Multiple HIV-1-specific IgG3 responses decline during acute HIV-1: implications for detection of incident HIV infection.

Published

Journal Article

OBJECTIVE: Different HIV-1 antigen specificities appear in sequence after HIV-1 transmission and the immunoglobulin G (IgG) subclass responses to HIV antigens are distinct from each other. The initial predominant IgG subclass response to HIV-1 infection consists of IgG1 and IgG3 antibodies with a noted decline in some IgG3 antibodies during acute HIV-1 infection. Thus, we postulate that multiple antigen-specific IgG3 responses may serve as surrogates for the relative time since HIV-1 acquisition. DESIGN: We determined the magnitude, peak, and half-life of HIV-1 antigen-specific IgG1 and IgG3 antibodies in 41 HIV-1-infected individuals followed longitudinally from acute infection during the first appearance of HIV-1-specific antibodies through approximately 6 months after infection. METHODS: We used quantitative HIV-1-binding antibody multiplex assays and exponential decay models to estimate concentrations of IgG1 and IgG3 antibodies to eight different HIV-1 proteins including gp140 Env, gp120 Env, gp41 Env, p66 reverse transcriptase, p31 Integrase, Tat, Nef, and p55 Gag proteins during acute/recent HIV-1 infection. RESULTS: Among HIV-1-specific IgG3 responses, anti-gp41 IgG3 antibodies were the first to appear. We found that anti-gp41 Env IgG3 and anti-p66 reverse transcriptase IgG3 antibodies, in addition to anti-Gag IgG3 antibodies, each consistently and measurably declined after acute infection, in contrast to the persistent antigen-specific IgG1 responses. CONCLUSION: The detailed measurements of the decline in multiple HIV-specific IgG3 responses simultaneous with persistent IgG1 responses during acute and recent HIV-1 infection could serve as markers for detection of incident HIV infection.

Full Text

Duke Authors

Cited Authors

  • Yates, NL; Lucas, JT; Nolen, TL; Vandergrift, NA; Soderberg, KA; Seaton, KE; Denny, TN; Haynes, BF; Cohen, MS; Tomaras, GD

Published Date

  • November 13, 2011

Published In

Volume / Issue

  • 25 / 17

Start / End Page

  • 2089 - 2097

PubMed ID

  • 21832938

Pubmed Central ID

  • 21832938

Electronic International Standard Serial Number (EISSN)

  • 1473-5571

Digital Object Identifier (DOI)

  • 10.1097/QAD.0b013e32834b348e

Language

  • eng

Conference Location

  • England