PMID- 34256025
OWN - NLM
STAT- MEDLINE
DCOM- 20210831
LR  - 20220824
IS  - 1678-4391 (Electronic)
IS  - 1413-8670 (Print)
IS  - 1413-8670 (Linking)
VI  - 25
IP  - 3
DP  - 2021 May-Jun
TI  - Pathogenesis of HTLV-1 infection and progression biomarkers: An overview.
PG  - 101594
LID - S1413-8670(21)00063-5 [pii]
LID - 10.1016/j.bjid.2021.101594 [doi]
LID - 101594
AB  - 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(+) T 
      and CD8(+) T lymphocytes and the imbalance between proinflammatory and 
      anti-inflammatory cytokines. The compartmentalization of HBZ suggests that this 
      protein may be an additional tool for assessing immune and inflammatory 
      responses, in addition to those already recognized as potential biomarkers 
      associated with progression from infection to disease (including human leukocyte 
      antigen (HLA), killer immunoglobulin-like receptors (KIR), interleukin (IL)-6, 
      IL-10, IL-28, Fas, Fas ligand, interferon (IFN)-gamma, tumor necrosis factor (TNF)-alpha, 
      and mannose-binding lectin).
CI  - Copyright (c) 2021 Sociedade Brasileira de Infectologia. Published by Elsevier 
      Espana, S.L.U. All rights reserved.
FAU - Brites, Carlos
AU  - Brites C
AD  - Federal University of Bahia (UFBA), Professor Edgard Santos University Hospital 
      Complex, Laboratory of Infectious Diseases Research, Salvador, BA, Brazil.
FAU - Grassi, Maria Fernanda
AU  - Grassi MF
AD  - Oswaldo Cruz Foundation, Advanced Laboratory of Public Health, Salvador, BA, 
      Brazil.
FAU - Quaresma, Juarez Antonio Simoes
AU  - Quaresma JAS
AD  - Federal University of Para (UFPA), Nucleus of Tropical Medicine, Belem, PA, 
      Brazil.
FAU - Ishak, Ricardo
AU  - Ishak R
AD  - Federal University of Para (UFPA), Institute of Biological Sciences, Laboratory 
      of Virology, Belem, PA, Brazil.
FAU - Vallinoto, Antonio Carlos Rosario
AU  - Vallinoto ACR
AD  - Federal University of Para (UFPA), Institute of Biological Sciences, Laboratory 
      of Virology, Belem, PA, Brazil. Electronic address: vallinoto@ufpa.br.
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20210710
PL  - Brazil
TA  - Braz J Infect Dis
JT  - The Brazilian journal of infectious diseases : an official publication of the 
      Brazilian Society of Infectious Diseases
JID - 9812937
RN  - 0 (Basic-Leucine Zipper Transcription Factors)
RN  - 0 (Biomarkers)
RN  - 0 (Retroviridae Proteins)
SB  - IM
MH  - Basic-Leucine Zipper Transcription Factors
MH  - Biomarkers
MH  - *HTLV-I Infections
MH  - *Human T-lymphotropic virus 1
MH  - Humans
MH  - Retroviridae Proteins
PMC - PMC9392164
OTO - NOTNLM
OT  - Biomarkers
OT  - HBZ
OT  - HTLV-1
OT  - Pathogenesis
OT  - TAX
COIS- Conflict of Interest The authors declare no conflicts of interest.
EDAT- 2021/07/14 06:00
MHDA- 2021/09/01 06:00
PMCR- 2021/07/10
CRDT- 2021/07/13 20:08
PHST- 2021/04/08 00:00 [received]
PHST- 2021/05/12 00:00 [revised]
PHST- 2021/06/03 00:00 [accepted]
PHST- 2021/07/14 06:00 [pubmed]
PHST- 2021/09/01 06:00 [medline]
PHST- 2021/07/13 20:08 [entrez]
PHST- 2021/07/10 00:00 [pmc-release]
AID - S1413-8670(21)00063-5 [pii]
AID - 101594 [pii]
AID - 10.1016/j.bjid.2021.101594 [doi]
PST - ppublish
SO  - Braz J Infect Dis. 2021 May-Jun;25(3):101594. doi: 10.1016/j.bjid.2021.101594. 
      Epub 2021 Jul 10.