Human T cell leukemia virus type-1 (HTLV-1) is the first discovered human retrovirus. HTLV-1 infects at least 10 million people worldwide. 3-5 % of infected people develop a severe, still untreatable, form of blood cancer (Adult T-cell leukemia(lymphoma). HTLV-1 infection may also cause chronic inflammatory diseases including HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP). Molecular studies of HTLV-1 viral proteins have provided new information about functions of specific viral proteins such as Tax-1 and HBZ in the infected cells. Tax-1 and HBZ are strongly involved in the mechanism of HTLV-1-mediated oncogenesis, although the intimate molecular mechanisms of their action, particularly for HBZ, is still not completely clarified. The immune response against the virus plays a critical role in prevention and/or protection of the pathological consequences of infection, although aspects of immunity and particularly the role of lymphocyte subpopulations and their products in either protecting or accelerating disease onset deserves further elucidation.
The goal of this Topic is to provide a clear and up-to-date information on the present status of HTLV-1 infection. Many unanswered questions remain in relation to the virus life cycle and the mechanism of latent infection, aspects of the immune response to the virus (intrinsic, innate and adaptive), the possible new avenues of prevention and treatment of the disease.
Themes to be addressed are: infection and pathogenesis; immune response to HTLV-1 infection, molecular and cellular correlates of oncogenicity. Papers are expected to cover the biology of the infected cells as results of combined effects of viral factors not only in T cells but also in myeloid cells, the immune response in the various phases of infection from asymptomatic carriers to patients affected by inflammatory processes and finally in cancer patients. Furthermore, contributions are expected to cover the topic of remote effects in uninfected cells in the body through cytokines and/or viral exosomes. Contributions are also expected to cover studies in animal models such as monkeys and mice to understand the virus life cycles.
Both original research papers and reviews are accepted.
Human T cell leukemia virus type-1 (HTLV-1) is the first discovered human retrovirus. HTLV-1 infects at least 10 million people worldwide. 3-5 % of infected people develop a severe, still untreatable, form of blood cancer (Adult T-cell leukemia(lymphoma). HTLV-1 infection may also cause chronic inflammatory diseases including HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP). Molecular studies of HTLV-1 viral proteins have provided new information about functions of specific viral proteins such as Tax-1 and HBZ in the infected cells. Tax-1 and HBZ are strongly involved in the mechanism of HTLV-1-mediated oncogenesis, although the intimate molecular mechanisms of their action, particularly for HBZ, is still not completely clarified. The immune response against the virus plays a critical role in prevention and/or protection of the pathological consequences of infection, although aspects of immunity and particularly the role of lymphocyte subpopulations and their products in either protecting or accelerating disease onset deserves further elucidation.
The goal of this Topic is to provide a clear and up-to-date information on the present status of HTLV-1 infection. Many unanswered questions remain in relation to the virus life cycle and the mechanism of latent infection, aspects of the immune response to the virus (intrinsic, innate and adaptive), the possible new avenues of prevention and treatment of the disease.
Themes to be addressed are: infection and pathogenesis; immune response to HTLV-1 infection, molecular and cellular correlates of oncogenicity. Papers are expected to cover the biology of the infected cells as results of combined effects of viral factors not only in T cells but also in myeloid cells, the immune response in the various phases of infection from asymptomatic carriers to patients affected by inflammatory processes and finally in cancer patients. Furthermore, contributions are expected to cover the topic of remote effects in uninfected cells in the body through cytokines and/or viral exosomes. Contributions are also expected to cover studies in animal models such as monkeys and mice to understand the virus life cycles.
Both original research papers and reviews are accepted.
