A search for human T‐cell leukemia virus type I in the lesions of patients with tropical spastic paraparesis and polymyositis

Abstract

We searched for the presence of human T-cell leukemia virus type I (HTLV-I) sequences in central nervous system and muscle lesions of 3 patients with tropical spastic paraparesis/HTLV-I-associated myelopathy (TSP/HAM) and 3 patients with HTLV-I-associated polymyositis. Proviral DNA coding for the Tax protein was found by polymerase chain reaction amplification in DNA extracted from lesions of every patient with TSP/HAM or HTLV-I-associated polymyositis. In contrast, viral RNA was found occasionally by in situ hybridization in muscle lesions of some patients with polymyositis, but was never found in central nervous system lesions of TSP/HAM patients.

Human T Cell Leukemia Virus Type I Expression in Salivary Glands of Infected Patients

“…The virus has been detected in lymph nodes of ATL patients, circulating dendritic cells, and lymphocyte progenitors in bone marrow [1]. Outside the immune system, low levels of HTLV-I antigen and mRNA have been found in central nervous system and muscle lesions of TSP/HAM and HTLV-I-induced polymyositis [8,10,11]. Excepted for a few infected astrocytes in a case of HAM/TSP [12], infected cells in the central nervous system appear to be infiltrating CD4 lymphocytes.…”

“…sections using TRI-Reagent (Molecular Research Center, Cincinnati). cDNA was synthesized from 10 mg of RNA with avian myeloblastosis virus reverse transcriptase and hexamers as described [8]. Amplifications were performed with Taq DNA polymerase in 100 mL of standard buffer, with 200-500 ng of DNA or cDNA.…”

“…DNA was extracted from paraffin sections as previously described [8]. RNA was extracted from frozen unfixed Table 1.…”

“…ISH was performed as described with a 35 S-labeled antisense riboprobe corresponding to the tax region [8]. HTLV-Iinfected MT2 cells were used as the positive control.…”

Polimiosite associada a infecção por HTLV-I: relato de caso

“…Já foi constatada a ocorrência de predominância de linfócitos CD8 no endomísio, com macrófagos e linfócitos CD4 no infiltrado que circunda as fibras musculares sadias comprometendo o MHC-I ( major histocompatibility complex class I) 12 ; como também já foi verificado que o vírus não penetra nas fibras musculares e sim nos macrófagos endomisiais, não sendo observada a presença de antígenos HTLV-I em pacientes portadores de PM 12 . Estes achados dão conta de que a PM associada a infecção pelo HTLV-I não decorre de comprometimento direto da fibra muscular pelo vírus; os miotubos são resistentes à infecção, mas devido a um processo imunopatológico restrito desencadeado pela liberação de citocinas (interferon, TNF-alfa) e interleucinas-2, as quais interferem no MHC-I, proporcionando reconhecimento estranho das células T e produzindo resposta autoimune anormal 12,13 . Este mecanismo também está presente em outras doenças imunomediadas associadas a infecção pelo HTLV-I, como a mielopatia, polineurite e a sindrome de Sjögren 12 .…”