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1 April 2007

Volume 195, Number 7
The Journal of Infectious Diseases 2007;195:960–964
© 2007 by the Infectious Diseases Society of America. All rights reserved.
0022-1899/2007/19507-0008$15.00
DOI: 10.1086/511988
BRIEF REPORT

Apolipoprotein B mRNA–Editing Enzyme, Catalytic Polypeptide–Like 3G: A Possible Role in the Resistance to HIV of HIV‐Exposed Seronegative Individuals

Mara Biasin,1,a

Luca Piacentini,1,a

Sergio Lo Caputo,2

Yasuyoshi Kanari,3

Giuliana Magri,1

Daria Trabattoni,1

Valentina Naddeo,1

Lucia Lopalco,4

Alberto Clivio,5

Eugenio Cesana,5

Francesca Fasano,1

Cristina Bergamaschi,1

Francesco Mazzotta,2

Masaaki Miyazawa,3 and

Mario Clerici1

Departments of 1Immunology and 5Biology, Dipartimento di Scienze Precliniche Laboratorio Interdisciplinare Tecnologie Avanzate Vialba, Milano University Medical School, Milano, and 2Infectious Diseases Clinic, S. M. Annunziata Hospital, Antella, Firenze, Italy; 3Department of Immunology, Kinki University School of Medicine, Osaka‐Sayama, Osaka, Japan; and 4Duke University Medical Center, Department of Surgery, Laboratory for AIDS Vaccine Research and Development, Durham, North Carolina

Apolipoprotein B mRNA–editing enzyme, catalytic polypeptide–like 3G (APOBEC3G), a human cytidine deaminase, is a potent inhibitor of HIV replication. To explore a possible role of this protein in modulating in vivo susceptibility to HIV infection, we analyzed APOBEC3G expression in HIV‐exposed seronegative individuals, HIV‐seropositive patients, and healthy control subjects. The results showed that the expression of APOBEC3G is significantly increased in peripheral blood mononuclear cells (PBMCs)—mainly CD14+ cells—and in cervical tissues of HIV‐exposed seronegative individuals. Higher APOBEC3G expression correlated with a reduced susceptibility of PBMCs to in vitro infection with the HIV‐1Ba‐L R5 strain. APOBEC3G could be important in modulating in vivo susceptibility to sexually transmitted HIV infection.

Received 20 September 2006; accepted 3 November 2006; electronically published 16 February 2007.

Reprints or correspondence: Dr. Mario Clerici, Chair of Immunology, University of Milan DISP LITA Vialba, Via G.B. Grassi 74, 20157 Milano, Italy ().

Cited by

D Tudor, M Derrien, L Diomede, A-S Drillet, M Houimel, C Moog, J-M Reynes, L Lopalco, M Bomsel. (2009) HIV-1 gp41-specific monoclonal mucosal IgAs derived from highly exposed but IgG-seronegative individuals block HIV-1 epithelial transcytosis and neutralize CD4+ cell infection: an IgA gene and functional analysis. Mucosal Immunology
Online publication date: 8-Aug-2009.
CrossRef
BM Baker, BL Block, AC Rothchild, BD Walker. (2009) Elite control of HIV infection: implications for vaccine design. Expert Opinion on Biological Therapy 9:1, 55-69
Online publication date: 1-Feb-2009.
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L. Piacentini, M. Biasin, C. Fenizia, M. Clerici. (2009) Genetic correlates of protection against HIV infection: the ally within. Journal of Internal Medicine 265:1, 110-124
Online publication date: 1-Feb-2009.
CrossRef
Masaaki Miyazawa, Lucia Lopalco, Francesco Mazzotta, Sergio Lo Caputo, Francisco Veas, Mario Clerici. (2009) The ‘immunologic advantage’ of HIV-exposed seronegative individuals. AIDS 23:2, 161-175
Online publication date: 1-Feb-2009.
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Nzovu K. Ulenga, Abdoulaye Dieng Sarr, Seema Thakore‐Meloni, Jean‐Louis Sankalé, Geoff Eisen, and Phyllis J. Kanki. (2008) Relationship between Human Immunodeficiency Type 1 Infection and Expression of Human APOBEC3G and APOBEC3F. The Journal of Infectious Diseases 198:4, 486-492
Online publication date: 15-Aug-2008.
Abstract-Full Text-PDF Version (162 kB)
Melissa A Farrow, Ann M Sheehy. (2008) Vif and Apobec3G in the innate immune response to HIV: a tale of two proteins. Future Microbiology 3:2, 145-154
Online publication date: 1-May-2008.
CrossRef

  • Potential conflicts of interest: none reported.

    Presented in part: AIDS 2006, XVI International AIDS Conference, 13–18 August 2006, Toronto, Canada (abstract MOPE0023).

    Financial support: Istituto Superiore di Sanità “Programma Nazionale di Ricerca sull’AIDS”; Centro di Eccellenza CISI: Center for Biomolecular Interdisiplinary Studies and Industrial Applications; European Microbicides Project and AIDS Vaccine Integrated Project (European Community WP6 projects); Japan Health Science Foundation; Tuscany Region, DG Right to Health and Solidarity Policy.

  • M.B. and L.P. contributed equally to this work.

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