Search Results

You are looking at 1 - 2 of 2 items for

  • Author or Editor: Yuji Inaba x
  • Refine by Access: All Content x
Clear All Modify Search

SUMMARY

Heparin inhibited hemagglutination (ha) by pseudorabies virus (prv), but not ha by Akabane virus, bovine adenovirus type 7, Fukuoka virus, Getah virus, Japanese encephalitis virus, and parainfluenza virus type 3 belonging to the families Bunyaviridae, Adenoviridae, Rhabdoviridae, Togaviridae, Flaviviidae, and Paramyxoviridae, respectively. The minimal inhibitory concentration of heparin required to inhibit 8 ha U of prv ranged from 0.005 to 0.01 U/ml. Mouse erythrocytes failed to combine with the ha inhibitory factor of heparin. On the other hand, mouse erythrocytes treated with heparinase had greatly reduced agglutinability by prv. Virus-heparin complex formation could be observed by sedimenting heparin with the virus particles.

Free access
in American Journal of Veterinary Research

Abstract

Objective

To investigate whether heparin has any effect on the growth of porcine reproductive and respiratory syndrome virus (PRRSV).

Sample Population

2 isolates of PRRSV, and as control viruses, 1 isolate of pseudorabies virus (PRV) and 1 isolate of parainfluenza 3 virus (PIV-3).

Procedures

Plaque assays, using a continuous cell line (MARC-145) derived from African green monkey kidney cell line (MA104), were performed for determination of inhibitory effect of heparin on PRRSV, PRV, and PIV-3. The effect of various doses of heparin and heparinase on the growth of PRRSV, PRV, and PIV-3 was evaluated and compared. In each experiment, values were expressed as the mean value for duplicate samples.

Results

The number of plaques formed by PRRSV and PRV was reduced to 24 to 25 and 15% of the untreated control (100%), respectively, by 1 U of heparin/ml, but could not be reduced below 6 to 7 and 3%, respectively, by use of concentrations up to 50 U/ml. An inhibitory effect of heparin, at a concentration up to 50 U/ml, was not observed on PIV-3. Delaying addition of heparin for 30 minutes after the addition of PRRSV and PRV reduced plaque formation by 48 to 51 and 68%, respectively, compared with 91 to 92 and 95%, respectively, if heparin was added at the time of infection. In addition, most PRRSV added was retained by heparin beads, as was PRV. Heparinase treatment of MARC-145 cells reduced the number of PRRSV-, as well as PRV-induced plaques. On the other hand, the number of PIV-3-induced plaques did not decrease after treatment of MARC-145 cells with heparinase.

Conclusions

Addition of heparin to PRRSV or to the MARC-145 cells before virus inoculation and treatment of the cells with heparinase prevented the virus from infecting the cells. (Am J Vet Res 1997;58:488–491)

Free access
in American Journal of Veterinary Research