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  4. Characterization of anti-HIV-1 neutralizing and binding antibodies in chronic HIV-1 subtype C infection

Characterization of anti-HIV-1 neutralizing and binding antibodies in chronic HIV-1 subtype C infection

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Author(s)
Archary, Derseree
•
Rong, Rong
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Gordon, Michelle L.
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Boliar, Saikat
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Madiga, Maphuti
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Gray, Elin S.
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Dugast, Anne-Sophie
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Hermanus, Tandile
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Goulder, Philip J. R.
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Coovadia, Hoosen M.
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Date Issued
September 2012
Journal
Virology
Publisher
Elsevier
Citation
Archary, Derseree, Rong Rong, Michelle L. Gordon, Saikat Boliar, Maphuti Madiga, Elin S. Gray, Anne-Sophie Dugast, et al. “Characterization of Anti-HIV-1 Neutralizing and Binding Antibodies in Chronic HIV-1 Subtype C Infection.” Virology 433, no. 2 (November 2012): 410–420. © 2012 Elsevier Inc.
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Final published version
Abstract
Neutralizing (nAbs) and high affinity binding antibodies may be critical for an efficacious HIV-1 vaccine. We characterized virus-specific nAbs and binding antibody responses over 21 months in eight HIV-1 subtype C chronically infected individuals with heterogeneous rates of disease progression. Autologous nAb titers of study exit plasma against study entry viruses were significantly higher than contemporaneous responses at study entry (p=0.002) and exit (p=0.01). NAb breadth and potencies against subtype C viruses were significantly higher than for subtype A (p=0.03 and p=0.01) or B viruses (p=0.03; p=0.05) respectively. Gp41-IgG binding affinity was higher than gp120-IgG (p=0.0002). IgG–FcγR1 affinity was significantly higher than FcγRIIIa (p<0.005) at study entry and FcγRIIb (p<0.05) or FcγRIIIa (p<0.005) at study exit. Evolving IgG binding suggests alteration of immune function mediated by binding antibodies. Evolution of nAbs was a potential marker of HIV-1 disease progression.
MIT Department
Massachusetts Institute of Technology. Department of Biological Engineering
Ragon Institute of MGH, MIT and Harvard
Terms of Use
Article is made available in accordance with the publisher's policy and may be subject to US copyright law. Please refer to the publisher's site for terms of use.
Persistent DSpace Link
http://hdl.handle.net/1721.1/90266
DOI of Published Version
https://doi.org/10.1016/j.virol.2012.08.033
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