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Bovine immunodeficiency virus (BIV) is a bovine lentivirus that infects animals world-wide. The authors have cloned the BIV env and gag proteins and several sub-unit peptides spanning the entire coding regions of the two proteins as fusions to the bacterial trpE protein and expressed them in Escherichia coli (Spindler et al. 1984). These recombinant proteins can readily be expressed but the expression levels of these peptides varied. When these proteins were tested against a panel of bovine sera, only sera from BIV-infected animals reacted specifically. One major antigenic determinant was identified in the cartoxyl terminus of the p26 gag protein and another was identified in the transmembrane (TM) domain of the envelope glycoprotein.
The pathogenesis of the BIV infection has not been well characterized. Experimentally-infected animals did not develop immunodeficiency. It is possible that co-factors may play a role in enhancing the pathogenesis of BIV infection; and one of these co-factors could be bovine herpesviruses (BHV). BHV-1 co-infection of BIV-infected cells enhanced BIV replication and an immediate early gene of BHV-1 is involved. This herpes-viral gene product acts on the BIV promotor element to stimulate BIV expression. In vivo co-infection of animals with BIV and BIV-1 demonstrated that these viruses can interact in vivo, with BHV-l reactivated BIV expression in infected animals.