It has been established that the human T cell lymphotropic viruses type I and II (HTLV-I and HTLV-II) are both present in some indigenous peoples of the Americas. While HTLV-I has been identified in coastal British Columbia Indians (BCIs), HTLV-II has not been previously reported in the BCIs or other Canadian Amerindians. The prevalence of HTLV-I and HTLV-II in these populations has not been extensively studied. In this article, we examine a group of BCIs from Vancouver Island who belong to the Nuu-Chah-Nulth and are known to have an increased incidence of rheumatic disease. In 494 serum samples from this tribe, the levels of prevalence of HTLV-I and HTLV-II were 2.8 and 1.6%, respectively. No association could be made between arthropathy and HTLV-I infection. In addition, we characterized an HTLV-II isolate of a BCI from the coastal mainland of British Columbia and with a history of intravenous drug abuse. This case represents the first molecular characterization of a Canadian Amerindian HTLV-II isolate: a subtype IIa virus with phylogenetic affinity for intravenous drug user isolates and containing an extended form of the Tax protein. These results are consistent either with this strain having been sampled from a polymorphic ancestral pool of HTLV-II that gave rise to the current epidemic spread of this virus by intravenous drug use and sexual transmission, or with its being "back-transmitted" into the BC Amerindian population in association with intravenous drug use.
Sera from various Swiss population groups were tested for antibodies against the human T-cell leukemia virus type I (HTLV-I). Particle agglutination and ELISA were performed for screening; Western blot was done for confirmation. True-positive sera were found at a prevalence of 0.12% in a cohort of 846 individuals at risk for AIDS tested in 1984-1985. Prevalences of 0.35% were found among 575 HIV-I positives tested in 1987, and of 1.3% among 292 HIV-I positives of a different group tested in 1988. The 6 positives found in our study represent the first cases of HTLV-I infection, or HIV-I/HTLV-I double infection, diagnosed in Switzerland. In addition, high proportions of sera, regardless of whether they were from normal blood donors, HIV-positives, or individuals at risk for AIDS, had antibodies that reacted weakly with one or several proteins of the size of viral gag proteins. The prevalence of such antibodies in normal donors was in the range of 10 to 40%, depending on the strictness of interpretation. Competition Western blots performed with some of these sera showed that these antibodies reacted with HTLV-I, but not with HIV-I or cellular antigens, and had a lower affinity to HTLV-I proteins than the antibodies of human or goat antisera. The results indicate that these antibodies may be induced by agents immunologically related to, but different from, HTLV-I, which are highly prevalent in the Swiss population. Oligopeptide stretches with sequence homology to HTLV-I are known to exist in various normal body proteins, several infectious agents including common viruses and protozoa, but the results might also indicate the existence of additional human retroviruses. Screening of blood donors with sensitive tests for antibodies to HTLV-I might produce an unacceptably high rate of false-positive results, if stringent rules of interpretation analogous to those common in HIV screening are not used.
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