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Journal of Virology, January 2009, p. 150-158, Vol. 83, No. 1
0022-538X/09/$08.00+0     doi:10.1128/JVI.01652-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

Follicular Dendritic Cells and Human Immunodeficiency Virus Type 1 Transcription in CD4+ T Cells{triangledown}

Tyler C. Thacker ,{dagger},{ddagger} Xueyuan Zhou,{dagger} Jacob D. Estes,§ Yongjun Jiang, Brandon F. Keele,|| Terry S. Elton,{dagger}{dagger} and Gregory F. Burton*

Department of Chemistry and Biochemistry, Brigham Young University, Provo, Utah 84602

Received 2 August 2008/ Accepted 16 October 2008

HIV replication occurs throughout the natural course of infection in secondary lymphoid tissues and in particular within the germinal centers (GCs), where follicular dendritic cells (FDCs) are adjacent to CD4+ T cells. Because FDCs provide signaling that increases lymphocyte activation, we postulated that FDCs could increase human immunodeficiency virus (HIV) replication. We cultured HIV-infected CD4+ T cells alone or with FDCs and measured subsequent virus expression using HIV-p24 production and reverse transcription-PCR analyses. When cultured with FDCs, infected CD4+ T cells produced almost fourfold more HIV than when cultured alone, and the rate of virus transcription was doubled. Both FDCs and their supernatant increased HIV transcription and resulted in nuclear translocation of NF-{kappa}B and phosphorylated c-Jun in infected cells. FDCs produced soluble tumor necrosis factor alpha (TNF-{alpha}) ex vivo, and the addition of a blocking soluble TNF receptor ablated FDC-mediated HIV transcription. Furthermore, TNF-{alpha} was found highly expressed within GCs, and ex vivo GC CD4+ T cells supported greater levels of HIV-1 replication than other CD4+ T cells. These data indicated that FDCs increase HIV transcription and production by a soluble TNF-{alpha}-mediated mechanism. This FDC-mediated effect may account, at least in part, for the presence of persistent HIV replication in GCs. Therefore, in addition to providing an important reservoir of infectious virus, FDCs increase HIV production, contributing to a tissue microenvironment that is highly conducive to HIV transmission and expression.

* Corresponding author. Mailing address: Department of Chemistry and Biochemistry, Room C-211A BNSN, Brigham Young University, Provo, UT 84602. Phone: (801) 422-4917. Fax: (801) 422-0153. E-mail: gburton{at}chem.byu.edu

{triangledown} Published ahead of print on 29 October 2008.

{dagger} These individuals contributed equally to the work presented in this study.

{ddagger} Present address: National Animal Disease Center, Agricultural Research Service, USDA, 2300 Dayton Ave., Ames, IA 50010.

§ Present address: The AIDS and Cancer Virus Program, SAIC-Frederick, Inc., NCI—Frederick, Fort Detrick Campus, Bldg. 535, Rm. 413b, Frederick, MD 21702.

Present address: AIDS Research Center, No. 1 Hospital, China Medical University, Shenyang, Liaoning, People's Republic of China.

|| Present address: Department of Medicine, University of Alabama at Birmingham, 720 20th Street South, KAUL 806, Birmingham, AL 35294-0024.

{dagger}{dagger} Present address: Davis Heart and Lung Research Institute, The Ohio State University DHLRI 515, 473 West 12th Avenue, Columbus, OH 43210.

Journal of Virology, January 2009, p. 150-158, Vol. 83, No. 1
0022-538X/09/$08.00+0     doi:10.1128/JVI.01652-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.



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