Increased HTLV‐I proviral DNA in HTLV‐I–associated myelopathy: A quantitative polymerase chain reaction study

Jun‐ichi ‐i Kira, Yoshio Koyanagi, Takeshi Yamada, Yasuto Itoyama, Ikuo Goto, Naoki Yamamoto, Hiroyuki Sasaki, Yoshiyuki Sakaki

Research output: Contribution to journalArticle

143 Citations (Scopus)

Abstract

Using the polymerase chain reaction, we quantitated the amount of human T‐lymphotropic virus type I (HTLV‐I) proviral DNA in peripheral blood mononuclear cells from 18 patients with HTLV‐I–associated myelopathy/tropical spastic paraparesis; 17 HTLV‐I carriers without HTLV‐I–associated myelopathy/tropical spastic paraparesis, with or without other autoimmune or inflammatory diseases; and 19 seronegative control subjects. The HTLV‐I proviral DNA was 10‐ to 100‐fold higher in the patients and in the HTLV‐I carriers without HAM/TSP who had autoimmune or inflammatory diseases than in the carriers without autoimmune or inflammatory diseases. The patients who had had onset of myelopathy at a younger age (15 to 39 years) had an extremely high level of HTLV‐I proviral DNA in the early phase, as compared with findings in those with a late onset of myelopathy (at 44 to 61 years). The large increase in HTLV‐I proviral DNA in peripheral blood mononuclear cells is presumably closely related to the development of autoimmune or inflammatory processes in HTLV‐I carriers, including HTLV‐I–associated myelopathy/tropical spastic paraparesis.

Original languageEnglish
Pages (from-to)194-201
Number of pages8
JournalAnnals of Neurology
Volume29
Issue number2
DOIs
Publication statusPublished - Jan 1 1991

All Science Journal Classification (ASJC) codes

  • Neurology
  • Clinical Neurology

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