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Bacterial Artificial Chromosomes: A Functional Genomics Tool for the Study of Positive-strand RNA Viruses
Published on: December 29, 2015
Viral genomes and arterial disease
A L Robertson1, Y Katsura, R J Stein
1Department of Pathology, University of Illinois, College of Medicine, Chicago.
Annals of the New York Academy of Sciences
|January 17, 1995
Summary
Herpesvirus DNA fragments can induce arterial smooth muscle cell proliferation, potentially initiating atherogenesis. This study demonstrates a new rabbit model for studying early stages of this inflammatory disease.
Area of Science:
- Cardiovascular Biology
- Virology
- Cellular Transformation
Background:
- Atherogenesis involves inflammatory-proliferative responses of intimal arterial cells.
- Herpesviruses may induce cellular transformation, contributing to atheroma development.
- Challenges exist in modeling herpesvirus-induced atherogenesis in vitro.
Purpose of the Study:
- To investigate the role of herpesvirus genome sequences in inducing atherogenesis.
- To develop a reproducible in vivo rabbit model for studying early atherogenesis.
Main Methods:
- Intraarterial injection of HSV-1 or HSV-2 genome fragments into Watanabe heritable hyperlipemic rabbits.
- Utilized specially designed catheters for targeted arterial delivery.
- Compared lesion development in normolipemic and hyperlipemic rabbits with placebo controls.
Main Results:
- Normolipemic rabbits developed localized intimal tumors composed of smooth muscle cells and macrophages.
- Hyperlipemic rabbits exhibited larger intimal lesions with lipid-laden macrophages.
- Placebo-injected controls showed no lesion development.
Conclusions:
- Selective transfection with viral genome sequences can induce smooth muscle cell growth promoters.
- Herpesvirus DNA may play a significant role in the initial stages of atherogenesis.
- The developed rabbit model is suitable for studying herpesvirus-induced atherogenesis.
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