Increased human T lymphotropic virus type-1 (HTLV-1) proviral DNA in peripheral blood mononuclear cells and bronchoalveolar lavage cells from Japanese patients with HTLV-1-associated myelopathy.

Abstract

Human T lymphotropic virus type-1 (HTLV-1)-associated myelopathy/tropical spastic paraparesis (HAM/TSP) is endemic in tropical areas and in southwestern Japan, and has now been identified among risk groups in the United States and some European countries. Patients with HAM/TSP may also have T lymphocyte alveolitis related to the HTLV-1 infection. To quantify proportions of HTLV-1-infected cells, a fragment of HTLV-1 proviral DNA was amplified from peripheral blood mononuclear cells (PBMC) and bronchoalveolar lavage (BAL) cells obtained from patients with HAM/TSP, non-HAM/TSP HTLV-1 carriers with chronic pulmonary inflammation, and asymptomatic HTLV-1 carriers. The proportion of HTLV-1-infected cells in PBMC from patients with HAM/TSP was much higher (3-30%) than that from asymptomatic HTLV-1 carriers (mostly < 1%), based on findings with the quantitative polymerase chain reaction. In non-HAM/TSP carriers with chronic pulmonary inflammation, HTLV-1-infected cells in PBMC were also increased, but not as markedly as that seen in patients with HAM/TSP. Integration of HTLV-1 was also noted in BAL cells from patients with HAM/TSP or non-HAM/TSP carriers with chronic pulmonary inflammation. However, in patients with HAM/TSP, there was a marked increase in HTLV-1-infected cells in the lung (7.5-30% of BAL cells), as compared with findings in non-HAM/TSP carriers (< 5%). These results suggest that increased HTLV-1 proviral DNA loading may play an important role in the development of T lymphocyte alveolitis and myelopathy in patients with HAM/TSP.