Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 1986 Jul;22(7):397-401.
doi: 10.1007/BF02623529.

Susceptibility of endothelial cells derived from different blood vessels to common viruses

Susceptibility of endothelial cells derived from different blood vessels to common viruses

H M Friedman et al. In Vitro Cell Dev Biol. 1986 Jul.

Abstract

We examined whether endothelial cells derived from different blood vessels vary in their susceptibility to viral infection. Five common viral pathogens of humans (herpes simplex 1, measles, mumps, echo 9, and coxsackie B4 viruses) were evaluated for growth in endothelial cells derived from bovine fetal pulmonary artery, thoracic aorta, and vena cava. All five viruses replicated in each type of endothelial cell. There were apparent differences in the quantities of measles and mumps viruses produced in pulmonary artery endothelium compared with thoracic aorta and vena cava when endothelial cells were obtained from different animals. However, when pulmonary artery endothelial cells were compared with vena cava cells from the same animal, growth of each virus was similar in the two cell types. Four of the viruses replicated in the various endothelial cells without producing appreciable changes in cell morphology. These results indicate that endothelial cells from different blood vessels are equally susceptible to the human viruses evaluated, and that viral replication can occur without major alterations in cell morphology. Endothelial cells could serve as permissive cells permitting viruses to leave the circulation and initiate infection in adjacent tissues, including subendothelial smooth muscle cells.

PubMed Disclaimer

References

    1. Am J Clin Pathol. 1981 Aug;76(2):197-200 - PubMed
    1. N Engl J Med. 1969 Sep 11;281(11):585-9 - PubMed
    1. Atherosclerosis. 1978 Nov;31(3):295-306 - PubMed
    1. J Virol. 1985 Dec;56(3):839-45 - PubMed
    1. J Infect Dis. 1981 Feb;143(2):266-73 - PubMed

Publication types

LinkOut - more resources