No abstract

Factors that influence the response of chickens to avian nephritis virus (ANV) were studied. Day-old specific-pathogen-free chicks were inoculated with the G-4260 strain of ANV by oral, subcutaneous, intratracheal, intramuscular, and intracerebral routes at a dose of 10(5.0) plaque-forming units (PFUs) per chick. Inoculation induced only nephritis, and contact infection ANV occurred very easily. When 1-, 14-, 28-, 56-, and 300-day-old chickens were inoculated orally with 10(5.0) PFUs of the virus, the day-old chicks appeared to be most susceptible; histopathological responses to the virus became weak as chicks aged. The serological response of 28-day-old chickens to ANV was stronger that those of other groups. Pathologically, the adult chickens hardly responded to the virus, but they produced antibodies against the virus.

Monoclonal antibodies against 3 different glycoproteins of bovine herpesvirus type 1 (BHV-1) involved in virus neutralization were used in indirect immunofluorescence (IIF) tests to characterize the appearance and transport to the plasma membrane of virus antigens in the infected cells. Antibodies against gp 117 and gp 71 glycoproteins first showed pronounced ring-like nuclear fluorescence at 4 hours post-infection (PI), followed by staining of the perinuclear region, presumably the Golgi apparatus. In contrast, antibody against gp 87 produced staining in cell-to-cell junctional areas at 3 hours PI before any staining close to the nucleus. The expression of the 3 glycoproteins at the surface of the infected cells was confirmed by the use of monoclonal antibodies having neutralizing activity, but not by non-neutralizing antibodies against gp 117 and gp 71. Non-neutralizing antibody against gp 87 detected the surface fluorescence only in those cells showing marked degeneration. Inhibition of glycosylation of the viral glycoproteins with tunicamycin (TM) was followed by interference with transport of gp 117 and gp 87 to the plasma membrane. On the other hand, gp 71 was incorporated into the plasma membrane despite the lack of N-linked glycosylation.

Plaque formation, replication and related cytopathic function of 9 strains of transmissible gastroenteritis (TGE) virus were examined in primary cells and cell lines such as CPK, IB-RS-2, ESK, and PK-15 originated from porcine kidney and the effects of trypsin on the replication of TGE virus were examined in CPK cells. All strains produced a cytopathic effect and grew well in CPK cells as well as in primary porcine kidney cells. The effect of trypsin on the plaque formation was different from strains. The number of plaques produced by strains TO-163, Ukiha and Niigata increased from 2.6 to 3.52 times when trypsin was present in the medium during incubation at 37 degrees C for 1 hr after adsorption of the virus at 4 degrees C for 2 hr. The plaque sizes of TO-163, h-5, Ukiha and Niigata became larger from 1.4 to 1.7 times, when trypsin was present in the agar MEM overlay.

The 87,000-dalton glycoprotein (gp87) of bovine herpesvirus type 1 (BHV-1) was found to selectively attach to susceptible cells. The attachment of gp87 to the cells was markedly decreased by the prior adsorption of intact virions. Anti-gp87 (site Ia) monoclonal antibody, which inhibited BHV-1 adsorption to the cells and neutralized the virus without complement [Okazaki et al., Virology 250: 260-264], was effective in inhibiting the adsorption of gp87. Only the same antibody was able to inhibit the hemagglutination activity of BHV-1. Other monoclonal antibodies to the glycoproteins of BHV-1, including antibodies directed to sites Ib and Ic on gp87, were ineffective in inhibiting either virus adsorption or hemagglutination. The results of this study indicate that site Ia of gp87 molecule is the critical site of virus attachment for initiation of infection as well as the hemagglutination of BHV-1.