The influence of vaccinia virus
infection on activity and subcellular localization of cellular
transcription factors YY1 and
C/EBPbeta in human blood monocytes derived macrophages was examined. YY1 activity, shown by electrophoretic mobility shift assay, decreased upon
infection in the nuclear extracts but remained unchanged in whole
cell extracts until 48h post-
infection (p.i.). Immunohistochemical staining of the fixed cells showed translocation of the factor to the cytoplasm of the infected macrophages. The nuclear export of YY1 was blocked by
leptomycin B, an inhibitor of the Crm1-dependent export system. C/EBP
DNA binding activity was transiently increased during
viral infection. Cytoplasmic translocation of the
C/EBPbeta has also been observed and was found to be blocked by
leptomycin B treatment of the cells. It appears that the Crm1 system is not impaired by the
virus infection in blood-derived macrophages and that it remains operative for redirection of subcellular localization of
transcription factors from the nucleus to the cytoplasm. Moreover, blockage of the nuclear export by
leptomycin B significantly affected the yield of infectious virus. The results might help to better understand the mechanism of protein transport during
viral infection of monocyte-derived cells.