Detection of human T-cell leukemia virus antibodies in a Japanese T-cell leukemia patient with hypercalcemia
Y NakaoSakan MaedaShinya MatsudaT TakuboT MasaokaShunichi ShiozawaT SugiyamaYôhei ItôPrem S. SarinRobert C. Gallo
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A T-cell line (KH-2) from a Japanese T-cell leukemia patient with hypercalcemia has been characterized and shown to be similar in its properties to Human T-cell leukemia virus (HTLV)-positive T-cell lines from T-cell leukemia patients from different parts of the world. The HTLV isolated from the Japanese T-cell leukemia patient with hypercalcemia belongs to the HTLV family and has properties similar to HTLV from T-cell leukemia patients from the United States, Israel, and the Caribbean.Provirus
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We report the detection of human T‐lymphotropic virus type I (HTLV‐I) genomic sequences by polymerase chain reaction in lymphocyte cultures of three unrelated native Solomon Islanders, including a patient with HTLV‐I myeloneuropathy, residing in widely separated regions. In addition, we have isolated HTLV‐I from T‐cell lines derived from two of these individuals. Virus‐specific proteins of 15, 19, 24, 46 and 53 kilodaltons were detected by immunofluorescence and Western immunoblot, using serum from a Colombian patient with HTLV‐I myeloneuropathy, sera from HTLV‐I‐infected rabbits, and monoclonal and polyclonal antibodies against HTLV‐I gag and env gene products. Amplification of HTLV‐I gag, pol and env sequences by polymerase chain reaction confirmed that the viral isolates were HTLV‐I, not HTLV‐II. Our data clearly demonstrate that HTLV‐I does exist in Melanesia. Although the Solomon Islands viral isolates resemble prototype strains of HTLV‐I, we believe they represent variants of HTLV‐I, particularly in the light of our recent isolation of an HTLV‐I variant from Papua New Guinea. Nucleotide sequence analysis of these viral strains, now in progress, should clarify the molecular epidemiology and phylogeny of HTLV‐I.
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Sixteen human T-cell lines were studied for the expression of a cell-adhesion molecule ICAM-1 and its counter-receptor LFA-1. The cell lines included 3 human T-cell-leukemia-virus-type-I (HTLV-1)-negative cell lines derived from acute lymphoblastic leukemia (ALL) and 13 HTLV-1-positive cell lines, 7 of them established from cord- or peripheral-blood T cells by in vitro transformation with HTLV-1, 2 derived from HTLV-1 carriers, and 4 derived from patients with adult T-cell leukemia (ATL). In sharp contrast to a basal level of ICAM-1 in 3 HTLV-1-negative ALL cell lines, strong induction of ICAM-1 was seen in all HTLV-1-positive T-cell lines except for MT-1, one of the 4 ATL cell lines used in the present study. On the other hand, the expression of LFA-1 (CD11a and CD18) was more or less similar among the cell lines with and without HTLV-1. Interestingly, however, 3 out of 4 ATL cell lines (TL-Om1, H582, HUT102) revealed striking depression of LFA-1 expression. Several lines of evidence strongly argued against direct involvement of the viral transactivator p40tax or some autocrine cytokines in the induction of ICAM-1 in HTLV-1-positive T-cell lines. It was also found that ICAM-1 and LFA-1 were involved in syncytium formation induced in the co-culture of HTLV-1-positive and HTLV-1-negative human T-cell lines. Implications of constitutive expression of ICAM-1 for certain clinical manifestations of ATL and of depression of either ICAM-1 or LFA-1 during progression of ATL are discussed.
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Abstract Previously, we reported that cells of the human T‐cell lymphotropic virus type 1 (HTLV‐I)‐transformed lines MT‐2 and MT‐4 were extensively killed by infection with AIDS retrovirus HTLY‐III. We have investigated this phenomenon more systematically using light and electron microscopy as well as immunofluorescence. The cell lines used in the present studies included 14 of those carrying not only human HTLY‐1 but also related simian agents and 6 HTLY‐I‐negative T‐ and B‐cell lines. The results showed that the cytocidal effects occurred in the HTLY‐I‐transformed cell lines exclusively and were not present in further subcultures. In these cell lines the cytotoxic response was closely correlated with the induction of HTLV‐III antigens after virus infection. However, cells of 6 HTLV‐I‐free lines were not killed to a marked extent by HTLV‐III and were passaged as continuous producers of AIDS virus. Only 2 cell lines were resistant to the cytocidal effect of HTLV‐III among 14 HTLV‐I carrying cell lines. They were also resistant to the replication of infected HTLV‐III. This AIDS virus‐specific cytotoxic effect observed in HTLV‐I‐transformed cell lines did not appear to be associated with gene expression of the gag and pXs region of HTLV‐I genomes. This result may indicate that HTLV‐III specifically interferes with some steps of HTLV‐I transformation.
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Human T‐cell leukemia virus type 1 (HTLV–1) is an etiologic agent of adult T‐cell leukemia/lymphoma and other HTLV‐1–associated diseases. However, the interaction between HTLV–1 and T cells in the pathogenesis of these diseases is poorly understood. Mouse cells have been reported to be resistant to cell‐free HTLV–1 infection. However, we recently reported that HTLV–1 DNA could be observed 24 h after cell‐free HTLV–1 infection of mouse cell lines. To understand HTLV–1 replication in these cells in detail, we concentrated the virus produced from c77 feline kidney cell line and established an efficient infection system. The amounts of adsorption of HTLV–1 are larger in mouse T cell lines, EL4 and RLml, than those in human T cell lines, Molt4 and HUT78, and are similar to that in human kidney cell line, 293T. Unexpectedly, however, the amounts of entry of HTLV–1 are about 10–fold larger in the two mouse cell lines than those in the three human cell lines employed. Moreover, viral DNA was detectable from 1 h in EL4 and RLml cells, but only from 2–3 h in 293T, Molt4 and HUT78 cells. However, the amount of viral DNA in EL4 cells became smaller than that in Molt4 cells. HTLV–1 expression could be detected until day 1–2 in RLml and EL4 cells, and until day 4 in Molt4 cells. Our results suggest that mouse cell experiments would give useful information to dissect the early steps of cell‐free HTLV–1 infection.
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This report describes serologic evidence for a virus similar to that known as simian T-lymphotropic virus type III of African Green monkeys (STLV-III AGM ) infecting apparently healthy people in Senegal, West Africa, and the isolation of virus from these individuals. Serum samples from selected healthy West African people showed unusual serologic profiles when tested with antigens of HTLV-III/LAV, the etiologic agent of AIDS, and of STLV-III AGM . The samples reacted strongly with all of the major viral antigens of STLV-III AGM but showed variable or no reactivity with the major viral antigens of HTLV-III/LAV by radioimmunoprecipitation and sodium dodecyl sulfate-polyacrylamide gel electrophoresis. A new human T-lymphotropic virus (HTLV-IV) isolated from these people was grown in vitro and shown to have retroviral type particles, growth characteristics, and major viral proteins similar to those of the STLV-III and HTLV-III/LAV group of retroviruses. The gp120/160, gp32, p64, p55, p53, p24, and p15 proteins precipitated were the same size as and reactive with STLV-III AGM proteins. The serologic data suggest that this virus shares more common epitopes with STLV-III AGM than with the prototype HTLV-III/LAV that infects people in the United States and Europe. Further study of this virus and of the origin of the HTLV-III/LAV group of viruses may expand our understanding of the human AIDS virus.
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Human T-lymphotropic virus
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