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J Virol, May 1998, p. 4408-4412, Vol. 72, No. 5
0022-538X/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.
Human and Simian T-Cell Leukemia Viruses Type 2 (HTLV-2 and STLV-2pan-p) Transform T Cells Independently of
Jak/STAT Activation
James C.
Mulloy,1,*
Thi-Sau
Migone,2,
Ted M.
Ross,3,
Nick
Ton,1
Patrick L.
Green,3,§
Warren J.
Leonard,2 and
Genoveffa
Franchini1
Basic Research Laboratory, National Cancer
Institute,1 and
Laboratory of Molecular
Immunology, National Heart, Lung, and Blood
Institute,2 Bethesda, Maryland, and
Department of Microbiology and Immunology, Vanderbilt
University School of Medicine, Nashville, Tennessee3
Received 5 December 1997/Accepted 6 February 1998
Human T-lymphotropic virus type 1 (HTLV-1) and HTLV-2 differ in
pathogenicity in vivo. HTLV-1 causes leukemia and neurologic and
inflammatory diseases, whereas HTLV-2 is less clearly associated with
human disease. Both retroviruses transform human T cells in vitro, and
transformation by HTLV-1 was found to be associated with the
constitutive activation of the Jak/STAT pathway. To assess whether
HTLV-2 transformation may also result in constitutive activation of the
Jak/STAT pathway, six interleukin-2-independent, HTLV-2-transformed
T-cell lines were analyzed for the presence of activated Jak and STAT
proteins by electrophoretic mobility shift assay. In addition, the
phosphorylation status of Jak and STAT proteins was assessed directly
by immunoprecipitation and immunoblotting with an antiphosphotyrosine
antibody. Jak/STAT proteins were not found to be constitutively
activated in any of the T-cell lines infected by the type 2 human and
nonhuman primate viruses, suggesting that HTLV-2 and the cognate virus simian T-lymphotropic virus type 2 from Pan paniscus
transform T cells in vitro by mechanisms at least partially different
from those used by HTLV-1.
*
Corresponding author. Mailing address: Basic Research
Laboratory, Bldg. 37, Room 6A09, National Cancer Institute, National Institutes of Health, 37 Convent Dr. MSC 4255, Bethesda, MD 20892-4255. Phone: (301) 496-2655. Fax: (301) 496-8394. E-mail:
jmulloy{at}helix.nih.gov.
Present address: DNAX, Palo Alto, CA 94304.

Present address: Department of Genetics, Duke University Medical
Center, Durham, NC 27710.
§
Present address: Departments of Veterinary Biosciences and Medical
Microbiology & Immunology, The Ohio State University, Columbus,
OH
43210.
J Virol, May 1998, p. 4408-4412, Vol. 72, No. 5
0022-538X/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.
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