HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Yamamoto, N. Articles by Hinuma, Y. Search for Related Content PubMed PubMed Citation Articles by Yamamoto, N. Articles by Hinuma, Y. Agricola Articles by Yamamoto, N. Articles by Hinuma, Y.

Viral Aetiology of Adult T-Cell Leukaemia

¹ Department of Virology and Parasitology, Yamaguchi University School of Medicine, Ube, Yamaguchi 755
and² Institute for Virus Research, Kyoto University, Sakyo-ku, Kyoto 606, Japan

Overall conclusions: Regarding the cause of leukaemias or malignant lymphomas, several advances in viral oncology and immunology have merged recently, resulting in a heightened appreciation of the associations between viral infection, immunodeficiency and genetic predisposition. In humans, EBV infection has been discussed thoroughly from these standpoints in relation to BL, X-linked lymphoproliferative syndrome, ataxia telangiectasia and malignant lymphomas after organ transplantations (Purtilo et al., 1984). In a previous section describing possible mechanisms of leukaemogenesis of ATL we discussed mainly transformation at the cellular level and not at the level of the host organism. It is apparent, however, that the fate of the transformed cell at the cellular level will be determined eventually by confrontation with the various immunological barriers of the host. Variation at the cellular level, of course, should be closely related to a changed response to the host immune mechanism. Cytogenetic alterations most probably endow transformed cells not only with a growth advantage at the cellular level but also with an ability to escape the immune surveillance of the host. The results described in this context clearly indicate that HTLV/ATLV is a prerequisite for the occurrence of ATL. It is also obvious, however, that this disease is ‘a chronic malignancy’ which requires a long period of time between viral infection and the occurrence of disease. This strongly indicates that some forces operate to select out a single cell and to initiate its monoclonal growth from the population of the cells which had been infected polyclonally with HTLV/ATLV. Although HTLV/ATLV is one of the major factors in the development of ATL, one or more additional factors seem to be necessary. Such factors can be assumed to be both exogenous and endogenous. It appears to us that ATL carcinogenesis results from the interaction of HTLV/ATLV with various biological, physical and chemical factors in the environment (Yamamoto, 1984).

Keywords: ATL, aetiology, human retrovirus

This article has been cited by other articles:

				K. Hieshima, D. Nagakubo, T. Nakayama, A.-K. Shirakawa, Z. Jin, and O. Yoshie Tax-Inducible Production of CC Chemokine Ligand 22 by Human T Cell Leukemia Virus Type 1 (HTLV-1)-Infected T Cells Promotes Preferential Transmission of HTLV-1 to CCR4-Expressing CD4+ T Cells J. Immunol., January 15, 2008; 180(2): 931 - 939. [Abstract] [Full Text] [PDF]

				O. Yoshie, R. Fujisawa, T. Nakayama, H. Harasawa, H. Tago, D. Izawa, K. Hieshima, Y. Tatsumi, K. Matsushima, H. Hasegawa, et al. Frequent expression of CCR4 in adult T-cell leukemia and human T-cell leukemia virus type 1-transformed T cells Blood, March 1, 2002; 99(5): 1505 - 1511. [Abstract] [Full Text] [PDF]