Abstract
Primary human and primate brain microvascular endothelial cells were tested for permissiveness to coronaviruses JHM and 229E. While sub-genomic viral RNAs could be detected up to 72 hours post-infection, primate cells were abortively infected and neither virus caused cytopathology. Human cells were non-permissive for JHM but permissive for 229E replication; peak production of progeny 229E and observable cytopathic effects occurred approximately 22 and 32 hour post-infection, respectively. Using the criterion of cytopathology induction in infected endothelial cells, 229E was compared to other human RNA and DNA viruses. In addition, virus induced modulation of intercellular adhesion molecule 1 (ICAM-1), vascular cell adhesion molecule 1 (VCAM-1) and HLA I was monitored by immunostaining of infected cells.
MeSH terms
-
Animals
-
Antibodies, Monoclonal
-
Antigens, Viral / analysis
-
Antigens, Viral / biosynthesis
-
Brain / blood supply*
-
Cell Line
-
Chlorocebus aethiops
-
Coronavirus / genetics
-
Coronavirus / pathogenicity*
-
Coronavirus / physiology*
-
Coronavirus 229E, Human*
-
Endothelium, Vascular / virology*
-
Gene Expression
-
Humans
-
Immunohistochemistry
-
Intercellular Adhesion Molecule-1 / analysis
-
Intercellular Adhesion Molecule-1 / biosynthesis
-
Kinetics
-
Microcirculation
-
Primates
-
RNA, Viral / analysis
-
RNA, Viral / biosynthesis
-
Species Specificity
-
Time Factors
-
Transcription, Genetic
-
Vascular Cell Adhesion Molecule-1 / analysis
-
Vascular Cell Adhesion Molecule-1 / biosynthesis
-
Vero Cells
-
Virus Replication
Substances
-
Antibodies, Monoclonal
-
Antigens, Viral
-
RNA, Viral
-
Vascular Cell Adhesion Molecule-1
-
Intercellular Adhesion Molecule-1