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J Virol, January 1998, p. 841-846, Vol. 72, No. 1
0022-538X/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.

Human T-Lymphocyte Transformation with Human T-Cell Lymphotropic Virus Type 2

Sara L. Tarsis,1 Ming-Tsung Yu,2 Elizabeth S. Parks,1 Deborah Persaud,3 José L. Muñoz,4 and Wade P. Parks1,*

Department of Pediatrics, New York University Medical Center,1 Prenatal Diagnosis Laboratory of New York City/MHRA,2 New York, New York 10016; Department of Pediatrics, Johns Hopkins Medical School, Baltimore, Maryland 212053; and Department of Pediatrics, New York Medical College, Valhalla, New York 105954

Received 19 February 1997/Accepted 28 September 1997

Human T-cell lymphotrophic virus type 2 (HTLV-2), a common infection of intravenous drug users and subpopulations of Native Americans, is uncommon in the general population. In contrast with the closely related HTLV-1, which is associated with both leukemia and neurologic disorders, HTLV-2 lacks a strong etiologic association with disease. HTLV-2 does shares many properties with HTLV-1, including in vitro lymphocyte transformation capability. To better assess the ability of HTLV-2 to transform lymphocytes, a limiting dilution assay was used to generate clonal, transformed lymphocyte lines. As with HTLV-1, the transformation efficiency of HTLV-2 producer cells was proportionately related to the number of lethally irradiated input cells and was comparable to HTLV-1-mediated transformation efficiency. HTLV-2-infected cells were reproducibly isolated and had markedly increased growth potential compared to uninfected cells; HTLV-2 transformants required the continued presence of exogenous interleukin 2 for growth for several months and were maintained for over 2 years in culture. All HTLV-2-transformed populations were CD2 and/or CD3 positive and B1 negative and were either CD4+ or CD8+ populations or a mixture of CD4+ and CD8+ lymphocytes. Clonality of the HTLV-2 transformants was confirmed by Southern blot analysis of T-cell receptor beta  chain rearrangement. Southern blot analysis revealed a range of integrated full-length genomes from one to multiple. In situ hybridization analysis of HTLV-2 integration revealed no obvious chromosomal integration pattern.


* Corresponding author. Mailing address: Department of Pediatrics, New York University School of Medicine, 550 First Ave., Rm. TH-501A, New York, NY 10016. Phone: (212) 263-6425. Fax: (212) 263-8172. E-mail: PARKSW01{at}mcrcr.med.nyu.edu.




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