Cytomegalovirus: a virus of increasing relevance to oral medicine and pathology

Epstein, Joel B.; Scully, Crispian

doi:10.1111/j.1600-0714.1993.tb01087.x

Cited by 24 publications

(9 citation statements)

References 92 publications

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“…20,87 There are suggestions that chronically elevated basal endogenous glucocorticoid levels, even at concentrations that might appear within the physiologic range as observed in the impoverished children (Table 3), promote a shift from a type 1 to a type 2 cytokine production profile. 88,89 Glucocorticoid excess enhances replication of a number of latent viruses, [90][91][92] and promotes increased susceptibility of the oral mucosa to viral infections. 91 Increased steroid levels in the mouth could also serve as a rich nutrient source for anaerobes.…”

Section: Discussionmentioning

confidence: 99%

“…88,89 Glucocorticoid excess enhances replication of a number of latent viruses, [90][91][92] and promotes increased susceptibility of the oral mucosa to viral infections. 91 Increased steroid levels in the mouth could also serve as a rich nutrient source for anaerobes. 20 Stress also impairs salivary gland function, reducing the volume of saliva and the availability of salivary proteins, which are protective against the growth and pathogenicity of oral microflora.…”

Section: Discussionmentioning

confidence: 99%

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Pathogenesis of cancrum oris (noma): confounding interactions of malnutrition with infection.

Enwonwu¹,

Falkler²,

Idigbe³

et al. 1999

The American Journal of Tropical Medicine and Hygiene

107

129

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Abstract. This study showed that impoverished Nigerian children at risk for cancrum oris (noma) had significantly reduced plasma concentrations of zinc (Ͻ 10.8 mol/L), retinol (Ͻ 1.05 mol/L), ascorbate (Ͻ 11 mol/L), and the essential amino acids, with prominently increased plasma and saliva levels of free cortisol, compared with their healthy counterparts. The nutrient deficiencies, in concert with previously reported widespread viral infections (measles, herpesviruses) in the children, would impair oral mucosal immunity. We postulate, subject to additional studies, that evolution of the oral mucosal ulcers including acute necrotizing gingivitis to noma is triggered by a consortium of microorganisms of which Fusobacterium necrophorum is a key component. Fusobacterium necrophorum elaborates several dermonecrotic toxic metabolites and is acquired by the impoverished children via fecal contamination resulting from shared residential facilities with animals and very poor environmental sanitation.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Pathogenesis of cancrum oris (noma): confounding interactions of malnutrition with infection.

Enwonwu¹,

Falkler²,

Idigbe³

et al. 1999

The American Journal of Tropical Medicine and Hygiene

107

129

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“…After the primary infection, which is usually subclinical and occurs at an early age, HCMV infection is thought to persist for the life of the host [Weller, 1971]. A number of reports have suggested that the virus may persist in a wide variety of cells, including lymphocytes, monocytes, and cells of the oropharynx, kidneys, lungs, liver, blood vessels, reproductive organs, and/or various secretory glands [Roche et al, 1981;Rice et al, 1984;Dudding and Garnett, 1987;Grundy, 1990;Mocarski et al, 1990;Nelson et al, 1990;Epstein and Scully, 1993;Kowalik et al, 1994]. Particularly germane to the possibility that HCMV may be involved in affecting the sensitivity to tobacco carcinogens are a series of reports from our laboratory and others indicating that HCMV infection in vitro induces genetic alterations and potentiates the genotoxic effects of some chemicals.…”

Section: Introductionmentioning

confidence: 98%

Differential mutagen sensitivity of peripheral blood lymphocytes from smokers and nonsmokers: Effect of human cytomegalovirus infection

Albrecht

Deng

Abdel‐Rahman

et al. 2004

Environ and Mol Mutagen

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We used the mutagen sensitivity assay to test the hypothesis that human cytomegalovirus (HCMV) infection modifies the sensitivity of cells to genetic damage from genotoxic agents. Chromosome aberration (CA) frequency in peripheral blood lymphocytes (PBLs) from 20 smokers who were matched with 20 nonsmokers by age (+/- 5 years), sex, and ethnicity was evaluated following in vitro exposure to bleomycin and/or HCMV infection. Bleomycin induced significant (P < 0.05) concentration-dependent increases in the frequency of aberrant cells, chromatid-type damage (breaks), and chromosome-type aberrations (deletions, rearrangements) in PBLs. The baseline (background) CA frequency was similar in both smokers and nonsmokers. Significantly higher frequencies of aberrant cells (P < 0.05) were observed in PBLs from smokers compared to nonsmokers at all bleomycin concentrations tested (10, 30 and 100 microg/ml). Infection of PBLs with HCMV induced a significant (P < 0.05) twofold increase in the frequency of CA (primarily chromatid breaks) in PBLs, regardless of the smoking status. PBLs from smokers and nonsmokers infected with HCMV prior to challenge with bleomycin demonstrated significant (P < 0.05) concentration-dependent increases in the levels of aberrant cells, chromatid-type damage (breaks), and chromosome-type aberrations (deletions, rearrangements) compared to noninfected cells challenged with bleomycin. The frequency of induced CA was consistently higher for PBLs derived from smokers relative to nonsmokers (P = 0.06 and 0.002). These data indicate that, individually, both smoking and HCMV infection significantly enhance the sensitivity of PBLs to bleomycin-induced genetic damage. More importantly, the data also suggest that smoking and HCMV infection interact synergistically to enhance the sensitivity of PBLs to such damage.

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“…Some infections, parti-cularly gram-negative, viral and fungal infections, are more frequent and severe in glucocorticoid-treated patients (Dale and Petersdorf, 1973). Glucocorticoid excess enhances replication of a number of latent viruses (Scully and Porter, 1994;Glaser et al, 1994), promotes increased susceptibility of the oral mucosa to viral infections (Epstein and Scully, 1993) and promotes a shift from a Type 1 to a Type 2 cytokine production profile (Clerici and Shearer, 1993).…”

Section: Discussion Of Proposed Pathogenesis Of Nomamentioning

confidence: 99%

Noma (cancrum oris): questions and answers

et al. 1999

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Noma (cancrum oris) is an infectious disease which destroys the oro‐facial tissues and other neighboring structures in its fulminating course. It affects predominantly children aged 2–16 years in sub‐Saharan Africa where the estimated frequency in some communities may vary from one to seven cases per 1000 children. The key risk factors are poverty, malnutrition, poor oral hygiene, deplorable environmental sanitation, close residential proximity to livestock, and infectious diseases, particularly measleS. Malnutrition acts synergistically with endemic infections in promoting an immuno‐deficient state, and noma results from the interaction of general and local factors with a weakened immune system as the common denominator. Acute necrotizing gingivitis (ANG) is considered the antecedent lesion. Current studies suggest that evolution of ANG to noma requires infection by a consortium of microorganisms with Fusobacterium necrophorum and Prevotella intermedia as the suspected key playerS. Without appropriate treatment, mortality rate is 70–90%.Survivors suffer the twofold affliction of oro‐facial disfigurement and functional impairment. Reconstructive surgery of the resulting deformity is time‐consuming and financially prohibitive for the victims who are poor.

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Cytomegalovirus: a virus of increasing relevance to oral medicine and pathology

Cited by 24 publications

References 92 publications

Pathogenesis of cancrum oris (noma): confounding interactions of malnutrition with infection.

Pathogenesis of cancrum oris (noma): confounding interactions of malnutrition with infection.

Differential mutagen sensitivity of peripheral blood lymphocytes from smokers and nonsmokers: Effect of human cytomegalovirus infection

Noma (cancrum oris): questions and answers

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