Table 2.
Salivary herpesviruses and oral diseases
| Study | Disease | Study material and methods | Study outcome | Comments |
|---|---|---|---|---|
| Şahin et al. (155) | Periodontitis | Whole saliva was collected from 14 systemically healthy periodontitis patients, 15 gingivitis patients and 13 complete denture wearers. Real‐time TaqMan PCR was used for detection of HCMV and EBV DNAs | Salivary HCMV (range, 3.3 × 103–4.2 × 104/ml) was detected in seven (50%) periodontitis patients, but not in any gingivitis or edentulous subjects (P < 0.001). Salivary EBV (range, 3.6 × 102–1.6 × 109/ml) was detected in 11 (79%) periodontitis patients, in five (33%) gingivitis patients and in seven (54%) edentulous subjects (P = 0.076) | Periodontitis lesions seem to constitute the main origin of salivary HCMV, but do not comprise the sole source of salivary EBV |
| Dawson et al. (48) | Periodontitis | Samples of whole saliva and subgingival plaque were collected from 65 adults with chronic periodontitis. Real‐time PCR detection of EBV DNA | Patients exhibiting EBV DNA in saliva were 10 times more likely to have EBV DNA in subgingival plaque than patients lacking EBV DNA in saliva (odds ratio = 10.1, P = 0.0009) | The presence of EBV DNA in saliva and subgingival plaque showed correlation with each other but not with periodontal disease severity |
| Imbronito et al. (84) | Periodontitis | Samples of whole saliva and of subgingival plaque were collected from 40 adults with chronic periodontitis. Nested PCR was used to detect EBV DNA and HCMV DNA | EBV‐1 DNA was detected in 45% of subgingival samples and in 38% of salivary samples. HCMV DNA was detected in 83% of subgingival samples and in 75% of salivary samples | The sensitivity for viral detection in saliva compared with subgingival plaque was low for EBV DNA (22%) and high for HCMV DNA (82%). Oral detection of EBV DNA may require both salivary and subgingival sampling |
| Sugano et al. (181) | Periodontitis | Salivary samples of 33 systemically healthy periodontitis patients, 25–68 years of age. Real‐time PCR was used to detect EBV DNA and Porphyromonas gingivalis | Forty‐nine percent of patients harbored salivary EBV DNA at a concentration of 4.48 ± 2.19 × 105/ml. EBV‐positive patients showed higher mean salivary proportion of P. gingivalis than EBV‐negative patients | P. gingivalis sonicate was able to re‐activate EBV, and P. gingivalis–EBV synergistic interaction may play a pathogenetic role in periodontitis |
| Raggam et al. (144) | Herpetic lesions | Salivary samples from 25 patients with herpetic lesions. Quantification of HSV DNA was based on liquid phase‐based saliva collection and an automated commercial molecular assay | Nineteen samples yielded HSV‐1 DNA (range, 1.2 × 104–2.1 × 105 copies/ml) and two samples yielded HSV‐2 DNA (range, 1.4 × 103–2.2 × 104 copies/ml) | A fully automated diagnostic system may be useful in identifying saliva‐borne viruses |
| Crawford et al. (44) | Infectious mononucleosis | Two‐hundred and forty‐one college students who were EBV‐seronegative at the time of entering college were followed‐up for 3 years | The annual EBV seroconversion rate was 15.2% and the annual mononucleosis rate was 3.7%. The seroconversion rate was 28% for students who had oral sex and 13% for students who did not (not significant) | Having a greater number of sex partners was a highly significant risk factor for EBV seropositivity |
| Abiko et al. (3) | Bell’s palsy | Sixteen patients with Bell’s palsy provided repeat samples of submandibular and parotid saliva from the affected and from the unaffected side. PCR detection of HSV‐1 DNA was carried out | Five patients (31%) showed a high detection rate of HSV DNA for up to 2 weeks after disease onset from the affected side, but a low HSV DNA detection rate from the unaffected side | HSV‐1 re‐activation may be a pathogenic factor in some cases of Bell’s palsy |
| Furuta et al. (62, 63) | Ramsay Hunt syndrome | Forty‐seven patients with the Ramsay Hunt syndrome. Real‐time PCR detection of VZV DNA | Patients with oropharyngeal herpes zoster lesions had a VZV DNA salivary load that was about 10,000 copies higher than patients with herpes zoster lesions of the skin. The salivary VZV copy number ranged from 38 to 1.3 × 106 copies/50 μl | The VZV DNA level in saliva seems to reflect the kinetics of VZV re‐activation in the facial nerve |
| Raggam et al. (144) | Ramsay Hunt syndrome | Ten patients with Ramsay Hunt syndrome. Quantification of VZV DNA was based on liquid phase‐based saliva collection and on an automated commercial molecular assay | Seven salivary samples (70%) yielded VZV DNA (range, 3.3 × 104–5.8 × 105 copies/ml) | A fully automated diagnostic system may be useful in identifying saliva‐borne viruses |
| Griffen et al. (74) | HIV infection | Forty‐one HIV‐1 seropositive persons provided daily swabs from gingiva, buccal mucosa and palate for a median of 61 consecutive days. PCR was used to detect HSV‐1, HSV‐2, EBV and HCMV DNAs | Persons with high EBV DNA shedding rates showed salivary HCMV DNA significantly more often than persons with low EBV DNA shedding rates. HSV DNA oral shedding was observed least frequently | Salivary shedding of herpesviruses was common even in HAART‐treated patients |
EBV, Epstein–Barr virus; HAART, highly active antiretroviral therapy; HCMV, human cytomegalovirus; HIV, human immunodeficiency virus; HSV, herpes simplex virus; MMR, measles, mumps and rubella; PCR, polymerase chain reaction; VZV, varicella‐zoster virus.