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High Incidence of Antibodies to HTLV-I "tax" in Blood Relatives of Adult T Cell Leukemia Patients
Akihiko Okayama, Yi-ming A. Chen, Nobuyoshi Tachibana, Shigemasa Shioiri, Tun-Hou Lee, Kazunori Tsuda and Max Essex
The Journal of Infectious Diseases
Vol. 163, No. 1 (Jan., 1991), pp. 47-52
Published by: Oxford University Press
Stable URL: http://www.jstor.org/stable/30119508
Page Count: 6
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Adult T cell leukemia (ATL) is caused by the human T cell leukemia virus type I (HTLV-I). Although the mechanisms of the leukemogenic process are unknown, the tax gene may have a role in this process. Because clustering occurs with HTLV-I and ATL, members of ATL families were examined for antibodies to the tax protein and compared with matched HTLV-I-positive blood donors. To investigate the antibody response to this protein, a plasmid, pBHX-4, was constructed to express a recombinant tax protein (Max). For ATL patients and their HTLV-I antibody-positive blood relatives, the rate of seroreactivity with the r-tax protein was 67.3% (35/52), compared with 51.6% (97/188) for HTLV-I antibody-positive control blood donors (> .05). The difference between direct offspring of ATL patients and matched HTLV-I blood donors was even greater (84.2% [16/19] vs. 44.2% [42/95]; > .005). Thus, tax antibody positivity in direct offspring of ATL patients may reflect differences in time or route of HTLV-I infection. Alternatively, it might reflect genetic differences in host susceptibility or virus strain.
The Journal of Infectious Diseases © 1991 Oxford University Press