Replication and cytopathic effects of ovine lentivirus strains in alveolar macrophages correlate with in vivo pathogenicity

Abstract

Ruminant lentiviruses share genomic sequences and biologic properties with human immunodeficiency viruses. Four ovine lentivirus strains were assessed for cytopathic effects and virus replication. Lentivirus isolate H/24 produced high virus titers and lysis of synovial cells but replicated slowly and caused no fusion of alveolar macrophages. Lentivirus isolates 84/28 and 85/14 produced low virus titers, less syncytia, and limited or no cell lysis in synovial cells and macrophages. In contrast, ovine lentivirus isolate 85/34 produced early peak virus titers and caused rapid fusion and lysis of both macrophages and synovial cells. Ovine lentivirus isolates which were cytopathic for macrophages induced lymphoproliferative disease when inoculated into lambs.

Efficient isolation and propagation of human immunodeficiency virus on recombinant colony-stimulating factor 1-treated monocytes.

“…Retention of virus within macrophages is not novel for retroviruses. Other lentiviruses, such as caprine arthritis encephalitis and ovine progressive pneumonia virus also bud into and accumulate in cytoplasmic vacuoles (27,28) . These viruses have strong tropism for blood monocytes or tissue macrophages, yet viral replication is restricted and entirely dependent upon host cell (macrophage) differentiation .…”

A single mutation within the V3 envelope neutralization domain of feline immunodeficiency virus determines its tropism for CRFK cells

“…A comparable phenomenon has been described for human immunodeficiency type 1 (HIV-1), in which case the presence of the CD4 receptor is not sufficient to allow replication of all HIV-1 isolates in each cell type (14,17). The in vitro cell tropism of lentivirus isolates appears to have pathogenetic consequences: sheep inoculated with a macrophage-lytic isolate of ovine lentivirus developed a lymphoproliferative disease, whereas animals inoculated with nonlytic isolates remained asymptomatic (22). Molecular clones of simian immunodeficiency virus differing in host cell range have a contrasting pathogenic potential (4).…”

Activation of caprine arthritis-encephalitis virus long terminal repeat by gamma interferon

“…Differentiation of infected monocytes into macrophages results in increased viral expression and an associated inflammatory response (19,21). Development of clinical manifestations localizes to tissues in which infected macrophages express CAEV (15). Thus, regulation of CAEV expression during monocyte differentiation is an essential step during disease pathogenesis.…”