Viral infection of vascular endothelial cells alters production of colony-stimulating activity.

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Abstract
Viral infections in humans are frequently associated with granulocytopenia and/or granulocytosis. Such changes in myelopoiesis could result from infection of the granulocyte-macrophage colony-forming cell (CFC-GM) or changes in the production of colony-stimulating activity (CSA). Endothelial cells are a known source of CSA and may be transiently or persistently infected during a number of viral infections, including infection with herpes simplex virus type I (HSV-I) and measles virus. Therefore, we examined the effect of endothelial cell infection with these two viruses on the production of CSA. Uninfected passaged endothelial cells produce CSA when stimulated by the continual presence of a factor present in medium conditioned by peripheral blood monocytes (MCM). Within 4 h of infection with HSV-I, endothelial cells no longer produced CSA in response to MCM. In contrast, measles virus infection induced CSA production by passaged endothelial cells even in the absence of MCM. Measles virus-induced CSA production was maximal at 24 h and required the presence of live virus within the endothelial cells. The effects of HSV-I and measles virus on CSA production were not dependent on alterations in the production of alpha- or gamma-interferon by the infected endothelial cells. Infection with HSV-I did not stimulate endothelial cells to release any detectable interferon. In contrast, the supernatants of the measles-infected cells contained only beta-interferon, a known inhibitor of CFC-GM development. These studies suggest that CSA production by endothelial cells is directly altered by infection with HSV-I and measles virus. An alteration in CSA production might contribute to changes in myelopoiesis that frequently accompany viral infection in humans.