PMID- 10357853
OWN - NLM
STAT- MEDLINE
DCOM- 19990701
LR  - 20210526
IS  - 1092-2172 (Print)
IS  - 1098-5557 (Electronic)
IS  - 1092-2172 (Linking)
VI  - 63
IP  - 2
DP  - 1999 Jun
TI  - Mechanisms of T-cell activation by human T-cell lymphotropic virus type I.
PG  - 308-33
AB  - The interactions between human T-cell lymphotropic virus type I (HTLV-I) and the 
      cellular immune system can be divided into viral interference with functions of 
      the infected host T cell and the subsequent interactions between the infected T 
      cell and the cellular immune system. HTLV-I-mediated activation of the infected 
      host T cell is induced primarily by the viral protein Tax, which influences 
      transcriptional activation, signal transduction pathways, cell cycle control, and 
      apoptosis. These properties of Tax may well explain the ability of HTLV-I to 
      immortalize T cells. It is not clear, though, how HTLV-I induces T-cell 
      transformation (interleukin-2 [IL-2] independence). Recent evidence suggests that 
      Tax may promote the G1- to S-phase transition, although this may involve 
      additional proteins. A role for other viral proteins that may constitutively 
      activate the IL-2 receptor pathway has also been suggested. By virtue of their 
      activated state, HTLV-I-infected T cells can nonspecifically activate resting, 
      uninfected T cells via virus-mediated upregulation of adhesion molecules. This 
      may favor viral dissemination. Moreover, the induction of a remarkably high 
      frequency of antiviral CD8(+) T cells does not appear to eliminate the infection. 
      Indeed, individuals with a high frequency of virus-specific CD8(+) T cells have a 
      high viral load, indicating a state of chronic immune system stimulation. Thus, 
      while an activated immune system is needed to eradicate the infection, the spread 
      of the HTLV-I is also accelerated under these conditions. A detailed knowledge of 
      the molecular interactions between virus-specific CD8(+) T cells and 
      immunodominant viral epitopes holds promise for the development of specific 
      antiviral therapy.
FAU - Hollsberg, P
AU  - Hollsberg P
AD  - Department of Medical Microbiology and Immunology, Aarhus University, Aarhus, 
      Denmark. ph@microbiology.au.dk
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
PL  - United States
TA  - Microbiol Mol Biol Rev
JT  - Microbiology and molecular biology reviews : MMBR
JID - 9706653
RN  - 0 (Epitopes)
RN  - 0 (Gene Products, tax)
RN  - 0 (Interleukin-2)
SB  - IM
MH  - Apoptosis/physiology
MH  - CD4-Positive T-Lymphocytes/immunology/metabolism/*virology
MH  - CD8-Positive T-Lymphocytes/immunology/physiology/virology
MH  - Cell Cycle/physiology
MH  - Cell Transformation, Viral/physiology
MH  - Epitopes/metabolism
MH  - Gene Products, tax/physiology
MH  - HTLV-I Infections/immunology
MH  - Human T-lymphotropic virus 1/*physiology
MH  - Humans
MH  - Immunity, Cellular
MH  - Interleukin-2/metabolism
MH  - Lymphocyte Activation/immunology/*physiology
MH  - Signal Transduction
MH  - Transcriptional Activation
PMC - PMC98968
EDAT- 1999/06/05 00:00
MHDA- 1999/06/05 00:01
PMCR- 1999/06/01
CRDT- 1999/06/05 00:00
PHST- 1999/06/05 00:00 [pubmed]
PHST- 1999/06/05 00:01 [medline]
PHST- 1999/06/05 00:00 [entrez]
PHST- 1999/06/01 00:00 [pmc-release]
AID - 0014 [pii]
AID - 10.1128/MMBR.63.2.308-333.1999 [doi]
PST - ppublish
SO  - Microbiol Mol Biol Rev. 1999 Jun;63(2):308-33. doi: 
      10.1128/MMBR.63.2.308-333.1999.