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Table 1 Studies providing evidence on the role of retroviruses in the pathogenesis of Sjögren's syndrome

From: Is Sjögren's syndrome a retroviral disease?

Retrovirus Study Origin Main findings
  [12] USA SS-like illness developed in HTLV-I-infected patients with tropical spastic paraparesis.
  [13] Europe An antigen reactive with a monoclonal antibody to HTLV-I p19 was present in the LSG of patients with SS.
  [14] Japan Thirty-six percent of patients with primary SS were found, by ELISA, to be positive for serum antibodies to HTLV-I.
  [15] Japan Rates of HTLV-1 seroprevalence were 23% (17/74) among patients with SS and 3% (916/27,284) among blood donors. However, the difference between patients with systemic lupus erythematosus and blood donors was insignificant.
  [17] Europe Serum antibodies to HTLV-I were detected in 2 to 5 out of 11 patients with SS.
  [18] Japan HTLV-I-infected T cells expressing TCR with a conserved motif accumulated in both HTLV-I-associated and idiopathic SS
  [19] Japan HTLV-I proviral DNA was present in the nucleus of the infiltrating T cells but not in either the epithelial cells or the acinar cells of the salivary glands of HTLV-I-seropositive patients with SS.
  [20] Japan Definitive SS was diagnosed in 6 patients and probable SS in 2 patients among 10 patients with HAM.
  [21] Japan Definite SS was diagnosed in 13 out of 20 patients with HAM.
  [22] Japan The HTLV-I tax gene, but not the HTLV-I gag, pol, or env genes, was detected in LSG samples from 4 out of 14 patients with SS.
  [23] Europe The HTLV-I tax gene, but not the gag, pol, or env genes, was detected in LSG sections from 2 out of 9 patients with SS and from none of the control subjects.
  [24] Europe The tax gene of HTLV-I was detected in LSG from 15 out of 50 of patients (30%) with SS, 9 out of 32 patients (28%) with other inflammatory processes (3/9 graft-versus-host disease, 5/19 extravasated cysts, and 1/4 sarcoidosis), and only 1 out of 26 patients (4%) with normal LSG.
  [25] Japan The HTLV-I tax gene was detected in LSG of 3 out of 17 seronegative patients (18%) with SS.
  [42] USA An autoimmune exocrinopathy with histopathological findings similar to those of SS was observed in HTLV-1 tax transgenic mice.
  [27] USA An SS-like illness was reported among HIV-1-infected patients.
  [28, 29] USA The DILS was described as a disorder affecting a subgroup of patients with HIV-1 infection.
  [30] Europe The prevalence of DILS among HIV-1-infected patients was 7.79%.
  [31] USA The prevalence of DILS among HIV-1-infected patients was 32.3%.
  [32] USA-Africa The prevalence of DILS in patients from the US was 6%. The prevalence in patients with HIV infection from Cameroon was 48%.
  [33] Europe The prevalence of HIV-1-related SS dropped from 8% in the pre-HAART era to 1.5% in the post-HAART era.
  [34] USA The prevalence of DILS dropped significantly in the post-HAART era.
  [37] USA HIAP-I has been identified in lymphoblastoid cells cocultured with homogenates of salivary glands from patients with SS.
  [40] Europe Novel sequences spanning parts of the protease and reverse transcriptase open reading frames of a retrovirus were detected in LSG tissues of eight patients with SS.
  [41] Europe Two out of 55 LSG samples from patients with SS were positive for HRV-5 proviral DNA.
  1. DILS, diffuse infiltrative lymphocytosis syndrome; ELISA, enzyme linked immunosorbent assay; HAART, highly active anti-retroviral treatment; HAM, HTLV-I (human T lymphotropic virus type 1)-associated myelopathy; HIAP-I, human intracisternal A-type retroviral particle; HIV-1, human immunodeficiency virus-1; HRV-5, human retrovirus-5; HTLV-1, human T lymphotropic virus type 1; LSG, labial salivary gland; SS, Sjögren's syndrome; TCR, T-cell receptor.