Shedding of herpes simplex virus Type 1 into saliva

Kameyama, Tadamitsu; Sujaku, Chokudo; Yamamoto, Shigeru; Hwang, Charles B. C.; Shillitoe, Edward J.

doi:10.1111/j.1600-0714.1988.tb01320.x

Cited by 74 publications

(47 citation statements)

References 11 publications

(4 reference statements)

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“…CMV and HHV-8 were not detected at consecutive appointments in any patient, and HSV-2 and VZV were not detected in any salivas. Overall, these data are consistent with the findings of others who have examined the duration of HHV shedding in saliva (21,32,38,50,88) and indicate that the prevalence of HHVs in the saliva of asymptomatic adults does not increase upon the stress of dental treatment.…”

Section: Discussionsupporting

confidence: 81%

Effect of Prophylactic Valacyclovir on the Presence of Human Herpesvirus DNA in Saliva of Healthy Individuals after Dental Treatment

Miller¹,

Avdiushko²,

Danaher³

et al. 2005

J Clin Microbiol

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Human herpesviruses (HHVs) are ubiquitous pathogens that intermittently reactivate from latency. Transmission is believed to be facilitated by their frequent appearance in saliva. This study sought to understand the factors that influence the appearance of these viruses in saliva by examining the prevalence, pattern, and quantity of all eight HHVs in saliva of immunocompetent adults with a history of recurrent oral herpes simplex virus (HSV) infections following dental treatment and antiviral therapy. Valacyclovir or matched placebo was given (2 g twice on the day of treatment and 1 g twice the following day) to 125 patients in a randomized, double-blind controlled trial. Saliva, collected on the day of dental treatment and 3 and 7 days later, was analyzed using real-time quantitative PCR. At all visits, HHVs coinfected saliva. Over the course of the week, the DNAs of HHV-6 and HHV-7 were detected significantly more often (97% to 99% of patients) than Epstein-Barr virus (EBV; 64.8%), HSV-1 (13.0%), HHV-8 (3.2%), cytomegalovirus (2.4%), HSV-2 (0%), and varicella-zoster virus (0%), irrespective of drug treatment (P < 0.002). Mean genome copy numbers were highest for HSV-1 and HHV-6. Dental treatment did not influence asymptomatic viral shedding patterns. However, valacyclovir treatment resulted in significantly fewer patients shedding EBV at both postoperative visits compared with placebo (P < 0.008). These results suggest that HHVs are simultaneously present in the saliva of healthy adults at levels that could facilitate transmission, and valacyclovir therapy decreases the prevalence of EBV in saliva but has little effect on HHV-6 and HHV-7.Herpesviruses are ubiquitous pathogens that infect many animal species, including humans. Eight distinct members of the human Herpesviridae family have been identified. They include herpes simplex virus type 1 (HSV-1), HSV-2, varicellazoster virus (VZV), Epstein-Barr virus (EBV), cytomegalovirus (CMV), human herpesvirus 6 (HHV-6), HHV-7, and HHV-8 (Kaposi's sarcoma herpesvirus [KSHV]) (62, 81). These large DNA viruses each express more than 70 genes that specify a number of proteins and enzymes that can cause destruction of infected cells during the lytic infection (12,63). Following the initial lytic infection, HHVs establish a latent state in a diverse group of cells that ensures survival of the viral genome throughout the life of the host. Periodic reactivation and viral recrudescence (i.e., appearance with or without clinical symptoms) occur after stress and alterations in immune surveillance. Frank immunosuppression is associated with more severe disease and complications (e.g., encephalitis, pneumonia, hepatitis, and various forms of cancer) (2,7,13,14,40,53,57,60,67,68,78,83,84).Over 95% of the adult population are infected with HHVs (28,39,70,71,86). Infections occur following intimate contact with virus-laden secretions and in some case by fomites (e.g., nurseries, day care centers) (22,72). Saliva harbors most of the HHVs and appears to be an important mode for viru...

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Section: Discussionsupporting

confidence: 81%

Effect of Prophylactic Valacyclovir on the Presence of Human Herpesvirus DNA in Saliva of Healthy Individuals after Dental Treatment

Miller¹,

Avdiushko²,

Danaher³

et al. 2005

J Clin Microbiol

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“…However, HSV-1 reactivation may also result in asymptomatic shedding. 8,11 It is unknown whether the viral load in an oral sample can distinguish between asymptomatic and symptomatic HSV-1 reactivation. Also, it is unknown whether prolonged HSV-1 excretion in HSCT recipients despite antiviral treatment is caused by the profound immunosuppressed status of HSCT recipients, or due to resistance of the virus to the antiviral medication.…”

Section: Introductionmentioning

confidence: 99%

Viral loads and antiviral resistance of herpesviruses and oral ulcerations in hematopoietic stem cell transplant recipients

Beek

Laheij

Raber-Durlacher

et al. 2012

Bone Marrow Transplant

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Ulcerative oral mucositis and infection are frequent complications in hematopoietic stem cell transplant (HSCT) recipients. The aim of this study was to investigate the relationship between oral ulcerations and HSV-1, EBV and CMV excretion and the presence of aciclovir-resistant HSV-1 strains in HSCT recipients. This prospective observational study included 49 adult patients who underwent allogeneic HSCT. In total, 26 patients received myeloablative and 23 received non-myeloablative conditioning. Ulcerations on non-keratinized and keratinized oral mucosa were scored and oral rinsing samples were taken twice weekly. Viral loads were determined by real-time PCR. Samples from patients remaining HSV-1 positive despite antiviral treatment were studied for resistance to antivirals. Having an HSV-1 or EBV DNA --positive sample was a significant predictor for ulceration of keratinized mucosa. HSV-1 was a significant predictor for ulcerations on non-keratinized mucosa as well. Persistent HSV-1 infection occurred in 12 of 28 patients treated with antiviral medication and aciclovir-resistant HSV-1 was found in 5 persistent infections. In conclusion, HSV-1 is a predictor of ulcerations on non-keratinized as well as keratinized oral mucosa following HSCT. The role of EBV deserves further study. Persistent HSV-1 replication despite antiviral treatment is common and is due to resistance in 18% of treated patients.

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“…he vast majority of people carry a combination of latent herpesviruses which may cause severe disease and death if they reactivate upon immune suppression (1)(2)(3)(4). It has been proposed that human cytomegalovirus (HCMV) infection may be a major environmental factor accelerating immune senescence in older people (5)(6)(7)(8)(9)(10).…”

mentioning

confidence: 99%

Immune Protection against Virus Challenge in Aging Mice Is Not Affected by Latent Herpesviral Infections

Marandu

Oduro

Borkner

et al. 2015

J Virol

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f Latent herpesvirus infections alter immune homeostasis. To understand if this results in aging-related loss of immune protection against emerging infections, we challenged old mice carrying latent mouse cytomegalovirus (CMV), herpes simplex virus 1 (HSV-1), and/or murine gammaherpesvirus 68 (MHV-68) with influenza virus, West Nile virus (WNV), or vesicular stomatitis virus (VSV). We observed no increase in mortality or weight loss compared to results seen with herpesvirus-negative counterparts and a relative but not absolute reduction in CD8 responses to acute infections. Therefore, the presence of herpesviruses does not appear to increase susceptibility to emerging infections in aging patients.

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Shedding of herpes simplex virus Type 1 into saliva

Cited by 74 publications

References 11 publications

Effect of Prophylactic Valacyclovir on the Presence of Human Herpesvirus DNA in Saliva of Healthy Individuals after Dental Treatment

Effect of Prophylactic Valacyclovir on the Presence of Human Herpesvirus DNA in Saliva of Healthy Individuals after Dental Treatment

Viral loads and antiviral resistance of herpesviruses and oral ulcerations in hematopoietic stem cell transplant recipients

Immune Protection against Virus Challenge in Aging Mice Is Not Affected by Latent Herpesviral Infections

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