Goat endothelial cells may be infected in vitro by transmigration of caprine arthritis-encephalitis virus-infected leucocytes.

The caprine arthritis-encephalitis lentivirus (CAEV) causes a lifelong persistent infection in goats, and induces infiltrations of leucocytes and tissue reorganization in target organs, with a cyclical pattern of viral expression. The mammary gland is an important site of infection, associated with mother-to-kid transmission by infected cells in colostrum and milk. The monocyte/macrophage is the principal target cell, but other cell types, including epithelial and endothelial cells and fibroblasts, are susceptible to in vitro infection with varying levels of viral replication. Such cells, perhaps at specific differentiation states, might play a role in the regulation and transfer of in vivo infection in target organs. In this paper we describe the in vitro infection of endothelial cell monolayers by the transmigration of monocytes carrying the CAEV provirus. The infected endothelial cells progress to expression of the viral p30 capsid antigen, suggesting viral proliferation. Such a process occurring in vivo during angiogenesis and leucocyte homing to the mammary gland in the final third of mammogenesis, might contribute to viral spread in this crucial target organ.

Viral expression and leukocyte adhesion after in vitro infection of goat mammary gland cells with caprine arthritis-encephalitis virus.

A characteristic lesion in goats infected by the lentivirus CAEV is mastitis with lymphoid hyperplasia. In order to investigate the mechanism of lesion formation, cultures highly enriched in microvascular endothelial cells, mature and immature luminal epithelial cells, fibroblasts and myoepithelial cells were established from goat mammary gland biopsies. Their susceptibility to in vitro infection with two distinct types of CAEV was investigated by PCR, antigen expression and cytopathy. The capacity of infected mammary gland cells to bind uninfected caprine leukocytes was determined by flow cytometry. All cell types tested were susceptible to CAEV infection in vitro, with different levels of sensitivity according to cell phenotype. Our results suggest that the limited extent of natural infection of mammary gland cells reflects a protective local immune response, and that the myoepithelial cell could act as a reservoir cell. After infection, the mature luminal cell acquires the capacity to bind leukocytes in vitro, which could indicate a facilitation of cellular interactions. The distinct reactions of the different cell types to CAEV infection may be correlated with events leading to progressive lesion development during the natural infection.