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Journal of Virology, February 1999, p. 1411-1418, Vol. 73, No. 2
Department of Virology, The Lerner Research
Institute, The Cleveland Clinic Foundation, Cleveland, Ohio 44195
Received 20 July 1998/Accepted 2 September 1998
Human parainfluenza virus type 3 (HPIV3) infection causes severe
damage to the lung epithelium, leading to bronchiolitis, pneumonia, and
croup in newborns and infants. Cellular immunity that plays a vital
role in normal antiviral action appears to be involved, possibly
because of inappropriate activation, in the infection-related damage to
the lung epithelium. In this study, we investigated the expression of
major histocompatibility complex (MHC) class I and II molecules on
human lung epithelial (A549) and epithelium-like (HT1080) cells
following HPIV3 infection. MHC class I was induced by HPIV3 in these
cells at levels similar to those observed with natural inducers such as
beta and gamma interferon (IFN-
0022-538X/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.
Human Parainfluenza Virus Type 3 Up-Regulates Major
Histocompatibility Complex Class I and II Expression on Respiratory
Epithelial Cells: Involvement of a STAT1- and
CIITA-Independent Pathway
and -
). MHC class II was also
efficiently induced by HPIV3 in these cells. UV-irradiated culture
supernatants from infected cells were able to induce MHC class I but
not MHC class II, suggesting involvement of released factors for the
induction of MHC class I. Quantitation of IFN types I and II in the
culture supernatant showed the presence of IFN-
as the major
cytokine, while IFN-
was undetectable. Anti-IFN-
, however,
blocked the HPIV3-mediated induction of MHC class I only partially,
indicating that viral antigens, besides IFN-
, are directly involved
in the induction process. The induction of MHC class I and class II
directed by the viral antigens was confirmed by using cells lacking
STAT1, an essential intermediate of the IFN signaling pathways. HPIV3 induced both MHC class I and class II molecules in STAT1-null cells.
Furthermore, MHC class II was also induced by HPIV3 in cells defective
in class II transactivator, an important intermediate of the
IFN-
-mediated MHC class II induction pathway. Together, these data
indicate that the HPIV3 gene product(s) is directly involved in the
induction of MHC class I and II molecules. The induction of MHC class I
and II expression by HPIV3 suggests that it plays a role in the
infection-related immunity and pathogenesis.
*
Corresponding author. Mailing address: Department of
Molecular Biology, The Lerner Research Institute, The Cleveland Clinic Foundation, 9500 Euclid Ave., NC20, Cleveland, OH 44195. Phone: (216)
444-0625. Fax: (216) 444-0512. E-mail:
banerja{at}cesmtp.ccf.org.
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