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Bronchoalveolar lymphocytosis correlates with human T lymphotropic virus type I (HTLV-I) proviral DNA load in HTLV-I carriers
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  1. S Mori1,
  2. A Mizoguchi2,
  3. M Kawabata1,
  4. H Fukunaga2,
  5. K Usuku1,
  6. I Maruyama3,
  7. M Osame1
  1. 1Third Department of Internal Medicine, Kagoshima University School of Medicine, 8-35-1 Sakuragaoka, Kagoshima 890-8520, Japan
  2. 2Department of Respiratory Medicine, Minamikyusyu National, Sanatorium, 1882 Kida, Kajikicho, Kagoshima 899-5241, Japan
  3. 3Department of Laboratory Medicine, Kagoshima University School of Medicine, 8-35-1 Sakuragaoka, Kagoshima 890-8520, Japan
  1. Correspondence to:
    Dr S Mori
    Department of Internal Medicine, Southern Region Hospital, 220 Midori Machi, Makurazaki City, Kagoshima 898-0011, Japan; msirmsi.biglobe.ne.jp

Abstract

Background: A study was undertaken to investigate the pathogenesis of pulmonary involvement in human T lymphotropic virus type I (HTLV-I) carriers.

Methods: The bronchoalveolar lavage (BAL) cell profile of 30 HTLV-I carriers (15 asymptomatic HTLV-I carriers (AHCs) and 15 symptomatic HTLV-I carriers (SHCs)) with chronic inflammatory diseases of respiratory tract and eight patients with HTLV-I associated myelopathy/tropical spastic paraparesis (HAM/TSP) was investigated. The HTLV-I proviral deoxyribonucleic acid (DNA) load in peripheral blood mononuclear cells (PBMCs) and BAL fluid from HTLV-I carriers was estimated using the quantitative polymerase chain reaction method and the correlation between the lymphocyte number in BAL fluid and the HTLV-I proviral DNA load in PBMCs and BAL fluid was examined.

Results: The percentage of lymphocytes in BAL fluid was increased (>18%) in 11 of 30 HTLV-I carriers although there was no significant difference compared with control subjects. In HTLV-I carriers the lymphocyte number in BAL fluid correlated well with the copy number of HTLV-I proviral DNA in PBMCs. In addition, the copy number of HTLV-I proviral DNA in BAL fluid correlated well with the number of lymphocytes (both CD4+ and CD8+ cells) in BAL fluid.

Conclusions: These findings suggest that pulmonary lymphocytosis can occur in a subset of HTLV-I carriers without HAM/TSP and that the increased HTLV-I proviral DNA load may be implicated in the pathogenesis of pulmonary involvement in HTLV-I carriers.

  • AHC, asymptomatic HTLV-I carrier
  • BAL, bronchoalveolar lavage
  • HAM/TSP, HTLV-I associated myelopathy/tropical spastic paraparesis
  • HTLV-I, human T lymphotropic virus type I
  • PBMC, peripheral blood mononuclear cell
  • PCR, polymerase chain reaction
  • SHC, symptomatic HTLV-I carrier
  • bronchoalveolar lymphocytosis
  • human T lymphotropic virus type I (HTLV-I)

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