Pathogenesis of human cytomegalovirus disease and the kidney

Abstract

Uncertainty still surrounds many aspects of the pathogenesis of human cytomegalovirus (HCMV) infection. During asymptomatic infection HCMV is probably present in a small fraction of peripheral blood mononuclear cells (most likely monocytes); in active infection HCMV is detectable in a wider range of cells. In vitro experiments suggest that cellular control of transcription of HCMV immediate early (IE) gene expression is one key determinant of HCMV reactivation. The cytotoxic T cell response to IE and other virus gene products is probably important in subsequently limiting dissemination of HCMV infection. The basis for any association between active HCMV disease and allograft rejection is unclear, although homologies between cellular and viral proteins suggest possible mechanisms. Although HCMV may be associated with tubulointerstitial disease, there is no unequivocally established role for HCMV in the pathogenesis of human glomerular disease.