PMID- 22309258
OWN - NLM
STAT- MEDLINE
DCOM- 20120809
LR  - 20191210
IS  - 1399-0039 (Electronic)
IS  - 0001-2815 (Linking)
VI  - 79
IP  - 3
DP  - 2012 Mar
TI  - Sequence evolution and escape from specific immune pressure of an HIV-1 Rev 
      epitope with extensive sequence similarity to human nucleolar protein 6.
PG  - 174-85
LID - 10.1111/j.1399-0039.2012.01837.x [doi]
AB  - Antigen-specific immunity is crucially important for containing viral replication 
      in human immunodeficiency virus (HIV)-1-infected hosts. Several epitopes have 
      been predicted for the early expressed HIV-1 proteins Tat and Rev, but few have 
      been studied in detail. We characterized the human leukocyte antigen 
      (HLA)-B44-restricted Rev epitope EELLKTVRL (EL9) in an HIV-1-infected subject 
      treated with antiretroviral therapy. Interestingly, a high sequence similarity 
      was found between the EL9 epitope and the human nucleolar protein 6 (NOL6). 
      However, this similarity does not seem to impede immunogenicity as CD8(+) 
      T-cells, previously stimulated with EL9-pulsed dendritic cells, were able to 
      specifically recognize the HIV-1 Rev epitope without cross-recognizing the human 
      self-antigen NOL6. After the subject interrupted antiretroviral therapy and virus 
      rebounded, mutations within the EL9 epitope were identified. Although the 
      emerging mutations resulted in decreased or abolished T-cell recognition, they 
      did not impair Rev protein function. Mutations leading to escape from T-cell 
      recognition persisted for up to 124 weeks following treatment interruption. This 
      study shows that the HLA-B44-restricted Rev CD8(+) T-cell epitope EL9 is 
      immunogenic notwithstanding its close resemblance to a human peptide. The epitope 
      mutates as a consequence of dynamic interaction between T-cells and HIV-1. 
      Clinical status, CD4(+) T-cell count and viral load remained stable despite 
      escape from T-cell recognition.
CI  - (c) 2012 John Wiley & Sons A/S.
FAU - Allard, S D
AU  - Allard SD
AD  - Laboratory of Molecular and Cellular Therapy, Department of Physiology and 
      Immunology, Medical School of the Vrije Universiteit Brussel, Brussels, Belgium.
FAU - de Goede, A L
AU  - de Goede AL
FAU - De Keersmaecker, B
AU  - De Keersmaecker B
FAU - Heirman, C
AU  - Heirman C
FAU - Lacor, P
AU  - Lacor P
FAU - Osterhaus, A D M E
AU  - Osterhaus AD
FAU - Demanet, C
AU  - Demanet C
FAU - Thielemans, K
AU  - Thielemans K
FAU - Gruters, R A
AU  - Gruters RA
FAU - Aerts, J L
AU  - Aerts JL
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Tissue Antigens
JT  - Tissue antigens
JID - 0331072
RN  - 0 (Anti-Retroviral Agents)
RN  - 0 (Epitopes, T-Lymphocyte)
RN  - 0 (HLA Antigens)
RN  - 0 (NOL6 protein, human)
RN  - 0 (Nuclear Proteins)
RN  - 0 (rev Gene Products, Human Immunodeficiency Virus)
SB  - IM
MH  - Amino Acid Sequence
MH  - Animals
MH  - Anti-Retroviral Agents/administration & dosage
MH  - Base Sequence
MH  - COS Cells
MH  - Cell Line, Tumor
MH  - Chlorocebus aethiops
MH  - Enzyme-Linked Immunosorbent Assay
MH  - Epitopes, T-Lymphocyte/genetics/immunology
MH  - *Evolution, Molecular
MH  - HIV Infections/drug therapy/*immunology
MH  - *HIV-1/genetics
MH  - HLA Antigens/genetics
MH  - HeLa Cells
MH  - Humans
MH  - Lymphocyte Activation/immunology
MH  - Molecular Mimicry
MH  - Molecular Sequence Data
MH  - Mutation
MH  - Nuclear Proteins/chemistry/*genetics
MH  - T-Lymphocytes/immunology/virology
MH  - rev Gene Products, Human Immunodeficiency Virus/*genetics/*immunology
EDAT- 2012/02/09 06:00
MHDA- 2012/08/10 06:00
CRDT- 2012/02/08 06:00
PHST- 2012/02/08 06:00 [entrez]
PHST- 2012/02/09 06:00 [pubmed]
PHST- 2012/08/10 06:00 [medline]
AID - 10.1111/j.1399-0039.2012.01837.x [doi]
PST - ppublish
SO  - Tissue Antigens. 2012 Mar;79(3):174-85. doi: 10.1111/j.1399-0039.2012.01837.x.