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Special Issue "Recent Advances in HTLV Research 2015"
Deadline for manuscript submissions: closed (1 October 2015).
A printed edition of this Special Issue is available here.
Institute for Molecular Virology, University of Minnesota, 18-242 Moos Tower, 515 Delaware St. SE, Minneapolis, MN 55455, USA
Interests: antiretroviral; nucleoside; mutation; drug synergy; therapeutic indices
Special Issues and Collections in MDPI journals
The human cancer-causing retroviruses—i.e., human T-cell leukemia virus types 1 and 2 (HTLV-1 and HTLV-2)—were both discovered over three decades ago. About 14 million people are infected with HTLV-1 and many millions with HTLV-2 worldwide. HTLV-1 is associated with the T-lymphocytic malignancy called adult T-cell leukemia/lymphoma (ATLL) in about 2 percent of individuals infected, and another 2 to 3 percent of individuals develop a neurologic disorder called HTLV-associated myelopathy (HAM). HTLV-2 causes HAM in approximately 1 to 2 percent of infected individuals, but does not cause ATLL. HTLV-1 and HTLV-2 have served as excellent models for the study of the epidemiology and pathogenesis of virus-associated cancers as well as autoimmune conditions such as multiple sclerosis. Recently, two new members—HTLV-3 and HTLV-4—have been discovered in bushmeat hunters from central Africa, which emphasizes the urgent need for continual surveillance for new human retroviruses and their capacity to cause disease.
The viral oncoprotein Tax-1 is encoded by HTLV-1 and is both necessary and sufficient for viral transformation, and Tax-2 is encoded by HTLV-2 and in animal models does not induce tumors. The HTLVs encode for other regulatory proteins, including the HTLV-1 basic leucine zipper factor (HBZ), which inhibits Tax-mediated gene expression and is encoded as an anti-sense viral transcript. The HTLV-1 p30II protein can act as an agonist of Tax-mediated transcription and serves as a multifunctional repressor of cellular gene expression.
Leukemogenesis mediated by HTLV-1 remains an intensive area of investigation. The focus of current research remains on the Tax effects on cellular transformation, the consequences of perturbing cell cycle control and genome stability, the role of HBZ and p30II on viral pathogenesis, HTLV-1 latency and reactivation, as well as therapeutic approaches. The study of HAM pathogenesis has great potential as a model for neuroimmunologic dieseases. New and exciting progress is being made in the basic understanding of viral replication of the HTLVs, particularly in virus assembly and particle structure.
Important public health issues remain open issues to be addressed in spite of the basic epidemiology of HTLV-1 and HTLV-2 being reasonably well defined—i.e., emergence patterns in new host populations, transmission prevention, improved blood donor screening, and potential human transmission of HTLV-3 and HTLV-4. Clinical research is needed in developing potential HTLV-1 and HTLV-2 vaccines, as well as development of treatment options for ATLL and HAM. This ‘recent advances issue’ contains both reviews and updates on research that encompasses these areas.
Prof. Louis M. Mansky
Manuscript Submission Information
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- adult T-cell leukemia