Table 3.
Salivary herpesviruses and immunosuppressive diseases and medications
| Study | Condition/disease | Study material and methods | Study outcome | Comments |
|---|---|---|---|---|
| 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 | HSV DNA was detected in saliva in 5% of days, HCMV DNA in 19% of days and EBV DNA in 71% of days. The median DNA copies per ml of HSV, HCMV and EBV were 104.0, 103.3 and 105.3, respectively | Salivary shedding of herpesviruses was common, even among HAART‐treated patients |
| Pauk et al. (134) | HIV infection | HHV‐8 DNA was detected by PCR in saliva and in oral swabs obtained daily from 23 HHV‐8‐seropositive men who had sex with men | HHV‐8 DNA was detected in 34% of oropharyngeal samples (382 of 1134), in 0.4% of urethral samples (3 of 848) and in 1% of anal samples (14 of 1087) | Oral exposure to infectious saliva is a potential risk factor for the acquisition of HHV‐8 among men who have sex with men |
| Kim et al. (90) | HIV infection | One‐hundred and nine HSV‐2‐seropositive men (50 HIV positive and 59 HIV negative) provided oral swabs for 64 consecutive days. PCR was used to detect HSV‐2 DNA in saliva | HSV‐2 DNA was detected from oral swabs in 40% of the subjects on at least 1 day. HIV‐positive men shed HSV‐2 DNA orally more frequently than HIV‐negative men (odds ratio, 2.7) | HSV‐2 oral re‐activation was common, especially in HIV‐positive men, was always asymptomatic and often occurred on days of genital HSV‐2 re‐activation |
| Miller et al. (119) | HIV infection | Fifty‐eight HIV‐seropositive individuals in a case–control study. PCR was used to detect various herpesvirus DNAs in saliva | Salivary DNA of EBV, HHV‐8, HCMV and HSV‐1 was detected in 90%, 57%, 31% and 16%, respectively, of HIV‐positive subjects, and in 48%, 24%, 2% and 2%, respectively, of HIV‐negative subjects | HHVs were significantly more prevalent in the saliva of HIV‐seropositive subjects (odds ratios, 4.2–26.2). Saliva of HIV‐infected persons is a potential risk factor for transmission of multiple HHVs |
| Fidouh‐Houhou et al. (59) | HIV infection | Ninety‐eight HIV‐infected subjects with no history of HCMV disease. PCR was used for detection of HCMV DNA in saliva | Prior salivary shedding of HCMV DNA was associated with a high risk of developing HCMV disease (P = 0.04) | HIV‐related immunosuppression can re‐active a latent HCMV infection and cause clinical HCMV infections |
| Lucht et al. (109) | HIV infection/oral hairy leukoplakia (OHL) | Fifteen HIV‐1‐infected subjects with OHL and 45 HIV‐1‐infected subjects without OHL. PCR was used to detect EBV DNA in saliva | All 15 patients with OHL demonstrated EBV DNA oral shedding, whereas only 35 (78%) subjects without OHL revealed salivary EBV DNA (P = 0.04) | Increased excretion of EBV in saliva occurs soon after the primary HIV‐1 infection, and OHL may occur early on during the HIV‐1 infection |
| Lucht et al. (110) | HIV infection | Forty‐four HIV‐infected and 15 healthy HIV‐seronegative subjects. PCR was used to detect DNA of HCMV, HHV‐6, HHV‐7, and HHV‐8 in saliva | HCMV DNA was found most often in patients with AIDS. HHV‐8 DNA was found only in symptomatic HIV‐1‐infected patients (33%). Oral shedding of HHV‐6 and HHV‐7 was not elevated in HIV‐infected subjects | Oral shedding of HCMV DNA and HHV‐8 DNA correlated positively with the severity of the HIV‐associated immunodeficiency |
| Di Luca et al. (51) | Common cold, recurrent aphthous ulceration, HIV infection | Sixteen subjects with the common cold, 12 subjects with recurrent aphthous ulceration and 26 HIV‐infected subjects. PCR was used to detect HHV‐6 DNA and HHV‐7 DNA in saliva | Salivary HHV‐7 DNA was detected in 55% of healthy individuals, in 56% of individuals with the common cold, in 66% with recurrent aphthous ulcers and in 81% with HIV infection. HHV‐6 DNA was detected only in a few salivary specimens | HHV‐7 undergoes an active replication in salivary glands and sheds infectious virions into saliva, especially in HIV‐infected subjects |
| Rhinow et al. (148) | Bone marrow and stem cell transplantation | Unstimulated saliva from 20 patients before, during and after bone marrow and stem cell transplantation. PCR was used to detect HCMV | Salivary HCMV counts post‐transplantation showed evidence of HCMV re‐activation. HCMV infection from the transplant donor was not observed | Transplantation procedures may re‐active a latent HCMV infection |
| Al‐Otaibi et al. (9) | Renal allograft recipient | A 33‐year‐old renal allograft recipient provided pre‐ and post‐transplantation salivary samples. Real‐time PCR detection of HHV‐8 | HHV‐8 showed salivary loads of 2.6 × 106–4.1 × 106 genome‐copies/ml | Post‐transplantation, the salivary HHV‐8 DNA load declined precipitously following an increase in the dosage of valacyclovir |
AIDS, acquired immunodeficiency syndrome; EBV, Epstein–Barr virus; HAART, highly active antiretroviral therapy; HCMV, human cytomegalovirus; HHV, human herpesvirus; HIV, human immunodeficiency virus; HSV, herpes simplex virus; PCR, polymerase chain reaction; VZV, varicella‐zoster virus.