Pa. Luciw et al., GENETIC AND BIOLOGICAL COMPARISONS OF PATHOGENIC AND NONPATHOGENIC MOLECULAR CLONES OF SIMIAN IMMUNODEFICIENCY VIRUS (SIVMAC), AIDS research and human retroviruses, 8(3), 1992, pp. 395-402
Simian immunodeficiency virus (SIV) is a designation for a group of re
lated but unique lentiviruses identified in several primate species. A
viral isolate from a rhesus macaque (i.e., SIV(mac)) causes a fatal A
IDS-like disease in experimentally infected macaques, and several infe
ctious molecular clones of this virus have been characterized. This re
port presents the complete nucleotide sequence of molecularly cloned S
IV(mac1A11), and comparisons are made with the sequence of molecularly
cloned SIV(mac239), SIV(mac1A11) has delayed replication kinetics in
lymphoid cells but replicates as well as uncloned SIV(mac) in macropha
ge cultures. Macaques infected with virus from the SIV(mac1A11) clone
develop antiviral antibodies, but virus does not persist in peripheral
blood mononuclear cells and no disease signs are observed. SIV(mac239
) infects lymphoid cells, shows restricted replication in cultured mac
rophages, and establishes a persistent infection in animals that leads
to a fatal AIDS-like disease. Both viruses are about 98% homologous a
t the nucleotide sequence level. In SIV(mac1A11), the vpr gene as well
as the transmembrane domain of env are prematurely truncated, whereas
the nef gene of SIV(mac239) is prematurely truncated. Sequence differ
ences are also noted in variable region 1 (V1) in the surface domain o
f the env gene. The potential implications of these and other sequence
differences are discussed with respect to the phenotypes of both viru
ses. This animal model is critically important for investigating the r
oles of specific viral genes in viral/host interactions that cannot be
studied in individuals infected with the human immunodeficiency virus
(HIV).