ReviewCancer treatment and research2007
Molecular biology of KSHV in relation to AIDS-associated oncogenesis.
Review in Cancer treatment and research, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
72 citing papers in PubMed, 130 citations in OpenAlex.
- Signatures of oral microbiome in HIV-infected individuals with oral Kaposi's sarcoma and cell-associated KSHV DNA.PLoS pathogens · 2020Trial
- The inflammatory kinase MAP4K4 promotes reactivation of Kaposi's sarcoma herpesvirus and enhances the invasiveness of infected endothelial cells.PLoS pathogens · 2013Trial
- Immunological Determinants of Oncogenic Virus-Driven Cancers in Africa: Mechanisms, Co-Infections and Public Health Challenges.Pathogens (Basel, Switzerland) · 2026Review
- Molecular detection of HPV, EBV, and polyomaviruses in thyroid tumors and their clinicopathological relevance.Journal of cancer research and clinical oncology · 2025Article
- Implications of EBV-Encoded and EBV-Related miRNAs in Tumors.Current gene therapy · 2025Review
- Thymus capitatus flavonoids inhibit infection of Kaposi's sarcoma-associated herpesvirus.FEBS open bio · 2022Article
- MicroRNA let-7 and viral infections: focus on mechanisms of action.Cellular & molecular biology letters · 2022Review
- The KSHV ORF20 Protein Interacts with the Viral Processivity Factor ORF59 and Promotes Viral Reactivation.Microbiology spectrum · 2021Article
- Inter-regulatory role of microRNAs in interaction between viruses and stem cells.World journal of stem cells · 2021Review
- Review
- Article
- NCOA2 promotes lytic reactivation of Kaposi's sarcoma-associated herpesvirus by enhancing the expression of the master switch protein RTA.PLoS pathogens · 2019Article
- Arachidonic Acid Derived Lipid Mediators Influence Kaposi's Sarcoma-Associated Herpesvirus Infection and Pathogenesis.Frontiers in microbiology · 2019Review
- Upregulation of MicroRNA 711 Mediates HIV-1 Vpr Promotion of Kaposi's Sarcoma-Associated Herpesvirus Latency and Induction of Pro-proliferation and Pro-survival Cytokines by Targeting the Notch/NF-κB-Signaling Axis.Journal of virology · 2018Article
- SYK inhibition blocks proliferation and migration of glioma cells and modifies the tumor microenvironment.Neuro-oncology · 2018Article
- Role of Pattern Recognition Receptors in KSHV Infection.Cancers · 2018Review
- TLR4-Mediated Inflammation Promotes KSHV-Induced Cellular Transformation and Tumorigenesis by Activating the STAT3 Pathway.Cancer research · 2017Article
- Quantitative Analysis of the KSHV Transcriptome Following Primary Infection of Blood and Lymphatic Endothelial Cells.Pathogens (Basel, Switzerland) · 2017Article
- RNA NInflammation and cell signaling · 2017Article
- SIRT1-mediated downregulation of p27Kip1 is essential for overcoming contact inhibition of Kaposi's sarcoma-associated herpesvirus transformed cells.Oncotarget · 2016Article
12 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
7 authors at 1 institution in 1 country.
Funding
Abstract
KSHV has been established as the causative agent of KS, PEL, and MCD, malignancies occurring more frequently in AIDS patients. The aggressive nature of KSHV in the context of HIV infection suggests that interactions between the two viruses enhance pathogenesis. KSHV latent infection and lytic reactivation are characterized by distinct gene expression profiles, and both latency and lytic reactivation seem to be required for malignant progression. As a sophisticated oncogenic virus, KSHV has evolved to possess a formidable repertoire of potent mechanisms that enable it to target and manipulate host cell pathways, leading to increased cell proliferation, increased cell survival, dysregulated angiogenesis, evasion of immunity, and malignant progression in the immunocompromised host. Worldwide, approximately 40.3 million people are currently living with HIV infection. Of these, a significant number are coinfected with KSHV. The complex interplay between the two viruses dramatically elevates the risk for development of KSHV-induced malignancies, KS, PEL, and MCD. Although HAART significantly reduces HIV viral load, the entire T-cell repertoire and immune function may not be completely restored. In fact, clinically significant immune deficiency is not necessary for the induction of KSHV-related malignancy. Because of variables such as lack of access to therapy noncompliance with prescribed treatment, failure to respond to treatment and the development of drug-resistant strains of HIV, KSHV-induced malignancies will continue to present as major health concerns.
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What OpenQuestion holds
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.