PMID- 8497046
OWN - NLM
STAT- MEDLINE
DCOM- 19930621
LR  - 20200724
IS  - 0022-538X (Print)
IS  - 1098-5514 (Electronic)
IS  - 0022-538X (Linking)
VI  - 67
IP  - 6
DP  - 1993 Jun
TI  - Endogenous expression of E1A in human cells enhances the effect of adenovirus E3 
      on class I major histocompatibility complex antigen expression.
PG  - 3176-81
AB  - Group C human adenovirus (Ad) serotypes (e.g., Ad type 2 [Ad2] and Ad5) cause 
      persistent infections in humans. One explanation for Ad persistence is an 
      ineffective cytotoxic T-lymphocyte response due to diminished cell surface 
      expression of class I major histocompatibility antigen (MHC Ag) on Ad-infected 
      cells, an effect mediated by the Ad E3 19-kDa glycoprotein (E3 effect). However, 
      we previously reported that, except for the Ad5 E1-transformed human cell line 
      293, a variety of human lymphoid, epithelial, and fibroblastic cells are 
      resistant to the E3 effect during Ad5 infection (J. M. Routes and J. L. Cook, J. 
      Immunol. 144:2763-2770, 1990). The present study tested the hypothesis that 
      endogenous expression of E1A proteins in 293 cells sensitizes cells to this E3 
      effect, resulting in an enhanced downregulation of surface class I MHC Ag 
      expression following Ad5 infection. Human epithelial and fibroblastic cells 
      expressing E1A gene products for at least 72 h exhibited an enhanced E3 effect 
      following Ad5 infection that was independent of baseline levels of surface class 
      I MHC Ag expression and of E1A induction of E3 19-kDa glycoprotein expression. 
      There was a direct correlation between the level of endogenous E1A expressed and 
      the magnitude of the E3 effect. We postulate that the in vivo existence of cells 
      stably expressing either E1A proteins or E1A-like activities in the 
      microenvironment of Ad5 infection provides a reservoir of Ad-infected cells that 
      is relatively protected from the virus-specific cytotoxic T-lymphocyte response, 
      thereby favoring Ad persistence in humans.
FAU - Routes, J M
AU  - Routes JM
AD  - Department of Medicine, National Jewish Center for Immunology and Respiratory 
      Medicine, Denver, Colorado 80206.
FAU - Metz, B A
AU  - Metz BA
FAU - Cook, J L
AU  - Cook JL
LA  - eng
GR  - AI-32136/AI/NIAID NIH HHS/United States
GR  - CA43187/CA/NCI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Virol
JT  - Journal of virology
JID - 0113724
RN  - 0 (Adenovirus E1A Proteins)
RN  - 0 (Adenovirus E3 Proteins)
SB  - IM
MH  - Adenovirus E1A Proteins/biosynthesis/*immunology
MH  - Adenovirus E3 Proteins/biosynthesis/*immunology
MH  - Adenoviruses, Human/growth & development/*immunology
MH  - Cell Line, Transformed
MH  - Cytotoxicity, Immunologic
MH  - Down-Regulation
MH  - Genes, MHC Class I/*immunology
MH  - Humans
PMC - PMC237656
EDAT- 1993/06/01 00:00
MHDA- 1993/06/01 00:01
PMCR- 1993/06/01
CRDT- 1993/06/01 00:00
PHST- 1993/06/01 00:00 [pubmed]
PHST- 1993/06/01 00:01 [medline]
PHST- 1993/06/01 00:00 [entrez]
PHST- 1993/06/01 00:00 [pmc-release]
AID - 10.1128/JVI.67.6.3176-3181.1993 [doi]
PST - ppublish
SO  - J Virol. 1993 Jun;67(6):3176-81. doi: 10.1128/JVI.67.6.3176-3181.1993.