HCMV infection of HFF cells resulted in increased abundance of ornithine decarboxylase, thymidine kinase, heat-shock protein 70 (hsp70), and brain creatine kinase transcripts.
HCMV infection of HFF cells resulted in increased abundance of ornithine decarboxylase, thymidine kinase, heat-shock protein 70 (hsp70), and brain creatine kinase transcripts.
To do this, we primarily investigated the influence of HCMV infection on IL-1 beta-mRNA expression in peripheral blood monocytes and the promyelocytic cell line, ML-3 as well as the inflammatory response genes TNF-alpha, MAD-9, MAD-6, and MAD-2 in the promyelocytic ML-3 cell line.
We find that, as with RA induction, transfection of T2 cells with oncogenic human Ha-ras results in cells which are permissive for HCMV infection and gene expression.
To do this, we primarily investigated the influence of HCMV infection on IL-1 beta-mRNA expression in peripheral blood monocytes and the promyelocytic cell line, ML-3 as well as the inflammatory response genes TNF-alpha, MAD-9, MAD-6, and MAD-2 in the promyelocytic ML-3 cell line.
To do this, we primarily investigated the influence of HCMV infection on IL-1 beta-mRNA expression in peripheral blood monocytes and the promyelocytic cell line, ML-3 as well as the inflammatory response genes TNF-alpha, MAD-9, MAD-6, and MAD-2 in the promyelocytic ML-3 cell line.
To do this, we primarily investigated the influence of HCMV infection on IL-1 beta-mRNA expression in peripheral blood monocytes and the promyelocytic cell line, ML-3 as well as the inflammatory response genes TNF-alpha, MAD-9, MAD-6, and MAD-2 in the promyelocytic ML-3 cell line.
To do this, we primarily investigated the influence of HCMV infection on IL-1 beta-mRNA expression in peripheral blood monocytes and the promyelocytic cell line, ML-3 as well as the inflammatory response genes TNF-alpha, MAD-9, MAD-6, and MAD-2 in the promyelocytic ML-3 cell line.
To do this, we primarily investigated the influence of HCMV infection on IL-1 beta-mRNA expression in peripheral blood monocytes and the promyelocytic cell line, ML-3 as well as the inflammatory response genes TNF-alpha, MAD-9, MAD-6, and MAD-2 in the promyelocytic ML-3 cell line.
Secretion by peripheral blood mononuclear cells is increased if they are cultured with host fibroblasts infected with CMV in vitro and the levels of gamma IFN and TNF produced are within the range that protects fresh fibroblasts from CMV infection.
Secretion by peripheral blood mononuclear cells is increased if they are cultured with host fibroblasts infected with CMV in vitro and the levels of gamma IFN and TNF produced are within the range that protects fresh fibroblasts from CMV infection.
Secretion by peripheral blood mononuclear cells is increased if they are cultured with host fibroblasts infected with CMV in vitro and the levels of gamma IFN and TNF produced are within the range that protects fresh fibroblasts from CMV infection.
Patients with AIDS and disseminated CMV infection display the maximum activation of HIV p24 antigenaemia and the greatest deficiency of CD8+ T lymphocytes.
Patients with AIDS and disseminated CMV infection display the maximum activation of HIV p24 antigenaemia and the greatest deficiency of CD8+ T lymphocytes.
Patients with AIDS and disseminated CMV infection display the maximum activation of HIV p24 antigenaemia and the greatest deficiency of CD8+ T lymphocytes.
Patients with AIDS and disseminated CMV infection display the maximum activation of HIV p24 antigenaemia and the greatest deficiency of CD8+ T lymphocytes.
Patients with AIDS and disseminated CMV infection display the maximum activation of HIV p24 antigenaemia and the greatest deficiency of CD8+ T lymphocytes.
Patients with AIDS and disseminated CMV infection display the maximum activation of HIV p24 antigenaemia and the greatest deficiency of CD8+ T lymphocytes.
When both primary astrocytes and SK-N-MC cells were transfected with (a) HIV LTR-CAT alone, (b) HIV LTR-CAT plus HCMV-IE gene, or (c) HIV LTR-CAT plus HCMV infection 2 days before the transfection, both HCMV infection and its IE gene trans-activated the HIV LTR promoter.
No differences in local immunological changes, characterized by interstitial mononuclear leukocyte infiltration as well as by aberrant expression of HLA-class II antigens and of ICAM1 on proximal tubular epithelial cells, could be detected by further immunohistological analysis between grafted kidneys at late stage of rejection with and without CMV infection.
The influence of HLA A-B-DR matching on cytomegalovirus disease after renal transplantation. Evidence that HLA-DR7-matched recipients are more susceptible to cytomegalovirus disease.