ArticleVirology2020
STING is dispensable during KSHV infection of primary endothelial cells.
Article in Virology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 11 citations in OpenAlex.
- CD46 Is a Protein Receptor for Human Adenovirus Type 64.Viruses · 2024Article
- Alpha-defensin binding expands human adenovirus tropism.PLoS pathogens · 2024Article
- KSHV infection of endothelial precursor cells with lymphatic characteristics as a novel model for translational Kaposi's sarcoma studies.PLoS pathogens · 2023Article
- The battle between the innate immune cGAS-STING signaling pathway and human herpesvirus infection.Frontiers in immunology · 2023Review
- Nucleic Acid Sensing in the Tumor Vasculature.Cancers · 2021Review
- Immune Regulation of the cGAS-STING Signaling Pathway in the Tumor Microenvironment and Its Clinical Application.OncoTargets and therapy · 2021Review
- Evasion of Intracellular DNA Sensing by Human Herpesviruses.Frontiers in cellular and infection microbiology · 2021Review
- Defensin-driven viral evolution.PLoS pathogens · 2020Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
During DNA virus infections, detection of cytosolic DNA by the cGAS-STING pathway leads to activation of IFN-β. Kaposi's Sarcoma Herpesvirus (KSHV), an oncogenic DNA virus, is the etiological agent of Kaposi's Sarcoma, an endothelial cell (EC)-based tumor. To investigate the role of STING during KSHV infection of primary ECs we identified a primary lymphatic EC sample that is defective for STING activation and we also knocked out STING in blood ECs. Ablation of STING in EC does not increase susceptibility to KSHV latent infection nor does it increase KSHV spread after lytic reactivation indicating STING signaling does not restrict KSHV. In contrast, STING ablation increases Adenovirus spread at low MOI, but STING is dispensable for blocking replication. These experiments reveal that the importance of STING depends on the DNA virus and that STING appears more important for restricting spread to bystander cells than for inhibition of viral replication.
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Registered trials
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