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Journal of Virology, October 2002, p. 10299-10306, Vol. 76, No. 20
0022-538X/02/$04.00+0     DOI: 10.1128/JVI.76.20.10299-10306.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

Addition of a Single gp120 Glycan Confers Increased Binding to Dendritic Cell-Specific ICAM-3-Grabbing Nonintegrin and Neutralization Escape to Human Immunodeficiency Virus Type 1

James Lue,1,{dagger} Mayla Hsu,1 David Yang,1 Preston Marx,2 Zhiwei Chen,1 and Cecilia Cheng-Mayer1*

Aaron Diamond AIDS Research Center, The Rockefeller University, New York, New York 10016,1 Tulane Regional Primate Research Center and Department of Tropical Medicine, Tulane Health Sciences Center, New Orleans, Louisiana2

Received 5 April 2002/ Accepted 11 July 2002

The potential role of dendritic cell-specific ICAM-3-grabbing nonintegrin (DC-SIGN) binding in human immunodeficiency virus transmission across the mucosal barrier was investigated by assessing the ability of simian-human immunodeficiency chimeric viruses (SHIVs) showing varying degrees of mucosal transmissibility to bind the DC-SIGN expressed on the surface of transfected cells. We found that gp120 of the highly transmissible, pathogenic CCR5-tropic SHIVSF162P3 bound human and rhesus DC-SIGN with an efficiency threefold or greater than that of gp120 of the nonpathogenic, poorly transmissible parental SHIVSF162, and this increase in binding to the DC-SIGN of the SHIVSF162P3 envelope gp120 translated into an enhancement of T-cell infection in trans. The presence of an additional glycan at the N-terminal base of the V2 loop of SHIVSF162P3 gp120 compared to that of the parental virus was shown to be responsible for the increase in binding to DC-SIGN. Interestingly, this glycan also conferred escape from autologous neutralization, raising the possibility that the modification occurred as a result of immune selection. Our data suggest that more-efficient binding of envelope gp120 to DC-SIGN could be relevant to the enhanced mucosal transmissibility of SHIVSF162P3 compared to that of parental SHIVSF162.

* Corresponding author. Mailing address: Aaron Diamond AIDS Research Center, 455 First Ave., New York, NY 10016. Phone: (212) 448-5080. Fax: (212) 448-5159. Email: cmayer{at}adarc.org.

{dagger} Present address: School of Medicine, University of California, San Francisco, Calif.

Journal of Virology, October 2002, p. 10299-10306, Vol. 76, No. 20
0022-538X/02/$04.00+0     DOI: 10.1128/JVI.76.20.10299-10306.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.



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