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  Vol. 291 No. 1, January 7, 2004 TABLE OF CONTENTS
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Relationship Between CCR5 Density and Viral Load After Discontinuation of Antiretroviral Therapy

Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

To the Editor: Discontinuation of combined antiretroviral therapy (CART) improves virological control and specific immunity in some persons infected with human immunodeficiency virus 1 (HIV-1),1 whereas in others it results in rapid viral rebound and decrease in the antiviral cytotoxic T cell responses below the pretherapeutic level.2 The host factors responsible for these opposite consequences are largely unknown. We have recently reported that the mean number of CCR5 coreceptors at the surface of CD4 T cells (CCR5 density) is logarithmically correlated with viral load3 and disease progression4 during HIV-1 infection. We have explained this link by showing in vitro that CCR5 density strongly determines the efficiency of HIV-1 life cycle, particularly at the reverse transcription stage.5 Herein we report a test of the hypothesis that CCR5 density, which is stable over time in a given individual but varies among individuals, might determine the intensity of viral rebound after cessation of . . . [Full Text of this Article]

Methods

Jacques Reynes, MD, PhD; Vincent Baillat, MD
Service des Maladies Infectieuses et Tropicales
Hôpital Gui de Chauliac

Pierre Portales, PharmD; Jacques Clot, MD, PhD
Laboratoire d'Immunologie
Hôpital Saint Eloi

Pierre Corbeau, MD, PhD
Institut de Génétique Humaine
Montpellier, France



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THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES

Reduction of CCR5 with low-dose rapamycin enhances the antiviral activity of vicriviroc against both sensitive and drug-resistant HIV-1
Heredia et al.
Proc. Natl. Acad. Sci. USA 2008;105:20476-20481.
ABSTRACT | FULL TEXT  





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