Evidence map›Paper›PMID 17151125›Full record

ArticleJournal of virology2007

Intracellular Tat of human immunodeficiency virus type 1 activates lytic cycle replication of Kaposi's sarcoma-associated herpesvirus: role of JAK/STAT signaling.

Yi Zeng, Xunhai Zhang, Zan Huang, Lin Cheng, Shuihong Yao, Di Qin, Xiuying Chen, Qiao Tang, Zhigang Lv, Ling Zhang and 1 more

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
72citing papers in PubMed, 1 pooled it
2.5field-weighted citation impact, top 11% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

72 citing papers in PubMed, 1 synthesis or guideline pooled it, 131 citations in OpenAlex.

  1. CD20-negative diffuse large B cell lymphoma: a comprehensive analysis of 695 cases.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Pooled it
  2. Article
  3. Article
  4. The STAT Signaling Pathway in HIV-1 Infection: Roles and Dysregulation.International journal of molecular sciences · 2025
    Review
  5. Review
  6. Article
  7. Review
  8. Review
  9. Review
  10. Article
  11. Kaposi Sarcoma, a Trifecta of Pathogenic Mechanisms.Diagnostics (Basel, Switzerland) · 2022
    Review
  12. Article
  13. Review
  14. Review
  15. Article
  16. Review
  17. Review
  18. Article
  19. Review
  20. Article

12 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors at 4 institutions in 3 countries.

Yi ZengDepartment of Microbiology and Immunology, Nanjing Medical University, Nanjing 210029, People's Republic of China.
Xunhai Zhang
Zan Huang
Lin Cheng
Shuihong Yao
Di Qin
Xiuying Chen
Qiao Tang
Zhigang Lv
Ling Zhang
Chun Lu
Nanjing Medical University · CNAnhui Science and Technology University · CNState Key Laboratory of Reproductive MedicineUniversity of Chicago · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Human immunodeficiency virus type 1 (HIV-1) infection significantly increases the risk of Kaposi's sarcoma (KS) occurrence in individuals infected with Kaposi's sarcoma-associated herpesvirus (KSHV). KSHV infection appears to be necessary but not sufficient for KS development without other cofactors. However, factors that facilitate KSHV to cause KS have not been well defined. Previously, we determined that human herpesvirus 6 was one of the cofactors that activated lytic cycle replication of KSHV. Here, we demonstrate that the Tat protein of HIV-1 is a potentially important factor in the pathogenesis of KS, as determined by production of lytic phase mRNA transcripts and viral proteins in BCBL-1 cells. Mechanistic studies showed ectopic expression of Tat induced the production of human interleukin-6 (huIL-6) and its receptor (huIL-6Ra) and activated STAT3 signaling. Neutralization of huIL-6 or huIL-6R or inhibition of STAT3 signaling enhanced the replication. In addition, IL-4/STAT6 signaling also partially contributed to Tat-induced KSHV replication. These findings suggest that Tat may participate in KS pathogenesis by inducing KSHV replication and increasing KSHV viral load. These data also suggest that JAK/STAT signaling may be of therapeutic value in AIDS-related KS patients.

Indexed as

AnimalsBase SequenceCallithrixCell LineDNA PrimersGene ExpressionGene Products, tatGenes, tatHerpesvirus 8, HumanHIV-1HIV InfectionsHumansInterleukin-4Interleukin-6Janus KinasesMiceDNA PrimersGene Products, tatIL4 protein, humanIL6 protein, humanInterleukin-4Interleukin-6Janus KinasesReceptors, Interleukin-6STAT6 protein, humanSTAT6 Transcription FactorSTAT Transcription Factorstat Gene Products, Human Immunodeficiency Virus

Identifiers

PMID17151125
PMCPMC1865948
OpenAlexW2100301498

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.