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Monocyte function in cattle experimentally infected with bovine immunodeficiency-like virus
A H Rovid1, S Carpenter, J A Roth
1Department of Microbiology, Immunology, and Preventive Medicine, Iowa State University, Ames 50011, USA.
Veterinary Immunology and Immunopathology
|March 1, 1995
Summary
Bovine immunodeficiency-like virus (BIV) infection minimally impacts cattle monocyte function in vivo, likely due to low viral load. In vitro, BIV enhances monocyte phagocytosis and migration while reducing cytotoxicity.
Area of Science:
- Veterinary Immunology
- Virology
- Cellular Immunology
Background:
- Bovine immunodeficiency-like virus (BIV) is a lentivirus affecting cattle.
- Monocytes play crucial roles in immune responses, including phagocytosis, migration, and cytotoxicity.
- Understanding BIV's impact on monocyte function is vital for managing BIV-infected cattle.
Purpose of the Study:
- To investigate the effects of BIV infection on bovine monocyte function in vivo and in vitro.
- To determine if observed effects are due to low viral burden or intrinsic viral properties.
Main Methods:
- Experimentally infected cattle and in vitro monocyte cultures were used.
- Monocyte functions assessed included phagocytosis of Staphylococcus aureus, random and chemotactic migration, and antibody-dependent cell-mediated cytotoxicity (ADCC).
- In vitro experiments involved treating normal monocytes with cell-free BIV.
Main Results:
- In vivo, BIV infection showed minimal effects on monocyte function for up to 2 years post-infection, with transiently reduced phagocytosis early on.
- In vitro, BIV treatment significantly increased monocyte phagocytosis and migration, and decreased ADCC in a dose-dependent manner.
- These findings suggest that the limited in vivo effects are likely due to a low BIV viral load.
Conclusions:
- BIV R29 infection has minimal impact on peripheral blood monocyte function in cattle, likely because of a low virus burden.
- In vitro studies demonstrate BIV's capacity to alter monocyte functions, indicating potential changes in monocyte-derived cells at replication sites.