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 investigated production of tumor necrosis factor alpha (TNF-alpha) by human alveolar macrophages and human umbilical vein endothelial cells (HUVEC) after infection with SNV. In addition, we examined the effect of TNF-alpha on HUVEC monolayer leakage. Our results reveal that although TNF-alpha decreases accumulation of viral nucleoproteins, TNF-alpha levels do not change in SNV-infected cells. In addition, supernatants from SNV-infected human alveolar macrophages did not cause a significant increase in endothelial monolayer permeability.
Khaiboullina
S F
SF
Department of Microbiology and Cell and Molecular Biology Program, School of Medicine, University of Nevada-Reno, Reno, Nevada 89557, USA.
Netski
D M
DM
Krumpe
P
P
St Jeor
S C
SC
D000818:Animals; D002463:Cell Membrane Permeability / Q000187:drug effects; D002522:Chlorocebus aethiops; D017077:Culture Media, Conditioned / Q000494:pharmacology; D004730:Endothelium, Vascular / Q000187:drug effects* / Q000378:metabolism / Q000821:virology*; D006476:Orthohantavirus; D018778:Hantavirus Infections / Q000188:drug therapy* / Q000821:virology; D006801:Humans; D016676:Macrophages, Alveolar / Q000378:metabolism / Q000821:virology; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology* / Q000627:therapeutic use*; D014709:Vero Cells
D017077:Culture Media, Conditioned; D014409:Tumor Necrosis Factor-alpha