AIDS-Associated Infections in Salivary Glands: Autopsy Survey of 60 Cases

Wagner, Randall P.; Tian, Haoyu; McPherson, Marcia J.; Latham, Patricia S.; Orenstein, Jan M.

doi:10.1093/clinids/22.2.369

Cited by 25 publications

(19 citation statements)

References 15 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Restriction of CMV replication to (a segment of) ductal cells in the rat model is in concert with the data obtained in the guinea-pig infection model using guinea-pig CMV (GPCMV), in which infection was limited to ductal segments [5,22,23,25]. In humans, CMV-infected ductal cells and acinar cells were found [24,39,45,50]. In mice, only infected acinar cells were described [26,27,28,29,31,34,36].…”

Section: Discussionsupporting

confidence: 65%

Rat cytomegalovirus replication in the salivary glands is exclusively confined to striated duct cells

Kloover¹,

Hillebrands

Wit

et al. 2000

Virchows Archiv

View full text Add to dashboard Cite

The salivary gland is the preferred organ for cytomegalovirus (CMV) replication and viral persistence. In order to identify the nature of infected cells and to study viral replication in more detail, several experiments were conducted. Using the rat CMV (RCMV) model, acutely infected young adult rats (6 weeks of age) and new-born rats (3 days of age) were infected, and submandibular, parotid and sublingual glands were harvested at different time points after infection. For identification of the nature of infected cells, immunohistochemistry, in situ hybridisation and electron microscopic techniques were used. In young adult animals, the submandibular gland was the preferred organ for RCMV replication. The parotid and sublingual glands contained fewer viruses than the submandibular gland. In contrast, in new-born rats, the main site of RCMV replication was the sublingual gland, while the submandibular and parotid glands contained low amounts of virus. No virus could be detected in the parotid glands. In all glands of RCMV-infected animals, the infection was exclusively confined to striated duct cells. Infection resulted in a cellular inflammatory response which was mostly located in the interlobular duct region, whereas only few inflammatory cells were found in the neighbourhood of infected striated duct cells. This phenomenon may contribute to the long persistence of the virus in this organ.

show abstract

Section: Discussionsupporting

confidence: 65%

Rat cytomegalovirus replication in the salivary glands is exclusively confined to striated duct cells

Kloover¹,

Hillebrands

Wit

et al. 2000

Virchows Archiv

View full text Add to dashboard Cite

show abstract

“…Human CMV (hCMV), both active and latent, has a particular tropism for salivary glands (Wagner et al, 1996; Nichols and Boeckh, 2000). In the immunocompromised patient, hCMV is a common cause of opportunistic infections, and subsequent morbidity and mortality (Kim et al, 2010; Mori and Kato, 2010).…”

Section: Discussionmentioning

confidence: 99%

“…As with other herpesviruses, hCMV has the ability to establish lifelong persistence and latent infection following primary exposure (Nichols and Boeckh, 2000), salivary glands being the primary site of both (Wagner et al, 1996; Nichols and Boeckh, 2000). hCMV shed in saliva from infected salivary glands are a key source for the etiology of oral and systematic disease in immunocompromised patients (Correia-Silva et al, 2007, 2010).…”

Section: Introductionmentioning

confidence: 99%

Small molecule inhibitors of the host cell COX/AREG/EGFR/ERK pathway attenuate cytomegalovirus-induced pathogenesis

Melnick¹,

Abichaker²,

Htet³

et al. 2011

Experimental and Molecular Pathology

View full text Add to dashboard Cite

As with other herpesviruses, human cytomegalovirus (hCMV) has the ability to establish lifelong persistence and latent infection following primary exposure, salivary glands (SMGs) being the primary site of both. In the immunocompromised patient, hCMV is a common cause of opportunistic infections, and subsequent morbidity and mortality. Elucidating the molecular pathogenesis of CMV-induced disease is critical to the development of more effective and safer drug therapies. In the present study, we used a novel mouse postnatal SMG organ culture model of mCMV-induced dysplasia to investigate a candidate signaling network suggested by our prior studies (COX-2/AREG/EGFR/ERK). The objective was to employ small molecule inhibitors to target several key steps in the autocrine loop, and in this way ameliorate pathology. Our results indicate that upregulation of ERK phosphorylation is necessary for initial mCMV-induced pathogenesis, and that ErbB receptor family phosphorylation and downstream signaling are highly relevant targets for drug discovery.

show abstract

“…There was a 100% infection of the CEM SS cells as detected by the p24 antigen assay. Although the reason is not clear, it is possible that HIV infection induces changes of the salivary glands which results in a decline in the amount of saliva and a change in its constituents [10]. This in turn may affect the glycosylation pattern or sugar composition of the salivary mucins, and if inhibition of the virus is through aggregation by the carbohydrate side chains, and if changes in these sugar side chains occurs as a result of infection [11], it is conceivable that this is the reason for the inability of mucins from HIV positive individuals to inhibit the virus in an in vitro assay.…”

Section: Discussionmentioning

confidence: 99%

Anti-HIV-1 activity of salivary MUC5B and MUC7 mucins from HIV patients with different CD4 counts

Habte

Beer

Lotz

et al. 2010

Virol J

View full text Add to dashboard Cite

BackgroundWe have previously shown that MUC5B and MUC7 mucins from saliva of HIV negative individuals inhibit HIV-1 activity by 100% in an in vitro assay. The purpose of this subsequent study was to investigate whether MUC5B and MUC7 from saliva of HIV patients or with full blown AIDS had a similar inhibitory activity against the virus.MethodsSalivary MUC5B and MUC7 from HIV patients with different CD4 counts (< 200, 200-400 and > 400) were incubated with HIV-1 prior to infection of the human T lymphoblastoid cell line (CEM SS cells). Cells were then cultured and viral replication was measured by a qualitative p24 antigen assay. The size, charge and immunoreactivity of mucins from HIV negative and positive individuals was also analysed by SDS-PAGE, Western blot and ELISA respectively.ResultsIt was shown that irrespective of their CD4 counts both MUC5B and MUC7 from HIV patients, unlike the MUC5B and MUC7 from HIV negative individuals, did not inhibit HIV-1 activity. Size, charge and immunoreactivity differences between the mucins from HIV negative and positive individuals and among the mucins from HIV patients of different CD4 count was observed by SDS-PAGE, Western blot and ELISA.ConclusionsPurified salivary mucins from HIV positive patients do not inhibit the AIDS virus in an in vitro assay. Although the reason for the inability of mucins from infected individuals to inhibit the virus is not known, it is likely that there is an alteration of the glycosylation pattern, and therefore of charge of mucin, in HIV positive patients. The ability to inhibit the virus by aggregation by sugar chains is thus diminished.

show abstract

AIDS-Associated Infections in Salivary Glands: Autopsy Survey of 60 Cases

Cited by 25 publications

References 15 publications

Rat cytomegalovirus replication in the salivary glands is exclusively confined to striated duct cells

Rat cytomegalovirus replication in the salivary glands is exclusively confined to striated duct cells

Small molecule inhibitors of the host cell COX/AREG/EGFR/ERK pathway attenuate cytomegalovirus-induced pathogenesis

Anti-HIV-1 activity of salivary MUC5B and MUC7 mucins from HIV patients with different CD4 counts

Contact Info

Product

Resources

About