Delay of HIV-1 rebound after cessation of antiretroviral therapy through passive transfer of human n

Author:  ["Alexandra Trkola","Herbert Kuster","Peter Rusert","Beda Joos","Marek Fischer","Christine Leemann","Amapola Manrique","Michael Huber","Manuela Rehr","Annette Oxenius","Rainer Weber","Gabriela Stiegler","Brigitta Vcelar","Hermann Katinger","Leonardo Aceto","Huldrych F Günthard"]

Publication:  Nature Medicine

CITE.CC academic search helps you expand the influence of your papers.

Tags:     Medicine

Abstract

To determine the protective potential of the humoral immune response against HIV-1 in vivo we evaluated the potency of three neutralizing antibodies (2G12, 2F5 and 4E10) in suppressing viral rebound in six acutely and eight chronically HIV-1–infected individuals undergoing interruption of antiretroviral treatment (ART). Only two of eight chronically infected individuals showed evidence of a delay in viral rebound during the passive immunization. Rebound in antibody-treated acutely infected individuals upon cessation of ART was substantially later than in a control group of 12 individuals with acute infection. Escape mutant analysis showed that the activity of 2G12 was crucial for the in vivo effect of the neutralizing antibody cocktail. By providing further direct evidence of the potency, breadth and titers of neutralizing antibodies that are required for in vivo activity, these data underline both the potential and the limits of humoral immunity in controlling HIV-1 infection.

Cite this article

Trkola, A., Kuster, H., Rusert, P. et al. Delay of HIV-1 rebound after cessation of antiretroviral therapy through passive transfer of human neutralizing antibodies. Nat Med 11, 615–622 (2005). https://doi.org/10.1038/nm1244

View full text

>> Full Text:   Delay of HIV-1 rebound after cessation of antiretroviral therapy through passive transfer of human n

Reversing systemic inflammatory response syndrome with chemokine receptor pepducins

TLR activation triggers the rapid differentiation of monocytes into macrophages and dendritic cells