Human cytomegalovirus is present in the odontogenic epithelium of ameloblastoma
TL;DR: In this article, the presence of human cytomegalovirus (HCMV) in dentigerous cyst (DC), odontogenic keratocyst (OKC), and ameloblastoma (AB) was investigated.
Abstract: Background: The factor behind the activation of the remnant odontogenic tissues and development of odontogenic cysts and tumors is poorly understood.This study aimed to investigate the presence of human cytomegalovirus (HCMV) in dentigerous cyst (DC), odontogenic keratocyst (OKC), and ameloblastoma (AB). Methods: The study included 41 samples, which distributed into DC (n=13), OKC (n=12), and AB (n=16). Conventional PCR assay and IHC analysis were used to detect the HCMV-DNA and HCMV glycoprotein B (HCMV-gB) respectively. Results: HCMV-DNA was detected in 10 samples (62.5%) of AB, four samples (30.8%) of DC, and three samples (25 %) of OKC respectively (χ2 test = 1.195, p= 0.247). Meanwhile, HCMV-gB was found in 12 (75%) of AB, in 2 (15.4%) of DC, and absent in OKC (0.0%) (χ2 test = 4.122, p= 0.042). Conclusions: The high prevalence of HCMV inside the odontogenic epithelium of AB could indicate a possible role of the virus in the oncogenesis and/or oncomodulation of the AB. Additionally, we recommend the IHC for the detection of HCMV in the odontogenic tumors like AB.
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TL;DR: The human cytomegalovirus (HCMV) can infect a remarkably broad cell range within its host, including parenchymal cells and connective tissue cells of virtually any organ and various hematopoietic cell types.
Abstract: The human cytomegalovirus (HCMV) can infect a remarkably broad cell range within its host, including parenchymal cells and connective tissue cells of virtually any organ and various hematopoietic cell types. Epithelial cells, endothelial cells, fibroblasts and smooth muscle cells are the predominant targets for virus replication. The pathogenesis of acute HCMV infections is greatly influenced by this broad target cell range. Infection of epithelial cells presumably contributes to inter-host transmission. Infection of endothelial cells and hematopoietic cells facilitates systemic spread within the host. Infection of ubiquitous cell types such as fibroblasts and smooth muscle cells provides the platform for efficient proliferation of the virus. The tropism for endothelial cells, macrophages and dendritic cells varies greatly among different HCMV strains, mostly dependent on alterations within the UL128-131 gene locus. In line with the classification of the respective proteins as structural components of the viral envelope, interstrain differences concerning the infectivity in endothelial cells and macrophages are regulated on the level of viral entry.
360 citations
TL;DR: Beyond the oncomodulation model, the direct transforming role of HMCV-infected cells and the potential classification of HCMV as an oncovirus are assessed.
Abstract: Besides its well-described impact in immunosuppressed patients, the role of human cytomegalovirus (HCMV) in the pathogenesis of cancer has been more recently investigated. In cancer, HCMV could favor the progression and the spread of the tumor, a paradigm named oncomodulation. Although oncomodulation could account for part of the protumoral effect of HCMV, it might not explain the whole impact of HCMV infection on the tumor and the tumoral microenvironment. On the contrary cases have been reported where HCMV infection slows down the progression and the spread of the tumor. In addition, HCMV proteins have oncogenic properties per se, HCMV activates pro-oncogenic pathways in infected cells, and recently the direct transformation of cells following HCMV infection has been described, which gave rise to tumors when injected in mice. Thus, beyond the oncomodulation model, this review will assess the direct transforming role of HMCV-infected cells and the potential classification of HCMV as an oncovirus.
100 citations
TL;DR: Unraveling the etiology and pathogenesis of periapical pathosis may require a broadening of experimental approaches to include studies on interactions among herpesviruses, bacteria, and host immune reactions.
Abstract: Background Much remains to be learned about the etiopathogenesis of periapical pathosis, especially about the molecular events preceding and causing disease onset. Human cytomegalovirus and Epstein-Barr virus, 2 herpesviruses, are discussed in this review as they relate to apical periodontitis in humans. Results Cytomegalovirus or Epstein-Barr virus active infections are detected in more than 90% of granulomas of symptomatic and large periapical lesions. Dual infection with cytomegalovirus and Epstein-Barr virus is closely associated with symptomatic lesions. Herpes simplex virus active infection has no apparent relationship to periapical disease. Discussion The available evidence suggests the involvement of active cytomegalovirus and Epstein-Barr infections in the etiopathogenesis of apical periodontitis. In periapical pathosis, herpesviruses may cause the release of tissue-destructive cytokines, the overgrowth of pathogenic bacteria, and the initiation of cytotoxic or immunopathologic events. Immune impairment resulting from herpesvirus infection may aid bacteria at several stages of the pathogenesis of periapical lesions, including growth in the periapical environment, possible invasion of tissue, and direct damage to tissue. Unraveling the etiology and pathogenesis of periapical pathosis may require a broadening of our experimental approaches to include studies on interactions among herpesviruses, bacteria, and host immune reactions. Understanding the significance of herpesviruses in the development of periapical lesions may aid in the diagnosis, prevention, and treatment of the diseases.
95 citations
TL;DR: The objective was to broadly review the current literature on the prevalence and incidence, clinical manifestations, potential limitations of different diagnostic modalities, prognosis, and therapeutic options of CMV disease in critically ill patients.
Abstract: Cytomegalovirus (CMV) infection is increasingly recognized in critically ill immunocompetent patients. Some studies have demonstrated an association between CMV disease and increased mortality rates, prolonged intensive care unit and hospital length of stay, prolonged mechanical ventilation, and nosocomial infections. However, there is a considerable controversy whether such association represents a causal relationship between CMV disease and unfavorable outcomes or just a marker of the severity of the critical illness. Detection of CMV using polymerase chain reaction and CMV antigenemia is the standard diagnostic approach. CMV may have variety of clinical manifestations reflecting the involvement of different organ systems. Treatment of CMV in critical care is challenging due to diagnostic challenge and drug toxicity, and building predictive model for CMV disease in critical care setting would be promising to identify patients at risk and starting prophylactic therapy. Our objective was to broadly review the current literature on the prevalence and incidence, clinical manifestations, potential limitations of different diagnostic modalities, prognosis, and therapeutic options of CMV disease in critically ill patients.
73 citations
TL;DR: The present data suggest that human cytomegalovirus or Epstein-Barr virus activation participate in the pathogenesis of symptomatic periapical lesions, thereby inducing overgrowth of endodontopathic bacteria and the clinical flare-up of inflammation.
61 citations