and cell survival.

Differential serum binding patterns predicting healthy subjects and cancer patients

The paper identifies differential serum binding patterns that classify healthy individuals from cancer patients using serological data from the VirScan platform.

KSHV miR-K12-9 Induces Transformation of Immortalized and Primary Endothelial Cells

This paper shows that KSHV miR-K12-9 induces transformation in endothelial cells, leading to uncontrolled growth and tumor formation in mice.

LINE-1 transposable element is expressed in Kaposi's sarcoma and regulates gene expression in KSHV-infected cells

This study shows that LINE-1 retrotransposons are upregulated in KSHV-infected cells and their knockdown impairs proliferation and alters gene expression.

Global Lipidomic Analysis of Lytic KSHV Infection: The Lipid Chaperone FABP4 is Required for Maximal Infectious Virion Production

EBV Triggers a Distinct Antiviral Response in HMC3 Cells

This study shows that UV-inactivated EBV suppresses microglial anti-tumor interferon production and upregulates proto-oncogenic genes, suggesting EBV may contribute to CNS malignancies by impairing microglial immunity.

Non-canonical histone H3.3 and its chaperones HIRA and DAXX participate in the regulation of KSHV latency

This study shows that H3.3 and its chaperones HIRA and DAXX regulate KSHV latency by promoting chromatinization and stability of the viral episome.

Integrating Epstein-Barr virus (EBV) status into diffuse large B cell lymphoma (DLBCL) genetics

This study integrates EBV status into DLBCL genetics by analyzing sequencing data and cell lines, finding EBV-positive DLBCL is heterogeneous and current cell lines poorly model tumor complexity.

CRISPR Screens Reveal Epstein-Barr Virus-activated JunB as a Key Lymphoblastoid B cell Dependency Factor that Represses Cyclin Dependent Kinase Inhibitor P18INK4c

This study identifies JunB as a key dependency factor in EBV-infected B cells that represses p18INK4c, revealing a potential therapeutic target for EBV-associated cancers.

A CRISPR-Cas9 screen Reveals STEEP1 as a Key Host Dependency Factor for Epstein-Barr Virus Latent Membrane Protein 1 Trafficking and Signaling

This paper identifies STEEP1 as a host factor critical for LMP1 trafficking and signaling using a CRISPR-Cas9 screen, showing its role in NF-kB and MAP kinase pathway activation.

Selective effects of cyclin dependent kinase inhibitors in gammaherpesvirus reactivation from latency

This study evaluates the effects of CDK inhibitors on gammaherpesvirus reactivation, finding that broad-spectrum inhibitors reduce reactivation while targeted CDK4/6 inhibitors have nuanced effects depending on timing.

Differential glucose uptake by endothelial cells in response to in-vitro Herpes Virus 8 infection, when challenged with serums from diabetes mellitus type 2 patients

This study shows HHV8-infected endothelial cells take up more glucose than uninfected cells, and DM2 serums further increase glucose uptake in infected cells but reduce it in uninfected ones.