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The Journal of Immunology, 2005, 174: 7995-8002.
Copyright © 2005 by The American Association of Immunologists

Neisseria gonorrhoeae Enhances Infection of Dendritic Cells by HIV Type 11

Jizhong Zhang2,*, Geling Li2,*, Andre Bafica2,{dagger},{ddagger}, Milica Pantelic*, Pei Zhang*, Hal Broxmeyer*, Ying Liu*, Lee Wetzler§, Johnny J. He* and Tie Chen3,*

* Department of Microbiology and Immunology, Division of Infectious Diseases, Walther Oncology Center, Walther Oncology Institute, Indiana University School of Medicine, Indianapolis, IN 46202;{dagger} Immunobiology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892;{ddagger} Laboratorio de Imunorregulacao e Microbiologia, Oswaldo Cruz Foundation, Salvador, Bahia, Brazil; and§ Department of Medicine, Division of Infectious Diseases, Boston Medical Center, Boston University School of Medicine, Evans Biomedical Research Center, Boston, MA 02118

Clinical studies indicate that Neisseria gonorrhoeae (gonococci (GC)) has the capacity to enhance HIV type 1 (HIV-1) infection. We studied whether GC enhances HIV infection of activated dendritic cells (DCs). The results show that GC can dramatically enhance HIV replication in human DCs during coinfection. The GC component responsible for HIV infection enhancement may be peptidoglycan, which activates TLR2. TLR2 involvement is suggested by bacterial lipoprotein, a TLR2-specific inducer, which stimulates a strong enhancement of HIV infection by human DCs. Moreover, participation of TLR2 is further implicated because GC is unable to stimulate expression of HIV in DCs of TLR2-deficient HIV-1-transgenic mice. These results provide one potential mechanism through which GC infection increases HIV replication in patients infected with both GC and HIV.




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