Effects of tumor necrosis factor alpha on Sin Nombre virus infection in vitro

Previous data indicate that immune mechanisms may be involved in developing capillary leakage during Sin Nombre virus (SNV) infection. Therefore, we i nvestigated production of tumor necrosis factor alpha (TNF-alpha) by human alveolar macrophages and human umbilical vein endothelial cells (HUVEC) aft er infection with SNV. In addition, we examined the effect of TNF-alpha on HUVEC monolayer leakage. Our results reveal that although TNF-alpha decreas es accumulation of viral nucleoproteins, TNF-alpha levels do not change in SNV-infected cells. In addition, supernatants from SNV-infected human alveo lar macrophages did not cause a significant increase in endothelial monolay er permeability.