title: Increased proviral load in HTLV-1-infected patients with rheumatoid arthritis or connective tissue disease.
abstract: BACKGROUND
  Human T-lymphotropic virus type 1 (HTLV-1) proviral load is related to the development of HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP) and has also been shown to be elevated in the peripheral blood in HTLV-1-infected patients with uveitis or alveolitis. Increased proliferation of HTLV-1-infected cells in, or migration of such cells into, the central nervous system is also seen in HAM/TSP. In the present study, we evaluated the proviral load in a cohort of HTLV-1-infected patients with arthritic conditions.
  
  
  RESULTS
  HTLV-1 proviral load in the peripheral blood from 12 patients with RA and 6 patients with connective tissue disease was significantly higher than that in matched asymptomatic HTLV-1 carriers, but similar to that in matched HAM/TSP controls. HAM/TSP was seen in one-third of the HTLV-1-infected patients with RA or connective tissue disease, but did not account for the higher proviral load compared to the asymptomatic carrier group. The proviral load was increased in the synovial fluid and tissue from an HTLV-1-infected patient with RA, the values suggesting that the majority of infiltrated cells were HTLV-1-infected. In the peripheral blood from HTLV-1-infected patients with RA or connective tissue disease, HTLV-1 proviral load correlated with the percentages of memory CD4+ T cells and activated T cells, and these percentages were shown to be markedly higher in the synovial fluid than in the peripheral blood in an HTLV-1-infected patient with RA.
  
  
  CONCLUSIONS
  These biological findings are consistent with a role of the retrovirus in the development of arthritis in HTLV-1-infected patients. A high level of HTLV-1-infected lymphocytes in the peripheral blood and their accumulation in situ might play a central role in the pathogenesis of HTLV-1-associated inflammatory disorders. Alternatively, the autoimmune arthritis, its etiological factors or treatments might secondarily enhance HTLV-1 proviral load.
authors.affiliation: INSERM UMR433, antenne du Centre hospitalier universitaire de Fort-de-France, Martinique. mariayakova@hotmail.com
authors.forename: Maria
authors.initials: M
authors.lastname: Yakova
authors.forename: Agnès
authors.initials: A
authors.lastname: Lézin
authors.forename: Fabienne
authors.initials: F
authors.lastname: Dantin
authors.forename: Gisèle
authors.initials: G
authors.lastname: Lagathu
authors.forename: Stéphane
authors.initials: S
authors.lastname: Olindo
authors.forename: Georges
authors.initials: G
authors.lastname: Jean-Baptiste
authors.forename: Serge
authors.initials: S
authors.lastname: Arfi
authors.forename: Raymond
authors.initials: R
authors.lastname: Césaire
mesh_terms: D000328:Adult; D000368:Aged; D001172:Arthritis, Rheumatoid / Q000150:complications / Q000821:virology*; D002353:Carrier State / Q000821:virology; D003240:Connective Tissue Diseases / Q000150:complications / Q000821:virology*; D004279:DNA, Viral / Q000097:blood; D005260:Female; D015490:HTLV-I Infections / Q000150:complications / Q000821:virology*; D015368:Human T-lymphotropic virus 1 / Q000502:physiology*; D006801:Humans; D008297:Male; D008875:Middle Aged; D015493:Paraparesis, Tropical Spastic / Q000821:virology; D011533:Proviruses / Q000502:physiology*; D019562:Viral Load
chemical_list: D004279:DNA, Viral