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Availability of activated [CD4.sup.+] T cells dictates the level of viremia in naturally SIV-infected sooty mangabeys
- Source :
- Journal of Clinical Investigation. June, 2008, Vol. 118 Issue 6, p2039, 11 p.
- Publication Year :
- 2008
-
Abstract
- Naturally SIV-infected sooty mangabeys (SMs) remain asymptomatic despite high virus replication. Elucidating the mechanisms underlying AIDS resistance of SIV-infected SMs may provide crucial information to better understand AIDS pathogenesis. In this study, we assessed the determinants of set-point viremia in naturally SIV-infected SMs, i.e., immune control of SIV replication versus target cell limitation. We depleted [CD4.sup.+] T cells in 6 naturally SIV-infected SMs by treating with humanized anti-CD4 mAb (Cdr-OKT4A-huIgG1). [CD4.sup.+] T cells were depleted almost completely in blood and BM and at variable levels in mucosal tissues and LNs. No marked depletion of [CD14.sup.+] monocytes was observed. Importantly, [CD4.sup.+] T cell depletion was associated with a rapid, significant decline in viral load, which returned to baseline level at day 30-45, coincident with an increased fraction of proliferating and activated [CD4.sup.+] T cells. Throughout the study, virus replication correlated with the level of proliferating [CD4.sup.+] T cells. [CD4.sup.+] T cell depletion did not induce any changes in the fraction of Tregs or the level of SIV-specific [CD8.sup.+] T cells. Our results suggest that the availability of activated [CD4.sup.+] T cells, rather than immune control of SIV replication, is the main determinant of set-point viral load during natural SIV infection of SMs.<br />Introduction The HIV epidemic in humans arose after zoonotic transmission of simian [CD4.sup.+] T cell tropic lentiviruses, which naturally infect a range of African monkey host species and are now [...]
Details
- Language :
- English
- ISSN :
- 00219738
- Volume :
- 118
- Issue :
- 6
- Database :
- Gale General OneFile
- Journal :
- Journal of Clinical Investigation
- Publication Type :
- Academic Journal
- Accession number :
- edsgcl.180241328