Neuroinvasion of fluorescein-positive monocytes in acute simian immunodeficiency virus infection.

Monocytes and macrophages play a central role in the pathogenesis of human immunodeficiency virus (HIV)-associated dementia. They represent prominent targets for HIV infection and are thought to facilitate viral neuroinvasion and neuroinflammatory processes. However, many aspects regarding monocyte brain recruitment in HIV infection remain undefined.

Distinct chemokine triggers and in vivo migratory paths of fluorescein dye-labeled T Lymphocytes in acutely simian immunodeficiency virus SIVmac251-infected and uninfected macaques.

To define the possible impact of T-lymphocyte trafficking parameters on simian immunodeficiency virus (SIV) pathogenesis, we examined migratory profiles of carboxyfluorescein diacetate succinimidyl ester (CFSE)-labeled T lymphocytes in acutely SIVmac251-infected and uninfected macaques within 48 h after autologous transfer. Despite significant upregulation of homeostatic chemokine CCL19/macrophage inflammatory protein 3beta and proinflammatory chemokine CXCL9/monokine induced by gamma interferon in secondary lymphoid tissue in SIV infection, no differences in CFSE+ T-lymphocyte frequencies or cell compartmentalization in lymph nodes were identified between animal groups. By contrast, a higher frequency of CFSE+ T lymphocytes in the small intestine was detected in acute SIV infection.

Chemokine networks and in vivo T-lymphocyte trafficking in nonhuman primates.

T-lymphocyte migratory circuits in human and nonhuman primates remain largely unexplored due to the difficulty of defining cell trafficking in vivo. However, this knowledge may reveal critical aspects of immunity and T-lymphocyte homeostasis in both health and disease. Furthermore, in vivo T-lymphocyte trafficking studies may facilitate defining mechanism(s) of immune dysfunction in the nonhuman primate model for acquired immunodeficiency syndrome (AIDS).

Induction of simian AIDS in infant rhesus macaques infected with CCR5- or CXCR4-utilizing simian-human immunodeficiency viruses is associated with distinct lesions of the thymus.

Newborn rhesus macaques were infected with two chimeric simian-human immunodeficiency virus (SHIV) strains which contain unique human immunodeficiency virus type 1 (HIV-1) env genes and exhibit distinct phenotypes. Infection with either the CCR5-specific SHIV(SF162P3) or the CXCR4-utilizing SHIV(SF33A) resulted in clinical manifestations consistent with simian AIDS. Most prominent in this study was the detection of severe thymic involution in all SHIV(SF33A)-infected infants, which is very similar to HIV-1-induced thymic dysfunction in children who exhibit a rapid pattern of disease progression.