ArticleThe American journal of pathology2000
Induction of HHV-8 lytic cycle replication by inflammatory cytokines produced by HIV-1-infected T cells.
Article in The American journal of pathology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
63 citing papers in PubMed, 1 synthesis or guideline pooled it, 140 citations in OpenAlex.
- HIV and human herpesvirus 8 co-infection across the globe: Systematic review and meta-analysis.International journal of cancer · 2016Pooled it
- Repression of EEF1D by KSHV RTA promotes viral lytic reactivation.Journal of virology · 2026Article
- The association between the oral microbiome and oral Kaposi's sarcoma-associated herpesvirus (KSHV) shedding is modified by age and HIV status in a rural Ugandan cohort.Journal of oral microbiology · 2026Article
- Human Herpes Virus-8 Oral Shedding Heterogeneity Is Due to Varying Rates of Reactivation from Latency and Immune Containment.Viruses · 2025Article
- Association between KSHV-Specific Humoral and T Cell Responses with Recurrence of HIV-Associated Kaposi Sarcoma.Tropical medicine and infectious disease · 2024Article
- The Impact of Co-Infections for Human Gammaherpesvirus Infection and Associated Pathologies.International journal of molecular sciences · 2023Review
- The Prevalence of EBV and KSHV in Odontogenic Lesions.International dental journal · 2023Article
- Host-Level Susceptibility and IRF1 Expression Influence the Ability of IFN-γ to Inhibit KSHV Infection in B Lymphocytes.Viruses · 2022Article
- Epidemiology of Kaposi's Sarcoma.Cancers · 2021Review
- Disseminated AIDS-Related Kaposi Sarcoma Immune Reconstitution Inflammatory Syndrome With Infiltrative Liver Disease.ACG case reports journal · 2021Article
- Review
- Herpesviral Latency-Common Themes.Pathogens (Basel, Switzerland) · 2020Review
- Association of NFκB and related-cytokines with the viral load and development of antibodies against HHV-8 in people living with HIV/AIDS.Medical microbiology and immunology · 2020Article
- Kaposi's sarcoma-associated herpesvirus vIRF2 protein utilizes an IFN-dependent pathway to regulate viral early gene expression.PLoS pathogens · 2019Article
- Malignant hepatic vascular tumors in adults: Characteristics, diagnostic difficulties and current management.World journal of clinical oncology · 2019Review
- Cell Type-Specific Interferon-γ-mediated Antagonism of KSHV Lytic Replication.Scientific reports · 2019Article
- Contribution of the KSHV and EBV lytic cycles to tumourigenesis.Current opinion in virology · 2018Review
- Article
- The Kaposi's sarcoma-associated herpesvirus (KSHV) non-structural membrane protein K15 is required for viral lytic replication and may represent a therapeutic target.PLoS pathogens · 2017Article
- Hepatic Kaposi sarcoma: A case report and review of the literature.World journal of hepatology · 2017Review
3 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Human herpesvirus 8 (HHV-8) is a gamma2-herpesvirus consistently identified in Kaposi's sarcoma (KS), primary effusion lymphoma, and multicentric Castleman's disease. Although HHV-8 infection appears to be necessary, it may not be sufficient for development of KS without the involvement of other cofactors. One potentially important cofactor is HIV-1. HIV-1-infected cells produce HIV-1-related proteins and cytokines, both of which have been shown to promote growth of KS cells in vitro. Though HIV-1 is not absolutely necessary for KS development, KS is the most frequent neoplasm in AIDS patients, and AIDS-KS is recognized as a particularly aggressive form of the disease. To determine whether HIV-1 could participate in the pathogenesis of KS by modulating HHV-8 replication (rather than by inducing immunodeficiency), HIV-1-infected T cells were cocultured with the HHV-8-infected cell line, BCBL-1. The results demonstrate soluble factors produced by or in response to HIV-1-infected T cells induced HHV-8 replication, as determined by production of lytic phase mRNA transcripts, viral proteins, and detection of progeny virions. By focusing on cytokines produced in the coculture system, several cytokines known to be important in growth and proliferation of KS cells in vitro, particularly Oncostatin M, hepatocyte growth factor/scatter factor, and interferon-gamma, were found to induce HHV-8 lytic replication when added individually to BCBL-1 cells. These results suggest specific cytokines can play an important role in the initiation and progression of KS through reactivation of HHV-8. Thus, HIV-1 may participate more directly than previously recognized in KS by promoting HHV-8 replication and, hence, increasing local HHV-8 viral load.
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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.