© 2001 by Oxford University Press
Journal of the National Cancer Institute, Vol. 93, No. 5, 336-337,
March 7, 2001
© 2001 Oxford University Press
EDITORIAL |
Sorting Out Mutations in Human T-Cell Leukemia Virus Type 1 Proviruses During In Vivo Clonal Expansion
Affiliations of author: Department of Molecular Virology, Immunology, and Medical Genetics, Center for Retrovirus Research, The Arthur James Cancer Hospital and Solove Research Institute, and Comprehensive Cancer Center, Ohio State University Medical Center, Columbus.
Correspondence to: Louis M. Mansky, Ph.D., Department of Molecular Virology, Immunology, and Medical Genetics, 2078 Graves Hall, 333 West 10th Ave., Columbus, OH 43210 (e-mail: mansky.3@osu.edu).
Retroviruses, like all RNA viruses, have reputations that precede them regarding genetic variability. The lack of proofreading and subsequent high error rates of reverse transcriptase have been linked directly to the tremendous diversity observed in retrovirus populations. Although this association is not straightforward, a fair amount of evidence supports the conclusion that reverse transcriptase plays a major role in generating virus diversity (1). Retrovirus variation relies on the mutation rate per replication cycle, the number of replication cycles, the rate of mutation fixation, and the rate of recombination (2).
Human T-cell leukemia virus type 1 (HTLV-1), the first pathogenic human retrovirus discovered, is the etiologic agent of an adult T-cell leukemia/lymphoma (ATLL) and of a chronic progressive neuromyelopathy, tropical spastic paraparesis (TSP)/HTLV-1-associated myelopathy (HAM). During the asymptomatic phase of infection, proviral loads are generally lower than they are once TSP/HAM develops, even though proviruses can be
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