ArticleThe Journal of clinical investigation2011
Active lytic infection of human primary tonsillar B cells by KSHV and its noncytolytic control by activated CD4+ T cells.
Article in The Journal of clinical investigation, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed, 64 citations in OpenAlex.
- Associative study of human herpesvirus 8 and Kaposi's sarcoma: Mapping viral oncogenic properties and the clinical scenario in oncological patients.Immunologic research · 2025Review
- Macrophages drive KSHV B cell latency.Cell reports · 2023Article
- Kaposi's Sarcoma-Associated Herpesvirus Immediate Early Proteins Trigger FOXQ1 Expression in Oral Epithelial Cells, Engaging in a Novel Lytic Cycle-Sustaining Positive Feedback Loop.Journal of virology · 2023Article
- The ORF45 Protein of Kaposi's Sarcoma-Associated Herpesvirus and Its Critical Role in the Viral Life Cycle.Viruses · 2022Review
- Polyamine biosynthesis and eIF5A hypusination are modulated by the DNA tumor virus KSHV and promote KSHV viral infection.PLoS pathogens · 2022Article
- Kaposi's sarcoma-associated herpesvirus T cell responses in HIV seronegative individuals from rural Uganda.Nature communications · 2021Article
- RNA Granules in Antiviral Innate Immunity: A Kaposi's Sarcoma-Associated Herpesvirus Journey.Frontiers in microbiology · 2021Review
- Review
- Analysis of KSHV B lymphocyte lineage tropism in human tonsil reveals efficient infection of CD138+ plasma cells.PLoS pathogens · 2020Article
- Regulation of KSHV Latency and Lytic Reactivation.Viruses · 2020Review
- Distinct genetic architectures and environmental factors associate with host response to the γ2-herpesvirus infections.Nature communications · 2020Article
- Molecular Virology of KSHV in the Lymphocyte Compartment-Insights From Patient Samples andFrontiers in cellular and infection microbiology · 2020Review
- [IAssociation between Kaposi´s sarcoma and multiple myeloma: is it caused by HHV-8?]The Pan African medical journal · 2020Article
- Towards Understanding KSHV Fusion and Entry.Viruses · 2019Review
- How Kaposi's sarcoma-associated herpesvirus stably transforms peripheral B cells towards lymphomagenesis.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Glycoprotein K8.1A of Kaposi's Sarcoma-Associated Herpesvirus Is a Critical B Cell Tropism Determinant Independent of Its Heparan Sulfate Binding Activity.Journal of virology · 2019Article
- Cell Type-Specific Interferon-γ-mediated Antagonism of KSHV Lytic Replication.Scientific reports · 2019Article
- LL-37 disrupts the Kaposi's sarcoma-associated herpesvirus envelope and inhibits infection in oral epithelial cells.Antiviral research · 2018Article
- KSHV induces immunoglobulin rearrangements in mature B lymphocytes.PLoS pathogens · 2018Article
- Kaposi's Sarcoma-Associated Herpesvirus-Encoded Viral IL-6 (vIL-6) Enhances Immunoglobulin Class-Switch Recombination.Frontiers in microbiology · 2018Article
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Kaposi sarcoma-associated herpesvirus (KSHV) is a B-lymphotropic virus whose primary site of replication is the oropharynx. KSHV can infect both T and B cells from primary tonsillar explant cultures. However, T cells do not support lytic replication, while B cells spontaneously produce substantial amounts of infectious virus. Here, we provide evidence for a mechanism by which activated T cells may promote or stabilize latency of KSHV infection in B cells. When mixed cultures of B cells and activated T cells were exposed to KSHV, little spontaneous virus production was observed. Removing T cells from the mix or treating the mixed culture with immune suppressants enhanced virus production. Adding back activated T cells to purified infected B cells efficiently suppressed KSHV production, primarily due to CD4(+) T cells. This suppressive activity required T cell activation and direct cell-cell contact, but not prior exposure to KSHV antigen. Suppression was not MHC restricted and did not result in killing of the target cell. We therefore propose that oropharyngeal T cells activated by a variety of stimuli can recognize ligands on infected target B cells, leading to signaling events that prevent spontaneous lytic activation and promote latent infection in this compartment.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.