HTLV-1-associated inflammatory myopathies: low proviral load and moderate inflammation in 13 patients from West Indies and West Africa.
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Desdouits Marion, Cassar Olivier, Maisonobe Thierry, Desrames Alexandra, Aouba Achille, Hermine Olivier, Mikol Jacqueline, Polivka Marc, Penisson-Besnier Isabelle, Marcorelles Pascale, Zagnoli Fabien, Papo Thomas, Lacour Arnaud, Amoura Zahir, Haroche Julien, Cherin Patrick, Teixeira Antonio, Benveniste Olivier, Herson Serge, Morin Anne-Sophie, Mortreux Franck, Wattel Eric, Huerre Michel, Cumont Marie-Christine, Martin-Latil Sandra, Butler-Browne Gillian, Gout Olivier, Taylor Graham, Gessain Antoine, Ozden Simona, Ceccaldi Pierre-Emmanuel
Аннотация
OBJECTIVES: To characterize the histological and virological features of HAIM patients, in order to better understand the pathogenetic mechanisms and unravel new biological markers of this disease.
STUDY DESIGN: We conducted a retrospective study on 13 patients with HAIM, based on blood and muscle samples. We included blood samples from HTLV-1-infected individuals without myopathy as controls. Muscle biopsies were used for a broad immunohistological evaluation of tissue damage and inflammation, as well as identification of infected cells through in situ hybridization. DNA extracted from patients' PBMC was used to identify the virus genotype by sequencing and to assess the proviral load by quantitative PCR. Anti-viral antibodies in plasma samples were titrated by indirect immunofluorescence.
RESULTS: Patients originate from HTLV-1 endemic areas, the West Indies and West Africa. Histological alterations and inflammation in patients muscles were mostly moderate, with classical features of idiopathic myositis and rare HTLV-1-infected infiltrating cells. In all patients, HTLV-1 belonged to the A subtype, transcontinental subgroup. Anti-HTLV-1 antibodies titers were high, but the proviral load was not elevated compared to asymptomatic HTLV-1 carriers.
CONCLUSION: We show here that muscle inflammation is moderate in HAIM, and accompanied by a low HTLV-1 proviral load, suggesting that the pathogenetic events do not exactly mirror those of other HTLV-1-associated inflammatory diseases.