SHIV-KB9 infection of rhesus monkeys does not always cause disease-contribution of host immune factors and thymic output.

Simian-human immunodeficiency virus (SHIV) infection in the macaque is a model of HIV pathogenesis. KB9, a molecular clone of SHIV 89.6P, induced rapid and profound CD4(+) T cell loss in rhesus monkeys, followed by partial recovery in some. We describe another clinical outcome after intravenous SHIV-KB9 inoculation in two of six infected rhesus macaques: lack of signs of immunodeficiency with sustained CD4(+) T cell counts, despite virus load levels similar to those of the animals with CD4(+) lymphocyte decline. To dissect the role of host factors in determining pathogenicity of this viral clone, humoral and cellular immune responses were studied. Differences in CD8(+) T cell effector responses and activation profiles and in thymic output, but not in specific antibody production, were observed in animals with different disease outcomes during acute infection. Thymic involvement may thus be a critical factor in determining disease progression.