Correlation between Infections with Different Genotypes of Human Cytomegalovirus and Epstein-Barr Virus in Subgingival Samples and Periodontal Status of Patients

Abstract

Accumulating evidence indicates that herpesviruses may be putative pathogens in various types of periodontal diseases. The present study was performed to examine infections with different genotypes of human cytomegalovirus (HCMV) and Epstein-Barr virus (EBV) in subgingival samples from a Chinese population and to analyze the correlation with periodontal status. A nested PCR assay was used to identify the presence of HCMV, EBV type 1 (EBV-1), and EBV-2; and the amplicons were further analyzed by restriction fragment length polymorphism analysis. HCMV was detected in 79.0% of 143 chronic periodontitis (CP) patients, 78.5% of 65 gingivitis patients, and 76.3% of 76 periodontally healthy individuals, while EBV was found in 63.6%, 32.3%, and 30.3% of the three groups of subjects, respectively. The HCMV-positive PCR products from all the samples were identified as corresponding to gB genotype I (gB-I) or gB-II. HCMV gB-II (62.9%), EBV-1 (43.4%), and EBV-2 (18.2%) were associated with CP at higher frequencies (P < 0.05), whereas HCMV gB-I was more often observed in gingivitis patients (40.0%) and healthy individuals (40.8%) (P < 0.05). Furthermore, a higher rate of coinfection with HCMV and EBV was shown in CP patients (52.4%), especially dual infections with HCMV gB-II and EBV-1 (30.8%) or HCMV gB-II and EBV-2 (12.6%), compared with the rates of single infections with HCMV or EBV (P < 0.05). Infection with HCMV gB-II, EBV-1, or EBV-2 was correlated with higher rates of bleeding on probing (P < 0.05). In patients infected with HCMV gB-II or both HCMV and EBV, including HCMV gB-II and EBV-1, a deeper probing depth or more serious attachment loss was found (P < 0.05). These findings clearly indicate that HCMV gB-II is the dominant genotype detected in subgingival samples in CP. HCMV gB-II infection and HCMV gB-II coinfection with EBV-1 are closely associated with periodontal tissue inflammation and destruction.

Human Cytomegalovirus and Epstein-Barr Virus Genotypes in Apical Periodontitis Lesions

“…Only 2 of 4 HCMV gB genotypes were detected in periapical lesions, gB-I and gB-II. Our results are in accordance with previously reported occurrence of HCMV gB genotypes in generalized chronic periodontitis and periimplantitis tissues (25,26). Similarly, these studies reported the absence of HCMV gB-III and gB-IV in their samples.…”

“…Our results also corroborate some previous findings regarding EBV genotypes in oral pathologies. Wu et al (25) reported the presence of both EBV genotypes in tissue samples of generalized chronic periodontitis, with significantly higher frequencies of EBV-1, whereas Jankovic et al (26) found that EBV-1 was more frequent in samples of periimplantitis and mucositis compared with EBV-2. The occurrence of EBV-2 has been mostly found in immunocompromised patients such as HIV-infected and transplant recipients (24).…”

Prevalence of human cytomegalovirus and Epstein-Barr virus in subgingival plaque at peri-implantitis, mucositis and healthy sites. A pilot study

“…To obtain more precise information about the role of herpesviruses in the etiopathogenesis of peri-implantitis and periodontitis the highlights from the study by WU et al 30 must not be avoided. These findings clearly indicate that HCMV gB-II and EBV-1 are the dominant virus genotypes detected in subgingival samples in aggressive and chronic periodontitis.…”

“…The overall detection rate for HCMV DNA when nested PCR was used at individual sites with periodontitis was similar to the prevelance of CMV in peri-implantitis sites 65% (62% 14 , 64% 4 , 59% 26 , 63% 30 ). EBV DNA was detected in the subgingival plaque of periodontaly diseased sites in approximately 30% and in 8% of healthy sites 11,19,27,30 . In this study the presence of EBV DNA in peri-implantitis sites was higher at 45%.…”

Positively Selected Sites at HCMV gB Furin Processing Region and Their Effects in Cleavage Efficiency

“…While a number of studies found some possible association between gB genotype and infection course (Fries et al, 1994; Shepp et al, 1996; Rasmussen et al, 1997; Meyer-König et al, 1998; Cunha Ade et al, 2002; Wu et al, 2007; Roubalová et al, 2010; Madi et al, 2011; Xia et al, 2012; Vogel et al, 2013), other studies did not found any correlation (Lurain et al, 1999; Trincado et al, 2000; Sarcinella et al, 2002; Carraro and Granato, 2003; Tarragó et al, 2003; Tanaka et al, 2005; Yamamoto et al, 2007; Görzer et al, 2010; Wu et al, 2011; Paradowska et al, 2012). Some reports also indicated that infection with mixed genotypes could be related to disease progression (Sarcinella et al, 2002; Coaquette et al, 2004; Pang et al, 2008; Deckers et al, 2009).…”