K. Slezak et al., CHANGES IN ALPHA-1-ANTICHYMOTRYPSIN EXPRESSION IN VACCINIA VIRUS-INFECTED HEPG2 CELLS, Biological chemistry, 379(2), 1998, pp. 213-217
Human hepatoma cells (HepG2) synthesize and secrete several plasma pro
teins that are inhibited in a time-and dose-dependent manner after vac
cinia virus infection. However, infection of the HepG2 cells with a lo
w dose of the virus (up to 1 plaque forming unit/cell) stimulated the
expression of alpha-1-antichymotrypsin, which was demonstrated by mean
s of electroimmunoassay and Northern blot analysis. This stimulation a
ppeared to be on the level of transcription as shown in transient tran
sfection experiments using various alpha-1-antichymotrypsin gene promo
ter constructs. In contrast to interleukin-6, virus-induced activation
of the alpha-1-antichymotrypsin gene transcription does not require t
he STAT (signal transducers and activators of transcription) binding e
lements present in the alpha-1-antichymotrypsin gene promoter. Further
more, alpha-amanitin, which inhibits eukaryotic RNA polymerase II and
III, did not affect alpha-1-antichymotrypsin stimulation by the virus,
indicating involvement of the viral transcriptional apparatus in tran
sient activation of alpha-1-antichymotrypsin gene expression.