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American Family Physician Nov 2017Herpes zoster, or shingles, is caused by reactivation of varicella zoster virus, which causes chickenpox. There are an estimated 1 million cases in the Unites States... (Review)
Review
Herpes zoster, or shingles, is caused by reactivation of varicella zoster virus, which causes chickenpox. There are an estimated 1 million cases in the Unites States annually, with an individual lifetime risk of 30%. Patients with conditions that decrease cell-mediated immunity are 20 to 100 times more likely to develop herpes zoster. Patients may present with malaise, headache, low-grade fever, and abnormal skin sensations for two to three days before the classic maculopapular rash appears. The rash is usually unilateral, confined to a single dermatome, and typically progresses to clear vesicles that become cloudy and crust over in seven to 10 days. Herpes zoster can be treated with acyclovir, valacyclovir, or famciclovir, ideally within 72 hours of the development of the rash. Postherpetic neuralgia is the most common complication, occurring in about one in five patients. It is defined as pain in a dermatomal distribution sustained for at least 90 days after acute herpes zoster. Treatment is focused on symptom control and includes topical lidocaine or capsaicin and oral gabapentin, pregabalin, or tricyclic antidepressants. The varicella zoster virus vaccine decreases the incidence of herpes zoster and is approved for adults 50 years and older. The Centers for Disease Control and Prevention's Advisory Committee on Immunization Practices recommends this vaccine for adults 60 years and older, except for certain immunosuppressed patients.
Topics: Antiviral Agents; Female; Herpes Zoster; Herpes Zoster Vaccine; Humans; Male; Neuralgia, Postherpetic; Skin
PubMed: 29431387
DOI: No ID Found -
Clinical Microbiology Reviews Jul 1996Varicella-zoster virus (VZV) is a ubiquitous human alphaherpesvirus that causes varicella (chicken pox) and herpes zoster (shingles). Varicella is a common childhood... (Review)
Review
Varicella-zoster virus (VZV) is a ubiquitous human alphaherpesvirus that causes varicella (chicken pox) and herpes zoster (shingles). Varicella is a common childhood illness, characterized by fever, viremia, and scattered vesicular lesions of the skin. As is characteristic of the alphaherpesviruses, VZV establishes latency in cells of the dorsal root ganglia. Herpes zoster, caused by VZV reactivation, is a localized, painful, vesicular rash involving one or adjacent dermatomes. The incidence of herpes zoster increases with age or immunosuppression. The VZV virion consists of a nucleocapsid surrounding a core that contains the linear, double-stranded DNA genome; a protein tegument separates the capsid from the lipid envelope, which incorporates the major viral glycoproteins. VZV is found in a worldwide geographic distribution but is more prevalent in temperate climates. Primary VZV infection elicits immunoglobulin G (IgG), IgM, and IgA antibodies, which bind to many classes of viral proteins. Virus-specific cellular immunity is critical for controlling viral replication in healthy and immunocompromised patients with primary or recurrent VZV infections. Rapid laboratory confirmation of the diagnosis of varicella or herpes zoster, which can be accomplished by detecting viral proteins or DNA, is important to determine the need for antiviral therapy. Acyclovir is licensed for treatment of varicella and herpes zoster, and acyclovir, valacyclovir, and famciclovir are approved for herpes zoster. Passive antibody prophylaxis with varicella-zoster immune globulin is indicated for susceptible high-risk patients exposed to varicella. A live attenuated varicella vaccine (Oka/Merck strain) is now recommended for routine childhood immunization.
Topics: Acyclovir; Antibody Formation; Antiviral Agents; Chickenpox; Contraindications; Herpes Zoster; Herpesvirus 3, Human; Humans; Immunity, Cellular; Immunization, Passive; Serology; Vaccination; Vaccines, Attenuated
PubMed: 8809466
DOI: 10.1128/CMR.9.3.361 -
Molecules (Basel, Switzerland) Feb 2021Varicella-zoster virus (VZV), a common and ubiquitous human-restricted pathogen, causes a primary infection (varicella or chickenpox) followed by establishment of... (Review)
Review
Varicella-zoster virus (VZV), a common and ubiquitous human-restricted pathogen, causes a primary infection (varicella or chickenpox) followed by establishment of latency in sensory ganglia. The virus can reactivate, causing herpes zoster (HZ, shingles) and leading to significant morbidity but rarely mortality, although in immunocompromised hosts, VZV can cause severe disseminated and occasionally fatal disease. We discuss VZV diseases and the decrease in their incidence due to the introduction of live-attenuated vaccines to prevent varicella or HZ. We also focus on acyclovir, valacyclovir, and famciclovir (FDA approved drugs to treat VZV infections), brivudine (used in some European countries) and amenamevir (a helicase-primase inhibitor, approved in Japan) that augur the beginning of a new era of anti-VZV therapy. Valnivudine hydrochloride (FV-100) and valomaciclovir stearate (in advanced stage of development) and several new molecules potentially good as anti-VZV candidates described during the last year are examined. We reflect on the role of antiviral agents in the treatment of VZV-associated diseases, as a large percentage of the at-risk population is not immunized, and on the limitations of currently FDA-approved anti-VZV drugs. Their low efficacy in controlling HZ pain and post-herpetic neuralgia development, and the need of multiple dosing regimens requiring daily dose adaptation for patients with renal failure urges the development of novel anti-VZV drugs.
Topics: Antiviral Agents; Encephalitis, Varicella Zoster; Herpesvirus 3, Human; Humans; Microbial Sensitivity Tests; Pyrimidine Nucleosides
PubMed: 33672709
DOI: 10.3390/molecules26041132 -
Journal of Evidence-based Integrative... 2018Our previous articles showed that suppressive or preventive treatment with the herbal Gene-Eden-VIR/Novirin reduced the number and duration of genital herpes outbreaks... (Randomized Controlled Trial)
Randomized Controlled Trial
BACKGROUND
Our previous articles showed that suppressive or preventive treatment with the herbal Gene-Eden-VIR/Novirin reduced the number and duration of genital herpes outbreaks with no adverse effects. These studies also revealed that the herbal Gene-Eden-VIR/Novirin is mostly superior to acyclovir, valacyclovir, and famciclovir drugs in genital herpes. This study tested the effect of Gene-Eden-VIR/Novirin in oral herpes (also called cold sores and fever blisters).
METHODS
The framework of the study was a retrospective chart review. The study included 68 participants. The participants took 1 to 4 capsules per day over a period of 2 to 36 months. The study included 2 Food and Drug Administration-recommended controls: baseline and a no-treatment.
RESULTS
Gene-Eden-VIR/Novirin was effective in 89.3% of participants. The treatment reduced the mean number of outbreaks per year from 6.0 and 3.6 in the control groups to 2.0 in the treatment group ( P < .0001 and P = .07, respectively). Gene-Eden-VIR/Novirin reduced the mean duration of outbreaks from 9.8 and 5.8 days in the control groups to 3.2 days in the treatment group ( P < .0001 and P = .02, respectively). There were no reports of adverse experiences. Gene-Eden-VIR/Novirin was compared to acyclovir and valacyclovir in 6 tests. In all tests, Gene-Eden-VIR/Novirin showed higher efficacy. Gene-Eden-VIR/Novirin also showed superior safety.
CONCLUSIONS
This clinical study showed that suppressive or preventive treatment with the herbal Gene-Eden-VIR/Novirin reduced the number and duration of outbreaks in oral herpes without any adverse effects. The study also showed that the herbal Gene-Eden-VIR/Novirin had better clinical effects than acyclovir and valacyclovir, the leading drugs in the category. Based on these results, we recommend using the herbal Gene-Eden-VIR/Novirin as preventive treatment for oral herpes and, specifically, as an alternative to the acyclovir and valacyclovir drugs.
Topics: Adult; Aged; Aged, 80 and over; Antiviral Agents; Drug Combinations; Female; Herpes Labialis; Humans; Male; Middle Aged; Plant Extracts; Quercetin; Retrospective Studies; Selenium; Young Adult
PubMed: 30362389
DOI: 10.1177/2515690X18806269 -
Viruses Feb 2023Herpes simplex virus (HSV) and varicella zoster virus (VZV) are alpha herpesviruses that establish life-long latent infection in neuronal ganglia after primary... (Review)
Review
Herpes simplex virus (HSV) and varicella zoster virus (VZV) are alpha herpesviruses that establish life-long latent infection in neuronal ganglia after primary infection. Periodic reactivation of these viruses results in recurrent infections that can have significant impact on patients' quality of life. HSV commonly causes oral and genital mucocutaneous infections whereas VZV is responsible for varicella/chickenpox and herpes zoster/shingles, but cancer patients are at particularly higher risk of complications including disseminated and visceral infections due to impaired cell-mediated immunity. While diagnosis of more common HSV and/or VZV infections is frequently clinically based, immunocompromised hosts may have atypical skin presentation or visceral involvement. Thus, diagnostic confirmation using virus-specific tests such as polymerase chain reaction or immunohistochemical staining is crucial in some cases. Oral acyclovir, valacyclovir and famciclovir are usually used for mild to moderate infections and intravenous acyclovir is the drug of choice for severe or disseminated infections. Foscarnet can be used when acyclovir-resistance is confirmed or suspected. Pharmaceutical prophylaxis against HSV and/or VZV should be considered in high-risk cancers patients. Currently, there is no commercially available vaccine against HSV, but VZV vaccines are available to prevent varicella and zoster.
Topics: Humans; Chickenpox; Herpesvirus 3, Human; Simplexvirus; Quality of Life; Herpes Zoster; Varicella Zoster Virus Infection; Acyclovir; Neoplasms
PubMed: 36851652
DOI: 10.3390/v15020439 -
BMJ Clinical Evidence Apr 2011Chickenpox is extremely contagious. Over 90% of unvaccinated people become infected, but infection occurs at different ages in different parts of the world - over 80%... (Review)
Review
INTRODUCTION
Chickenpox is extremely contagious. Over 90% of unvaccinated people become infected, but infection occurs at different ages in different parts of the world - over 80% of people have been infected by the age of 10 years in the US, the UK, and Japan, and by the age of 20 to 30 years in India, South East Asia, and the West Indies.
METHODS AND OUTCOMES
We conducted a systematic review and aimed to answer the following clinical questions: What are the effects of interventions to prevent chickenpox in healthy adults and children? What are the effects of interventions to prevent chickenpox in children exposed prenatally? What are the effects of interventions to prevent chickenpox in immunocompromised adults and children? What are the effects of treatments for chickenpox in healthy adults and children? What are the effects of treatments for chickenpox in immunocompromised adults and children? We searched: Medline, Embase, The Cochrane Library, and other important databases up to June 2010 (Clinical Evidence reviews are updated periodically, please check our website for the most up-to-date version of this review). We included harms alerts from relevant organisations such as the US Food and Drug Administration (FDA) and the UK Medicines and Healthcare products Regulatory Agency (MHRA).
RESULTS
We found 11 systematic reviews, RCTs, or observational studies that met our inclusion criteria. We performed a GRADE evaluation of the quality of evidence for interventions.
CONCLUSIONS
In this systematic review we present information relating to the effectiveness and safety of the following interventions: aciclovir, famciclovir, live attenuated vaccine, valaciclovir, and varicella zoster immunoglobulin.
Topics: Chickenpox; Chickenpox Vaccine; Evidence-Based Medicine; Humans; Immunocompromised Host; Incidence; India; Vaccines, Attenuated
PubMed: 21486500
DOI: No ID Found -
The Cochrane Database of Systematic... Aug 2015Herpes simplex labialis (HSL), also known as cold sores, is a common disease of the lips caused by the herpes simplex virus, which is found throughout the world. It... (Meta-Analysis)
Meta-Analysis Review
BACKGROUND
Herpes simplex labialis (HSL), also known as cold sores, is a common disease of the lips caused by the herpes simplex virus, which is found throughout the world. It presents as a painful vesicular eruption, forming unsightly crusts, which cause cosmetic disfigurement and psychosocial distress. There is no cure available, and it recurs periodically.
OBJECTIVES
To assess the effects of interventions for the prevention of HSL in people of all ages.
SEARCH METHODS
We searched the following databases up to 19 May 2015: the Cochrane Skin Group Specialised Register, the Oral Health Group Specialised Register, CENTRAL in the Cochrane Library (Issue 4, 2015), MEDLINE (from 1946), EMBASE (from 1974), LILACS (from 1982), the China National Knowledge Infrastructure (CNKI) database, Airiti Library, and 5 trial registers. To identify further references to relevant randomised controlled trials, we scanned the bibliographies of included studies and published reviews, and we also contacted the original researchers of our included studies.
SELECTION CRITERIA
Randomised controlled trials (RCTs) of interventions for preventing HSL in immunocompetent people.
DATA COLLECTION AND ANALYSIS
Two authors independently selected trials, extracted data, and assessed the risk of bias. A third author was available for resolving differences of opinion.
MAIN RESULTS
This review included 32 RCTs, with a total of 2640 immunocompetent participants, covering 19 treatments. The quality of the body of evidence was low to moderate for most outcomes, but was very low for a few outcomes. Our primary outcomes were 'Incidence of HSL' and 'Adverse effects during use of the preventative intervention'.The evidence for short-term (≤ 1 month) use of oral aciclovir in preventing recurrent HSL was inconsistent across the doses used in the studies: 2 RCTs showed low quality evidence for a reduced recurrence of HSL with aciclovir 400 mg twice daily (risk ratio (RR) 0.26, 95% confidence interval (CI) 0.13 to 0.51; n = 177), while 1 RCT testing aciclovir 800 mg twice daily and 2 RCTs testing 200 mg 5 times daily found no similar preventive effects (RR 1.08, 95% CI 0.62 to 1.87; n = 237; moderate quality evidence and RR 0.46, 95% CI 0.20 to 1.07; n = 66; low quality evidence, respectively). The direction of intervention effect was unrelated to the risk of bias. The evidence from 1 RCT for the effect of short-term use of valaciclovir in reducing recurrence of HSL by clinical evaluation was uncertain (RR 0.55, 95% CI 0.23 to 1.28; n = 125; moderate quality evidence), as was the evidence from 1 RCT testing short-term use of famciclovir.Long-term (> 1 month) use of oral antiviral agents reduced the recurrence of HSL. There was low quality evidence from 1 RCT that long-term use of oral aciclovir reduced clinical recurrences (1.80 versus 0.85 episodes per participant per a 4-month period, P = 0.009) and virological recurrence (1.40 versus 0.40 episodes per participant per a 4-month period, P = 0.003). One RCT found long-term use of valaciclovir effective in reducing the incidence of HSL (with a decrease of 0.09 episodes per participant per month; n = 95). One RCT found that a long-term suppressive regimen of valaciclovir had a lower incidence of HSL than an episodic regimen of valciclovir (difference in means (MD) -0.10 episodes per participant per month, 95% CI -0.16 to -0.05; n = 120).These trials found no increase in adverse events associated with the use of oral antiviral agents (moderate quality evidence).There was no evidence to show that short-term use of topical antiviral agents prevented recurrent HSL. There was moderate quality evidence from 2 RCTs that topical aciclovir 5% cream probably has little effect on preventing recurrence of HSL (pooled RR 0.91, 95% CI 0.48 to 1.72; n = 271). There was moderate quality evidence from a single RCT that topical foscarnet 3% cream has little effect in preventing HSL (RR 1.08, 95% CI 0.82 to 1.40; n = 295).The efficacy of long-term use of topical aciclovir cream was uncertain. One RCT found significantly fewer research-diagnosed recurrences of HSL when on aciclovir cream treatment than on placebo (P < 0.05), but found no significant differences in the mean number of participant-reported recurrences between the 2 groups (P ≥ 0.05). One RCT found no preventive effect of topical application of 1,5-pentanediol gel for 26 weeks (P > 0.05). Another RCT found that the group who used 2-hydroxypropyl-β-cyclo dextrin 20% gel for 6 months had significantly more recurrences than the placebo group (P = 0.003).These studies found no increase in adverse events related to the use of topical antiviral agents.Two RCTs found that the application of sunscreen significantly prevented recurrent HSL induced by experimental ultraviolet light (pooled RR 0.07, 95% CI 0.01 to 0.33; n = 111), but another RCT found that sunscreen did not prevent HSL induced by sunlight (RR 1.13, 95% CI 0.25 to 5.06; n = 51). These RCTs did not report adverse events.There were very few data suggesting that thymopentin, low-level laser therapy, and hypnotherapy are effective in preventing recurrent HSL, with one to two RCTs for each intervention. We failed to find any evidence of efficacy for lysine, LongoVital® supplementation, gamma globulin, herpes simplex virus (HSV) type I subunit vaccine, and yellow fever vaccine in preventing HSL. There were no consistent data supporting the efficacy of levamisole and interferon, which were also associated with an increased risk of adverse effects such as fever.
AUTHORS' CONCLUSIONS
The current evidence demonstrates that long-term use of oral antiviral agents can prevent HSL, but the clinical benefit is small. We did not find evidence of an increased risk of adverse events. On the other hand, the evidence on topical antiviral agents and other interventions either showed no efficacy or could not confirm their efficacy in preventing HSL.
Topics: Antiviral Agents; Herpes Labialis; Humans; Randomized Controlled Trials as Topic; Recurrence; Secondary Prevention
PubMed: 26252373
DOI: 10.1002/14651858.CD010095.pub2 -
Antiviral Chemistry & Chemotherapy Jan 2013This review article focuses on the anti-herpesvirus agents effective against herpes simplex virus, varicella-zoster virus and cytomegalovirus, which have either been... (Review)
Review
This review article focuses on the anti-herpesvirus agents effective against herpes simplex virus, varicella-zoster virus and cytomegalovirus, which have either been licensed for clinical use (idoxuridine, trifluridine, brivudin, acyclovir, valaciclovir, valganciclovir, famciclovir and foscarnet) or are under clinical development (CMX001 [the hexadecyloxypropyl prodrug of cidofovir], the helicase-primase inhibitor BAY 57-1293 [now referred to as AIC316], FV-100 [the valine ester of Cf 1743] and the terminase inhibitor letermovir [AIC246]).
Topics: Animals; Antiviral Agents; Cytomegalovirus; Herpesviridae Infections; Herpesvirus 3, Human; Humans; Simplexvirus
PubMed: 23343513
DOI: 10.3851/IMP2533