Primary Sjogren's syndrome with antibodies to HTLV-I: clinical and laboratory features.

Eguchi, Katsuyuki; Matsuoka, Naoki; Ida, Hiroaki; Nakashima, Masahiro; Sakai, Masahiro; Sakito, S; Kawakami, Atsushi; Terada, Kaoru; Shimada, H; Kawabe, Yojiro

doi:10.1136/ard.51.6.769

Cited by 154 publications

(87 citation statements)

References 31 publications

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“…We did not find any specific association with class I1 HLA antigen expression and sicca syndrome in HCV-positive patients compared with HCV-negative patients. Other viruses have a salivary gland tropism: HCV, Epstein-Barr virus, and human T lymphotropic virus type I (HTLV-I) genes have been found in this tissue (28)(29)(30)(31). Moreover, a possible retroviral etiology of Sjogren's syndrome was suggested by the presence of antibodies against the retroviral protein p24 in 30% of the patients studied (32).…”

Section: Discussionmentioning

confidence: 99%

Sicca syndrome associated with hepatitis C virus infection

Jørgensen

Legouffe

Perney

et al. 1996

Arthritis & Rheumatism

135

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Objective. To determine the prevalence of hepatitis C virus (HCV) infection in patients with sicca syndrome, and to determine the clinical, immunologic, and genetic characteristics of sicca syndrome associated with HCV.Methods. We conducted a prospective study in a university hospital immunology-rheumatology department. Sixty-two consecutive patients with sicca syndrome according to the European criteria for Sjogren's syndrome were included. HCV infection was diagnosed in patients with positive recombinant immunoblot assay findings and the presence of viral RNA in serum and saliva. Rheumatoid factor (RF), cryoglobulins, antinuclear antibodies, and anti-SS-NSS-B antibodies were sought. HLA typing was performed on all patients.Results. The prevalence of HCV infection in patients with sicca syndrome was 19%. The incidence of neurologic involvement was significantly increased in patients with sicca syndrome associated with HCV infection (24% versus 4%; P c 0.03), as was elevations in transaminase levels (87.5% versus 16%; P < 0.0001). RF and cryoglobulins were more frequent in HCV-positive sicca syndrome patients (62% versus 30%; P C 0.03, and 56% versus 10%; P c 0.001, respectively). In contrast, anti-SS-NSS-B antibodies were present in 38% of HCVnegative sicca syndrome patients, but in only 1 HCVpositive sicca syndrome patient (P c 0.01). No significant difference in HLA type was observed. Viral RNA

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Section: Discussionmentioning

confidence: 99%

Sicca syndrome associated with hepatitis C virus infection

Jørgensen

Legouffe

Perney

et al. 1996

Arthritis & Rheumatism

135

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“…Furthermore, this virus has been associated, though to a lesser extent, to the development of a variety of in¯ammatory diseases (Eguchi et al, 1992;LaGrenade et al, 1990;Mattos et al, 1993;Mochizuki et al, 1994;Sato et al, 1991;Sherman et al, 1995). Among the 15 ± 25 million individuals infected worldwide, approximately 3 ± 5% will develop ATLL, depending on as yet unknown cofactors.…”

Section: Introductionmentioning

confidence: 99%

High circulating proviral load with oligoclonal expansion of HTLV-1 bearing T cells in HTLV-1 carriers with strongyloidiasis

et al. 2000

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Adult T cell leukemia (ATLL) develops in 3 ± 5% of HTLV-1 carriers after a long period of latency during which a persistent polyclonal expansion of HTLV-1 infected lymphocytes is observed in all individuals. This incubation period is signi®cantly shortened in HTLV-1 carrier with Strongyloides stercoralis (Ss) infection, suggesting that Ss could be a cofactor of ATLL. As an increased T cell proliferation at the asymptomatic stage of HTLV-1 infection could increase the risk of malignant transformation, the e ect of Ss infection on infected T lymphocytes was assessed in vivo in HTLV-1 asymptomatic carriers. After real-time quantitative PCR, the mean circulating HTLV-1 proviral load was more than ®ve times higher in HTLV-1 carriers with stongyloidiasis than in HTLV-1+ individuals without Ss infection (P50.009). This increased proviral load was found to result from the extensive proliferation of a restricted number of infected clones, i.e. from oligoclonal expansion, as evidenced by the semiquantitative ampli®-cation of HTLV-1¯anking sequences. The positive e ect of Ss on clonal expansion was reversible under e ective treatment of strongyloidiasis in one patient with parasitological cure whereas no signi®cant modi®cation of the HTLV-1 replication pattern was observed in an additional case with strongyloidiasis treatment failure. Therefore, Ss stimulates the oligoclonal proliferation of HTLV-1 infected cells in HTLV-1 asymptomatic carriers in vivo. This is thought to account for the shortened period of latency observed in ATLL patients with strongyloidiasis. Oncogene (2000) 19, 4954 ± 4960.

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“…However, serum antibodies of SS and SLE patients show a marked discordance between reactivity to these known autoantigens and reactivity to HIV Gag proteins (15,17). There is a region in the CA protein retroviruses known as the major homology region that is highly conserved among retroviruses, including IAP and human endogenous retroviruses.…”

Section: Can Findings Of Htlv Tax Expression In Ss Patients Be Generamentioning

confidence: 99%

New evidence for involvement of retroviruses in sjögren's syndrome and other autoimmune diseases

Garry¹

1994

Arthritis & Rheumatism

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Primary Sjogren's syndrome with antibodies to HTLV-I: clinical and laboratory features.

Cited by 154 publications

References 31 publications

Sicca syndrome associated with hepatitis C virus infection

Sicca syndrome associated with hepatitis C virus infection

High circulating proviral load with oligoclonal expansion of HTLV-1 bearing T cells in HTLV-1 carriers with strongyloidiasis

New evidence for involvement of retroviruses in sjögren's syndrome and other autoimmune diseases

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