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Author Notes:

Corresponding author. Mailing address: Department of Microbiology and Immunology, 3107 Rollins Research Center, Emory University, Atlanta, GA 30322. Phone: (404) 727-5948. Fax: (404) 727-0293. E-mail: linda.gooding@emory.edu

Present address Y.Z.: Gastroenteritis and Respiratory Viruses Branch, Centers for Disease Control and Prevention, Atlanta, GA.

We thank Dean Erdman, Tom Shenk, André Lieber, Baoling Ying, William Wold, Betty Moran, and Jerry Schaack for kindly providing viruses and James DeGregori for providing antibodies and viruses that were used in this study.

The content of this report is solely the responsibility of the authors and does not necessarily represent the official views of the National Institute of Allergy and Infectious Diseases, the National Cancer Institute, or the National Institutes of Health.

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Research Funding:

This research was supported by grants R01 AI052280 from the National Institute of Allergy and Infectious Diseases and RO1 CA127621 from the National Cancer Institute.

Modeling Adenovirus Latency in Human Lymphocyte Cell Lines

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Journal Title:

Journal of Virology

Volume:

Volume 84, Number 17

Publisher:

, Pages 8799-8810

Type of Work:

Article | Final Publisher PDF

Abstract:

Species C adenovirus establishes a latent infection in lymphocytes of the tonsils and adenoids. To understand how this lytic virus is maintained in these cells, four human lymphocytic cell lines that support the entire virus life cycle were examined. The T-cell line Jurkat ceased proliferation and died shortly after virus infection. BJAB, Ramos (B cells), and KE37 (T cells) continued to divide at nearly normal rates while replicating the virus genome. Viral genome numbers peaked and then declined in BJAB cells below one genome per cell at 130 to 150 days postinfection. Ramos and KE37 cells maintained the virus genome at over 100 copies per cell over a comparable period of time. BJAB cells maintained the viral DNA as a monomeric episome. All three persistently infected cells lost expression of the cell surface coxsackie and adenovirus receptor (CAR) within 24 h postinfection, and CAR expression remained low for at least 340 days postinfection. CAR loss proceeded via a two-stage process. First, an initial loss of cell surface staining for CAR required virus late gene expression and a CAR-binding fiber protein even while CAR protein and mRNA levels remained high. Second, CAR mRNA disappeared at around 30 days postinfection and remained low even after virus DNA was lost from the cells. At late times postinfection (day 180), BJAB cells could not be reinfected with adenovirus, even when CAR was reintroduced to the cells via retroviral transduction, suggesting that the expression of multiple genes had been stably altered in these cells following infection.

Copyright information:

© 2010, American Society for Microbiology

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