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Passive immunization against oral AIDS virus transmission: An approach to prevent mother‐to‐infant HIV‐1 transmission?

Regina Hofmann‐Lehmann

Dana‐Farber Cancer Institute, Boston, MA,

Harvard Medical School, Boston, MA,

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Robert A Rasmussen

Dana‐Farber Cancer Institute, Boston, MA,

Harvard Medical School, Boston, MA,

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Josef Vlasak

Dana‐Farber Cancer Institute, Boston, MA,

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Beverly A. Smith

Dana‐Farber Cancer Institute, Boston, MA,

Harvard Medical School, Boston, MA,

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Timothy W. Baba

Dana‐Farber Cancer Institute, Boston, MA,

Harvard Medical School, Boston, MA,

Tufts University School of Medicine, Boston, MA,

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Vladimir Liska

Dana‐Farber Cancer Institute, Boston, MA,

Harvard Medical School, Boston, MA,

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David C. Montefiori

Duke University Medical Center, Durham, NC,

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Harold M. McClure

Yerkes Regional Primate Research Center, Atlanta, GA,

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Daniel C. Anderson

Yerkes Regional Primate Research Center, Atlanta, GA,

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Bruce J. Bernacky

University of Texas MD Anderson Cancer Center, Bastrop, TX,

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Tahir A. Rizvi

University of Texas MD Anderson Cancer Center, Bastrop, TX,

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Russell Schmidt

University of Texas MD Anderson Cancer Center, Bastrop, TX,

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Lori R. Hill

University of Texas MD Anderson Cancer Center, Bastrop, TX,

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Michale E. Keeling

University of Texas MD Anderson Cancer Center, Bastrop, TX,

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Hermann Katinger

University of Agriculture, Vienna, Austria,

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Gabriela Stiegler

University of Agriculture, Vienna, Austria,

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Marshall R. Posner

Dana‐Farber Cancer Institute, Boston, MA,

Harvard Medical School, Boston, MA,

Beth Israel‐Deaconess Medical Center, Boston, MA,

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Lisa A. Cavacini

Harvard Medical School, Boston, MA,

Beth Israel‐Deaconess Medical Center, Boston, MA,

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Ting‐Chao Chou

Memorial Sloan‐Kettering Cancer Center, New York, NY

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Ruth M. Ruprecht

Dana‐Farber Cancer Institute, Boston, MA,

Harvard Medical School, Boston, MA,

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First published: 31 October 2003
Cited by: 17
Ruth M. Ruprecht, Dana‐Farber Cancer Institute, 44 Binney Street, JFB809, Boston, MA 02115‐6084.
E‐mail: [email protected]

Abstract

To develop immunoprophylaxis regimens against mother‐to‐child human immunodeficiency virus type 1 (HIV‐1) transmission, we established a simian–human immunodeficiency virus (SHIV) model in neonatal macaques that mimics intrapartum mucosal virus exposure (T.W. Baba, J. Koch, E.S. Mittler et al.: AIDS Res Hum Retroviruses 10:351–357, 1994). We protected four neonates from oral SHIV‐vpu+ challenge by ante‐ and postpartum treatment with a synergistic triple combination of immunoglobulin (Ig) G1 human anti‐HIV‐1 neutralizing monoclonal antibodies (mAbs) (T.W. Baba, V. Liska, R. Hofmann‐Lehmann et al.: Nature Med 6:200–206, 2000), which recognize the CD4‐binding site of Env, a glycosylation‐dependent gp120, or a linear gp41 epitope. Two neonates that received only postpartum mAbs were also protected from oral SHIV‐vpu+ challenge, indicating that postpartum treatment alone is sufficient. Next, we evaluated a similar mAb combination against SHIV89.6P, which encodes env of primary HIV89.6. One of four mAb‐treated neonates was protected from infection and two maintained normal CD4+ T‐cell counts. We conclude that the epitopes recognized by the three mAbs are important determinants for achieving protection. Combination immunoprophylaxis with synergistic mAbs seems promising to prevent maternal HIV‐1 transmission in humans.

Number of times cited: 17

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