Herpes simplex virus type 1 inhibits in vitro differentiation and selected functions of human blood‐derived monocytes

Abstract

We have studied the effect of herpes simplex virus type 1 (HSV1) infection on in vitro differentiation of blood‐derived human monocytes into macrophages using morphological, functional and biochemical parameters that alter during macrophage differentiation. Purified preparations of HSV modified the monocyte‐macrophage differentiation, in spite of the fact that the virus did not replicate in monocytes. Disappearance of expression of a monocyte‐specific surface antigen and the typical development of morphological appearance were delayed in HSV‐ infected cells. Production of the lysosomal enzyme acid phosphatase, which normally increases during differentiation, was also reduced in infected cells. Transcription of the oncogenes c‐myc and c‐fos, and the Hsp70 gene was modified in cells from some donors but not in other cell preparations. Possible mechanisms of these effects are discussed.

Herpes Simplex Virus Type 1-induced FasL Expression in Human Monocytic Cells and Its Implications for Cell Death, Viral Replication, and Immune Evasion

“…Previous studies showed that monocytes were resistant to HSV-1 infection, and only become susceptible to it upon differentiation towards macrophages (21)(22)(23). Another study showed that human peritoneal macrophages become partially permissive to viral infection upon treatment with thioglycollate, and are fully permissive after prior infection with Corynebacterium parvum (24).…”

Oncolytic HSV Exerts Direct Antiangiogenic Activity in Ovarian Carcinoma

“…We recently demonstrated that tumor endothelium in murine ID8-VEGF ovarian tumors (and human ovarian cancer) derives in significant part from monocyte/dendritic cell precursors (Conejo-García et al, 2004). Mouse (and human) monocytes and immature dendritic cells are susceptible to HSV infection (Hayward et al, 1993;Weir and Elkins, 1993;Bruun et al, 1998;Kobelt et al, 2003;Pollara et al, 2003). The potent inflammatory response set off by the viral infection may massively recruit such cells into the tumor.…”