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Delayed Maturation of Antibody Avidity but Not Seroconversion in Rhesus Macaques Infected With Simian HIV During Oral Pre-Exposure Prophylaxis

Curtis, Kelly A PhD*; Kennedy, M Susan BS*; Luckay, Amara MS*; Cong, Mian-er MD*; Youngpairoj, Ae S BS*; Zheng, Qi MS*; Smith, James PhD*; Hanson, Debra MS; Heneine, Walid PhD*; Owen, S Michele PhD*; García-Lerma, J Gerardo PhD*

JAIDS Journal of Acquired Immune Deficiency Syndromes: August 15th, 2011 - Volume 57 - Issue 5 - p 355-362
doi: 10.1097/QAI.0b013e3182234a51
Basic and Translational Science

Background: Pre-exposure prophylaxis (PrEP) is a novel intervention strategy for the prevention HIV transmission. Because several clinical trials are at various stages of completion, it is important to understand the impact of PrEP treatment on the development of the immune response to HIV, particularly in individuals who exhibit breakthrough infections despite PrEP.

Methods: A model of HIV infection, using rhesus macaques and the simian/human immunodeficiency virus (SHIV), was used to evaluate the effects of PrEP on the evolution of the humoral immune response. Time to seroconversion, neutralizing and binding antibody levels, and antibody avidity were measured in 12 rhesus macaques infected during daily or intermittent PrEP with FTC (emtricitabine) or Truvada (FTC/tenofovir combination) and compared with 11 untreated, simian HIV-infected controls.

Results: Macaques that became infected while receiving PrEP exhibited significantly lower peak virus loads during acute infection as compared with untreated animals. Although the timing of seroconversion and SHIV binding and neutralizing antibody levels were not impacted by treatment, lower maturation rates of antibody avidity for anti-p27, gp120, gp160, and gp41 were observed.

Conclusions: This study suggests that reduced virus loads associated with PrEP treatment have little impact on timing of seroconversion and neutralizing/binding antibody levels; however, maturation of antibody avidity was suppressed.

From the *Laboratory Branch and the †Quantitative Sciences and Data Management Branch, Division of HIV/AIDS Prevention, National Center for HIV/AIDS, Hepatitis, STD, and TB Prevention, Centers for Disease Control and Prevention, Atlanta, GA.

Received for publication March 10, 2011; accepted May 6, 2011.

This study was supported with intramural funding from the Centers for Disease Control and Prevention.

This work was presented as a poster presentation at CROI 2009 from February 8-11, 2009, in Montreal, Canada (Abstract #1072).

The findings and conclusions in this report are those of the authors and do not necessarily represent the views of the Centers for Disease Control and Prevention.

The authors have no conflicts of interest to disclose.

Supplemental digital content is available for this article. Direct URL citations appear in the printed text and are provided in the HTML and PDF versions of the journal's Web site (www.jaids.com).

Correspondence: Kelly A. Curtis, PhD, Centers for Disease Control and Prevention, 1600 Clifton Road NE, MS-A25, Atlanta, GA 30333 (e-mail: czv2@cdc.gov).

© 2011 Lippincott Williams & Wilkins, Inc.