Wild-type temperature-sensitive and -resistant visna viruses: Isolation and biological comparison

Abstract

The plaques formed by wild-type (WT) populations of strain K485 visna (V-K485) virus, strain K796 visna (V-K796) virus, and of progressive pneumonia virus in sheep choroid plexus (SCP) cell cultures are heterogeneous in size. Plaque purification procedures showed that this heterogeneity was due to the presence of two biologically different viruses, large plaque-forming (Lpf) virus and small plaque-forming (Spf) virus. The V-K796 Lpf virus, the V-K796 Spf virus, and the V-K796 WT virus are antigenically similar to each other. Although the V-K796 Spf virus is less cytopathic than the V-K796 Lpf virus, both viruses have a 14- to 16-hour latent period in SCP cells and have similar rates of synthesis for the initial 24 to 30 hours after infection. The V-K796 Spf virus is considered a temperature-sensitive visna virus since, unlike the V-K796 Lpf virus, it does not produce plaques at 41 degrees C and it is more thermosensitive than the V-K796 Lpf variant. Population analyses of two strains of wild-type visna virus and one strain of progressive pneumonia virus demonstrated that these populations contain variants with the phenotypes of V-K796 Spf virus and V-K796 Lpf virus, that the Spf virus was not selected against in sheep, and that cultivation of the wild type visna viruses at 37 degrees C selected against the temperature-sensitive variants. The existence of the temperature-sensitive Spf viruses in these wild-type virus populations suggests that the Spf variants maintain the persistent visna virus infection in sheep and delay the development of the host's cell-mediated immune response to the viral proteins.

Evidence for a role of virulent human immunodeficiency virus (HIV) variants in the pathogenesis of acquired immunodeficiency syndrome: studies on sequential HIV isolates

“…Although some features of the development of HIV infection have been linked to certain structural and regulatory properties of HIV isolates at the molecular level (11,21,31,32), little is known of the possible consequences of genomic variability for differences in pathogenic properties of divergent HIV strains. It is well known from studies with animal retroviruses, including lentiviruses (9,19,23,27,35), that virus strains may exhibit such differences in virulence. For these reasons, we and others (3, 4, 7, 10, 34, 37) studied the biological properties of HIV isolates in cell culture.…”

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

“…The in vivo target cell of ruminant lentiviruses is considered to be the monocyte or the macrophage (8,28,29). Lentivirus replication and cytopathic effects in monocytes or macrophages differ depending on virus strain as well as on source and maturation of the host cell (7,18,30). Recently, in addition to infection T-4+ lymphocytes, HIV has been demonstrated to infect and replicate in human monocytes (19), monocyte-derived macrophages (6), and alveolar macrophages (23).…”