THE INFLUENCE OF PROTEASE INHIBITORS OF THE ORGANISM, ESPECIALLY BOVINE APROTININ, ON THE PRODUCTION OF VIRULENT HOG-CHOLERA VIRUS IN TISSUE-CULTURES

Citation
G. Korn et W. Matthaeus, THE INFLUENCE OF PROTEASE INHIBITORS OF THE ORGANISM, ESPECIALLY BOVINE APROTININ, ON THE PRODUCTION OF VIRULENT HOG-CHOLERA VIRUS IN TISSUE-CULTURES, DTW. Deutsche tierarztliche Wochenschrift, 101(5), 1994, pp. 204-206
Citations number
32
Categorie Soggetti
Veterinary Sciences
ISSN journal
03416593
Volume
101
Issue
5
Year of publication
1994
Pages
204 - 206
Database
ISI
SICI code
0341-6593(1994)101:5<204:TIOPIO>2.0.ZU;2-H
Abstract
The influence of biological protease inhibitors, especially aprotinin, on the production of virulent hog cholera virus in cell cultures. Pro duction of number and size of fluorescent plaques after infection PK 1 5 cells with HC virus depended on properties of fetal calf sera added to the medium. By affinity chromatography on bovine alpha-chymotrypsin bound to CM-cellulose inhibitory proteins against chymortypsin-like p roteases could be eliminated from inhibiting sera- The fraction free f rom inhibitors did not inhibit plaque formation of HC virus in contras t to the fraction containing the eluted inhibitor (s). The inhibitory properties of fetal calf sera could be measured by a plaque inhibition test. By this test no inhibitory component could be demonstrated in 3 0 individual serum samples from pigs which on subsequent infection wit h HC virus exhibited virus growth to high titres The serum from one pi g, however, was found to inhibit HC virus plaque formation in PK 15 ce lls. When infected, this animal reacted with an unexpected low virus r eplication and mild disease symptoms. The production of virulent HC vi rus could likewise be inhibited by addition to the medium of the bovin e protease inhibitor aprotinin; the degree of inhibition being depende nt on the concentration. Virulent virus was produced again after elimi nation of this inhibitor from the medium. A weak inhibitory effect on plaque formation was also achieved by addition of the protease inhibit or chymostatin (3 mg/5 mg) and human alpha1x plasma inhibitor to the m edium of infected cells. The inhibitory effect appears to be very spec ific.