SJOGRENS-SYNDROME AND VIRUS

Virus are suspected to play a role in triggering lymphoid proliferation observed in Sjorgren's syndrome (SS). In this paper, attention is focused on the potential role of herpes virus, retrovirus and hepatitis C virus (HCV) in the pathogenesis of SS. Genes and proteins of Epstein-Barr virus (EBV) are detected in epithelial cells of salivary of lacrymal glands more often in SS patients than in controls. However, it could just be a consequence of the destruction of the glands by another mechanism. Endogenous retroviral sequences are detected with a higher frequence in salivary glands of SS patients, than in controls. Sicca syndrome may occur in HIV, HTLV-I and HCV-infected patients. We found the expression of the tax gene of HTLV-I in epithelial cells of salivary glands from two patients without any evidence of HTLV-I-associated disease and without any seric anti-HTLV-I antibodies. Anti-SSA and anti-SSB antibodies are usually not detected in serum of patients with sicca syndrome occurring during evolution of recognized viral diseases. Thus, this kind of sicca syndrome could be a little different from classical auto-immune SS. However, it is tempting to consider oropharynx like a site of latency of a lot of virus which could infect salivary epithelial cells. In some people with a particular genetic background, this could lead to a lymphoid proliferation and, secondary, to the destruction of the glands.