Evidence map›Paper›PMID 34256025›Full record

ReviewThe Brazilian journal of infectious diseases : an official publication of the Brazilian Society of Infectious Diseases

Pathogenesis of HTLV-1 infection and progression biomarkers: An overview.

Carlos Brites, Maria Fernanda Grassi, Juarez Antônio Simões Quaresma, Ricardo Ishak, Antonio Carlos Rosário Vallinoto

Open access · goldAbstract readReview
In one paragraph

Review in The Brazilian journal of infectious diseases : an official publication of the Brazilian Society of Infectious Diseases. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed, 1 pooled it
2.0field-weighted citation impact, top 13% 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

30 citing papers in PubMed, 1 synthesis or guideline pooled it, 41 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Observational
  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Observational
  11. Review
  12. Article
  13. Review
  14. Possible Trace of HTLV-1 Virus in Modulation of Cbl-b, ITCH, and PP2A Suppressor Genes.International journal of molecular and cellular medicine · 2025
    Article
  15. Frontiers in cellular and infection microbiology · 2025
    Article
  16. Review
  17. Article
  18. A promising advance in blocking HTLV-1 transmission: Addressing a global public health problem.Molecular therapy : the journal of the American Society of Gene Therapy · 2024
    Article
  19. Observational
  20. Article
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

5 authors at 3 institutions in 1 country.

Carlos BritesFederal University of Bahia (UFBA), Professor Edgard Santos University Hospital Complex, Laboratory of Infectious Diseases Research, Salvador, BA, Brazil.
Maria Fernanda GrassiOswaldo Cruz Foundation, Advanced Laboratory of Public Health, Salvador, BA, Brazil.
Juarez Antônio Simões QuaresmaFederal University of Pará (UFPA), Nucleus of Tropical Medicine, Belém, PA, Brazil.
Ricardo IshakFederal University of Pará (UFPA), Institute of Biological Sciences, Laboratory of Virology, Belém, PA, Brazil.
Antonio Carlos Rosário VallinotoFederal University of Pará (UFPA), Institute of Biological Sciences, Laboratory of Virology, Belém, PA, Brazil. Electronic address: vallinoto@ufpa.br.
Universidade Federal do Pará · BRFundação Oswaldo Cruz · BRUniversidade Federal da Bahia · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Infection by human T-cell lymphotropic virus type 1 (HTLV-1) occurs in lymphocytes, which travel throughout the body, thus affecting several target organs and causing varied clinical outcomes, particularly in populations that are underserved and do not have access to healthcare. However, the mechanism of pathogenesis is not yet fully understood. The TAX and HTLV-1 basic leucine zipper factor (HBZ) proteins maintain viral persistence and affect pathogenesis through cell proliferation and immune and inflammatory responses that accompany each clinical manifestation. TAX expression leads to inhibition of transcription error control, OX40 overexpression, and cell proliferation in adult T-cell leukemia (ATL). OX40 levels are elevated in the central nervous system (CNS), and the expression of TAX in the CNS causes neuronal damage and loss of immune reactivity among patients with HTLV-1-associated myelopathy (HAM). HBZ reduces viral replication and suppresses the immune response. Its cell compartmentalization has been associated with the pathogenesis of HAM (cytoplasmic localization) and ATL (nuclear localization). TAX and HBZ seem to act antagonistically in immune responses, affecting the pathogenesis of HTLV-1 infection. The progression from HTLV-1 infection to disease is a consequence of HTLV-1 replication in CD4

Indexed as

HTLV-I InfectionsHuman T-lymphotropic virus 1Basic-Leucine Zipper Transcription FactorsBiomarkersHumansRetroviridae ProteinsBasic-Leucine Zipper Transcription FactorsBiomarkersRetroviridae ProteinsBiomarkersHBZHTLV-1PathogenesisTAX

Identifiers

PMID34256025
PMCPMC9392164
OpenAlexW3178615274

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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 Socratic graph.