1887

Abstract

Summary

A recently described autoantibody-inducing agent in mice was further characterized. Tentatively designated AGIA (anti-Golgi apparatus-inducing agent), this agent has previously been shown to cause antibody production against Golgi apparatus (GA) antigen of cells from different vertebrate species as well as against tumour surface antigen of the Moloney murine sarcoma virus-non-producer transformant Sac. It was shown to possess the properties characteristic of lactate dehydrogenase-elevating virus (LDV). It induced elevation of lactate dehydrogenase levels in the blood, persistent lifelong viraemia in mice and serum titres of up to 10 infectious doses (ID) per ml in the acute phase of infection. Its replication was limited to subpopulations of murine peritoneal macrophages. Electron microscopy of AGIA-infected macrophages and of serum of infected mice revealed virus-like particles with a morphology resembling LDV. The buoyant density of AGIA was approximately 1.14 g/ml. Both the enzyme-elevating activity and the autoantibody-inducing activity were shown to belong to LDV. Infection of STU mice with two established strains of LDV (LDV and LDV) was also found to induce both autoantibody groups. In both cases, after infection with AGIA as well as after infection with the two known LDV isolates, anti-Sac cell antibodies occurred at comparable titres. However, anti-GA antibody titres were rather low after infection with LDV and LDV compared with AGIA infection. Serological cross-reactivity was demonstrated between AGIA-, LDV- and LDV-infected macrophages. AGIA induced anti-GA antibodies in all six mouse strains tested (STU, DBA/2, BALB/c, C3H/He, NMRI, C57BL/6); however, anti-Sac cell antibodies did not develop in C57BL/6 mice.

Loading

Article metrics loading...

/content/journal/jgv/10.1099/0022-1317-68-7-1983
1987-07-01
2019-11-19
Loading full text...

Full text loading...

http://instance.metastore.ingenta.com/content/journal/jgv/10.1099/0022-1317-68-7-1983
Loading

Most Cited This Month

This is a required field
Please enter a valid email address
Approval was a Success
Invalid data
An Error Occurred
Approval was partially successful, following selected items could not be processed due to error