Volume 36, Issue 6 pp. 651-655
Article
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Prevalence of HTLV-I in arctic regions

Marjorie Robert-Guroff

Corresponding Author

Marjorie Robert-Guroff

Laboratory of Tumor Cell Biology, Bethesda, MD 20205

Environmental Epidemiology Branch, National Cancer Institute, Bethesda, MD 20205

Laboratory of Tumor Cell Biology Radiumstationen, DK-8000 Aarhus C, DenmarkSearch for more papers by this author
Jeffrey Clark

Jeffrey Clark

Arctic Investigations Laboratory, Centers for Disease Control, Anchorage, AK 99501

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Anne P. Lanier

Anne P. Lanier

Department of Medical Genetics, University of Umea, Umea, Sweden

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Gunhild Beckman

Gunhild Beckman

Institute of Cancer Research, Radiumstationen, DK-8000 Aarhus C, Denmark

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Mads Melbye

Mads Melbye

Environmental Epidemiology Branch, National Cancer Institute, Bethesda, MD 20205

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Peter Ebbesen

Peter Ebbesen

Environmental Epidemiology Branch, National Cancer Institute, Bethesda, MD 20205

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William A. Blattner

William A. Blattner

Arctic Investigations Laboratory, Centers for Disease Control, Anchorage, AK 99501

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Robert C. Gallo

Robert C. Gallo

Laboratory of Tumor Cell Biology, Bethesda, MD 20205

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First published: 15 December 1985
Citations: 26

Abstract

Sera of native inhabitants of Arctic regions were assayed for antibodies to HTLV-I by the ELISA technique followed by competition experiments to confirm antibody specificity. Residents of 7 widely separated Alaskan villages exhibited prevalence rates of 0 to 12% for HTLV-I antibodies. Less than 1 % of Greenland Eskimos were HTLV-I antibody-positive. Residents of 3 northern Swedish regions ranged in HTLV-I antibody prevalence from 0 to 5%. Sera of healthy native inhabitants of Alaska and northern Sweden were similarly assayed for antibodies to HTLV-II. No additional sera were shown to be positive for HTLV-II antibodies. While some of the HTLV-I antibody-positive sera exhibited cross-reactivity with HTLV-II antigens, competition experiments using disrupted HTLV-II or purified HTLV-I p24 as test antigens indicated that the primary antibody response in all cases tested was elicited by HTLV-I. Our results show that HTLV-I distribution is not restricted to endemic areas in warm, humid climates, but extends to Arctic regions. Within these regions, HTLV-I exhibits the same restricted distribution seen in other areas where virus infection is prevalent. The Arctic does not seem to be a reservoir for HTLV-II infection. The origin of HTLV-I in Arctic areas is not known. One may speculate that foreign visitors introduced the virus into Aleut and Lapp populations, and that it has been maintained there and restricted in its distribution as a result of close familial relationships.

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