PMID- 15613312
OWN - NLM
STAT- MEDLINE
DCOM- 20050127
LR  - 20181113
IS  - 0022-538X (Print)
IS  - 1098-5514 (Electronic)
IS  - 0022-538X (Linking)
VI  - 79
IP  - 2
DP  - 2005 Jan
TI  - Epstein-Barr virus gp42 is posttranslationally modified to produce soluble gp42 
      that mediates HLA class II immune evasion.
PG  - 841-52
AB  - Epstein-Barr virus (EBV) resides as a persistent infection in human leukocyte 
      antigen (HLA) class II+ B lymphocytes and is associated with a number of 
      malignancies. The EBV lytic-phase protein gp42 serves at least two functions: 
      gp42 acts as the coreceptor for viral entry into B cells and hampers T-cell 
      recognition via HLA class II molecules through steric hindrance of T-cell 
      receptor-class II-peptide interactions. Here, we show that gp42 associates with 
      class II molecules at their various stages of maturation, including immature 
      alphabetaIi heterotrimers and mature alphabeta-peptide complexes. When analyzing 
      the biosynthesis and maturation of gp42 in cells stably expressing the viral 
      protein, we found that gp42 occurs in two forms: a full-length type II membrane 
      protein and a truncated soluble form. Soluble gp42 is generated by proteolytic 
      cleavage in the endoplasmic reticulum and is secreted. Soluble gp42 is sufficient 
      to inhibit HLA class II-restricted antigen presentation to T cells. In an almost 
      pure population of Burkitt's lymphoma cells in the EBV lytic cycle, both 
      transmembrane and soluble forms of gp42 are detected. These results imply that 
      soluble gp42 is generated during EBV lytic infection and could contribute to 
      undetected virus production by mediating evasion from T-cell immunity.
FAU - Ressing, Maaike E
AU  - Ressing ME
AD  - Department of Medical Microbiology, Leiden University Medical Center, Bldg. 1 E4, 
      P P.O. Box 9600, 2300 RC Leiden, The Netherlands. m.ressing@lumc.nl
FAU - van Leeuwen, Daphne
AU  - van Leeuwen D
FAU - Verreck, Frank A W
AU  - Verreck FA
FAU - Keating, Sinead
AU  - Keating S
FAU - Gomez, Raquel
AU  - Gomez R
FAU - Franken, Kees L M C
AU  - Franken KL
FAU - Ottenhoff, Tom H M
AU  - Ottenhoff TH
FAU - Spriggs, Melanie
AU  - Spriggs M
FAU - Schumacher, Ton N
AU  - Schumacher TN
FAU - Hutt-Fletcher, Lindsey M
AU  - Hutt-Fletcher LM
FAU - Rowe, Martin
AU  - Rowe M
FAU - Wiertz, Emmanuel J H J
AU  - Wiertz EJ
LA  - eng
GR  - R01 AI020662/AI/NIAID NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Virol
JT  - Journal of virology
JID - 0113724
RN  - 0 (BZLF2 protein, Herpesvirus 4, Human)
RN  - 0 (Glycoproteins)
RN  - 0 (Histocompatibility Antigens Class II)
RN  - 0 (Viral Proteins)
SB  - IM
MH  - Amino Acid Sequence
MH  - B-Lymphocytes/virology
MH  - Cell Line, Tumor
MH  - Glycoproteins/chemistry/*physiology
MH  - Histocompatibility Antigens Class II/*physiology
MH  - Humans
MH  - Molecular Sequence Data
MH  - *Protein Processing, Post-Translational
MH  - T-Lymphocytes/*immunology
MH  - Viral Proteins/chemistry/*physiology
PMC - PMC538541
EDAT- 2004/12/23 09:00
MHDA- 2005/01/28 09:00
PMCR- 2005/01/01
CRDT- 2004/12/23 09:00
PHST- 2004/12/23 09:00 [pubmed]
PHST- 2005/01/28 09:00 [medline]
PHST- 2004/12/23 09:00 [entrez]
PHST- 2005/01/01 00:00 [pmc-release]
AID - 79/2/841 [pii]
AID - 1325-04 [pii]
AID - 10.1128/JVI.79.2.841-852.2005 [doi]
PST - ppublish
SO  - J Virol. 2005 Jan;79(2):841-52. doi: 10.1128/JVI.79.2.841-852.2005.