AI Article Synopsis
- The study compares two HTLV-I-infected rabbit T cell lines: one (RH/K34) that causes leukemia and another (RH/K30) that results in a non-symptomatic infection.
- It was found that the protooncogene Vav is constantly phosphorylated in the leukemia-causing cell line (RH/K34), but not in the asymptomatic one (RH/K30).
- The differences in Vav phosphorylation between the lines are attributed to specific sequences in the viral genome that regulate this process, suggesting that viral control of Vav might be linked to the development of leukemia in infected cells.
Article Abstract
Human T cell leukemia virus I (HTLV-I) causes acute leukemic disease in a low percentage of infected individuals through obscure mechanisms. Our studies compare two rabbit HTLV-I-infected T cell lines: one, RH/K34, causes lethal experimental leukemia and the other, RH/K30, mediates asymptomatic infection. We show herein that the product of the protooncogene vav is constitutively Tyr-phosphorylated in RH/K34 but not in RH/K30. A role for the retrovirus in phosphorylation of Vav was assigned by transfection experiments with molecular clones of HTLV-I derived from the two lines. The HTLV-I molecular clone from RH/K30, but not that from RH/K34, down-regulates Vav phosphorylation in a Herpesvirus ateles-transformed T cell line. Use of recombinant virus clones revealed that a pX region sequence differing by two nucleotides between the two clones mediates this down-regulation. Because Vav is involved in T cell signaling and Vav phosphorylation occurs upon activation of T cells, control of the activation state of Vav by viral proteins may relate to the leukemogenic potential of certain HTLV-I-infected cells.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC19190 | PMC |
| http://dx.doi.org/10.1073/pnas.95.4.1782 | DOI Listing |
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