Article

Paucity of Sjogren-like syndrome in a cohort of HIV-1-positive patients in the HAART era. Part II.

Academic Department of Pathophysiology, AIDS Unit, School of Medicine, National and Kapodistrian University of Athens, Greece.
Rheumatology (Impact Factor: 4.21). 11/2003; 42(10):1164-7. DOI: 10.1093/rheumatology/keg316
Source: PubMed

ABSTRACT This study was performed in order to investigate the prevalence of Sjögren-like syndrome (SLS) in the highly active anti-retroviral therapy (HAART) era in a cohort of HIV-1-positive Greek patients.
One hundred and thirty-one unselected patients were screened by the validated European Union (EU) criteria for Sjögren's syndrome. Of the 31 who gave a positive EU-validated questionnaire, 17 consented to undergo minor salivary gland biopsy and other tests.
Only two patients had a positive salivary gland biopsy and both belonged to the non-compliant HAART group, whereas none of the compliant HAART patients had histological findings.
It is concluded that SLS, the prevalence of which in the pre-HAART era was 7.8%, has disappeared, possibly as a result of the protective action of HAART.

0 Bookmarks
 · 
90 Views
  • [Show abstract] [Hide abstract]
    ABSTRACT: Ferritin-based nanoprobe (FBNP) hydrogel provides solutions to some of the traditional problems of bioassays. The schematic shows 3D and highly specific multiplex assays of markers for AIDS and Sjögren's syndrome using quantum-dot based reporters with different fluorescence emissions for the two syndromes. The advantages of using a hydrogel include that the stability of FBNPs is significantly enhanced within the hydrogel, FBNPs are distributed evenly throughout the hydrogel matrix, and the amount of FBNPs within the hydrogel can be well controlled.
    Advanced Materials 07/2012; 24(35):4739-44, 4730. · 14.83 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Autoimmune rheumatic diseases, such as RA and SLE, are caused by genetic, hormonal and environmental factors. Human Endogenous Retroviruses (HERVs) may be triggers of autoimmune rheumatic disease. HERVs are fossil viruses that began to be integrated into the human genome some 30-40 million years ago and now make up 8% of the genome. Evidence suggests HERVs may cause RA and SLE, among other rheumatic diseases. The key mechanisms by which HERVS are postulated to cause disease include molecular mimicry and immune dysregulation. Identification of HERVs in RA and SLE could lead to novel treatments for these chronic conditions. This review summarises the evidence for HERVs as contributors to autoimmune rheumatic disease and the clinical implications and mechanisms of pathogenesis are discussed.
    The Open Rheumatology Journal 01/2013; 7:13-21.
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: The transmission of herpesviruses depends on viral shedding at mucosal surfaces. The salivary gland represents a major site of persistent viral replication for many viruses, including cytomegalovirus. We established a mouse model of salivary gland dysfunction after acute viral infection and investigated the cellular requirements for the loss of secretion. Murine cytomegalovirus (MCMV) infection severely impaired saliva secretion independently of salivary gland virus levels. Lymphocytes or circulating monocytes/macrophages were not required for secretory dysfunction. Dysfunction occurred before glandular inflammation, suggesting that a soluble mediator initiated the disruption of acinar cell function. Despite genetic differences in innate resistance to MCMV, NK cells protected the host against acinar atrophy and the loss of secretions under conditions of an exceedingly low virus inoculum. NK cells also modulated the type of glandular inflammation after infection, as they prevented an influx of Siglec-F(+) polymorphonuclear leukocytes (PMNs). Therefore, beyond their recognized role in controlling MCMV replication, NK cells preserve organ integrity and function and regulate the innate inflammatory response within the gland.
    Journal of Virology 12/2011; 86(4):2132-42. · 5.08 Impact Factor

Full-text (2 Sources)

Download
4 Downloads
Available from
Sep 22, 2014