Detection of cytomegalovirus and Epstein‐Barr virus in labial salivary glands in Sjogren's syndrome and non‐specific sialadenitis

Maitland, Norman J.; Flint, Stephen; Scully, Crispian; Crean, St John

doi:10.1111/j.1600-0714.1995.tb01187.x

Cited by 31 publications

(17 citation statements)

References 41 publications

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“…Several studies have suggested an association between SS and, mainly, hepatitis C virus (7)(8)(9) and viruses of the herpes family, including Epstein-Barr virus (EBV) (10)(11)(12)(13)(14)(15) and cytomegalovirus (CMV) (1 6,17). Several studies have suggested an association between SS and, mainly, hepatitis C virus (7)(8)(9) and viruses of the herpes family, including Epstein-Barr virus (EBV) (10)(11)(12)(13)(14)(15) and cytomegalovirus (CMV) (1 6,17).…”

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confidence: 99%

Murine cytomegalovirus induces a Sj�gren's syndrome-like disease in C57Bl/6-lpr/lpr mice

Fleck

Kern

Zhou

et al. 1998

Arthritis & Rheumatism

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Objective. To analyze Fas and tumor necrosis factor receptor I (TNFRI) apoptosis pathways in sali-vary gland inflammatory disease induced by murine cytomegaloviru s (MCMV) infection. Methods. Four different strains of mice (C57B1/6 [B6]-+/ + , Fas-deficient B6-lprllpr, TNFRI-deficient B6-tnfrl"", and B6-tnfrlo"-lpr/lpr mice) were infected intra-peritoneally with the Smith strain of MCMV (1 X lo5 plaque-forming units). Viral load was determined by a plaque assay, inflammation and apoptosis by immuno-histochemistry and staining with terminal dUTP nick-end labeling, and autoantibodies by enzyme-linked im-munosorbent assay. Results. Infectious MCMV was not detectable by day 100. Although all MCMV-infected mice developed acute sialadenitis by day 28, a chronic (>lo0 days), severe salivary gland inflammation and anti-Ro and anti-La antibodies developed only in the B6-Zprllpr mice. Apoptotic cells were detected during the acute, but not the chronic, phase of inflammation. Conclusion. Both Fas-and TNFRI-mediated ap-optosis contribute to the clearance of MCMV-infected cells in the salivary glands. However, because Fas-. ~ ~~

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confidence: 99%

Murine cytomegalovirus induces a Sj�gren's syndrome-like disease in C57Bl/6-lpr/lpr mice

Fleck

Kern

Zhou

et al. 1998

Arthritis & Rheumatism

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“…Sicca syndrome may be associated with the herpesviruses CMV and Epstein-Barr virus (EBV) (11,29,45,55). Diffuse infiltrative lymphocytosis syndrome (DILS), a disorder of HIVpositive patients, is characterized in part by sicca symptoms (15).…”

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confidence: 99%

Natural Killer Cells Regulate Murine Cytomegalovirus-Induced Sialadenitis and Salivary Gland Disease

Carroll

Lundgren

Wei

et al. 2012

J Virol

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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.

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“…Whereas the limited data for CMV are not supporting a role in pSS [9], there are multiple studies of EBV infection in pSS.…”

Section: Detection Of Dna Viruses In the Salivary Glands Of Pss Patientsmentioning

confidence: 98%

“…Subsequent studies yielded variable results on the rate of EBV DNA detection by conventional polymerase chain reaction (PCR) or in situ hybridization, ranging from no difference [9,12] to statistically significantly increased rate of detection in pSS and secondary SS (sSS) patients vs controls [13][14][15][16].…”

Section: Detection Of Dna Viruses In the Salivary Glands Of Pss Patientsmentioning

confidence: 99%

Persistent Viral Infection in Primary Sjogren’s Syndrome: Review and Perspectives

Triantafyllopoulou

Moutsopoulos

2007

Clinic Rev Allerg Immunol

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Exocrine gland pathology in primary Sjogren's syndrome is characterized by destruction of acinar epithelial cells and chronic lymphocytic infiltrates surrounding ductal epithelial cells. These cells seem to be activated, as it is inferred by their immunophenotype. The cause of this activation and the chronic inflammatory response that targets epithelial cells remain unknown. Here, we will review the evidence pointing to a persistent viral infection as a probable cause of primary Sjogren's syndrome and discuss potential directions for future research.

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Detection of cytomegalovirus and Epstein‐Barr virus in labial salivary glands in Sjogren's syndrome and non‐specific sialadenitis

Cited by 31 publications

References 41 publications

Murine cytomegalovirus induces a Sj�gren's syndrome-like disease in C57Bl/6-lpr/lpr mice

Murine cytomegalovirus induces a Sj�gren's syndrome-like disease in C57Bl/6-lpr/lpr mice

Natural Killer Cells Regulate Murine Cytomegalovirus-Induced Sialadenitis and Salivary Gland Disease

Persistent Viral Infection in Primary Sjogren’s Syndrome: Review and Perspectives

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