Varicella-zoster virus infections treatment

WraZ/nfecf/on. Treatment with tacrolimus ointment may be associated with an increased risk of varicella zoster virus infection (chicken pox or shingles), herpes simplex virus infection, or eczema herpeticum. 

Snoeck R, Andrei G, DeClercq E (1999) Current pharmacological approaches to the therapy of varicella zoster virus infection A guide to treatment. Drugs 57 187-206. 

Shepp DH, Dandliker PS, Meyers ID. Treatment of varicella-zoster virus infection in severefy immunocompromised patients arandomizedcompaiisonof acyclovir and vidarabine. NEr l JMed 9 314,208-12. 

Neonatal herpes simplex virus infection Treatment of neonatal herpes infections. Parenteral Treatment of initial and recurrent mucosal and cutaneous herpes simplex virus (HSV)-I and -2 and varicella-zoster virus (VZV/shingles) infections in immunocompromised patients. 

Acyclovir (ACV) is not a true nucleoside, because the guanine residue is attached to an open-chain structure, but it mimics deoxyribose well enough for the compound to be accepted as a substrate by a thymidine kinase specified by certain herpes-type viruses. The normal thymidine kinase in mammalian cells does not recognize ACV as a substrate, however, so only virus-infected cells convert ACV to its monophosphate. Once the first phosphate has been added, the second phosphate is added by cellular guanylate kinase several other cellular kinases can add the third phosphate. The triphosphate is a more potent inhibitor of the viral DNA polymerases than of cellular DNA polymerases and also inactivates the former but not the latter. The net result is that ACV has been an effective treatment of, and prophylaxis for, genital herpes. Also it can result in dramatic relief of pain associated with shingles caused by reactivation of latent varicella-zoster virus, and has been successful in many patients with herpes encephalitis. 

Vidarabine [vye DARE a been] arabinofuranosyl adenine, ara-A, adenine arabinoside) is one of the most effective of the nucleoside analogs and is also the least toxic. However, it has been supplanted clinically by acyclovir, which is more efficacious and safe. Although vidarabine is active against herpes simplex virus type 1 (HSV-1), HSV-2, and varicella-zoster virus (VZV), its use is limited to treatment of immunocompromised patients with herpes simplex keratitis or encephalitis, or VZV infections. Vidarabine, an adenosine analog, is converted in the cell to its 5 -triphosphate analog (ara-ATP), which is postulated to inhibit viral DNA synthesis. Some resistant herpes virus... 

Cidofovir is an acyclic nucleotide analogue of the monophosphate of cytosine. When phosphorylated by host cellular enzymes, the active compound cidofovir diphosphate has broad activity against the herpes viruses, including CMV, herpes simplex viruses 1 and 2, varicella zoster virus and Epstein-Barr virus. Cidofovir is used primarily in treatment of CMV retinitis in patients who have failed treatment with ganciclovir or foscamet and in acyclovir-resistant herpes simplex infections. 

Foscamet is an antiviral agent that inhibits replication of all known herpes viruses, including cytomegalovirus (CMV), herpes simplex virus types 1 and 2 (HSV-1, HSV-2), human herpes virus 6 (HHV-6), Epstein-Barr virus (EBV) and varicella-zoster virus (VZV). It is indicated in the treatment of CMV retinitis in patients with AIDS treatment of acyclovir-resistant mucocutaneous HSV infections in immunocompromised patients and as combination therapy with ganciclovir for patients who have relapsed after monotherapy with either drug. 

The first systemically administered antiherpesvirus agent, vidarabine, was approved by the Food and Drug Administration (FDA) in 1977. However, its toxicities restricted its use to life-threatening infections of HSV and varicella-zoster virus (VZV). The discovery and development of acyclovir, approved in 1982, provided the first effective treatment for less severe HSV and VZV infections in ambulatory patients. Intravenous acyclovir is superior to vidarabine in terms of efficacy and toxicity in HSV encephalitis and in VZV infections of immunocompromised patients. Acyclovir is the prototype of a group of antiviral agents that are phosphorylated intraceUularly by a viral... 

Acyclovir [9-(2-hydroxyethoxymethyl)guanine] (ACV) is clinically useful in the treatment of infections caused by several members of the herpes virus (e.g., herpes simplex, varicella zoster and Epstein-Barr virus [2,38,39]). An enzyme coded for by the virus phosphorylates ACV to a monophosphate intermediate. This species in turn undergoes further phosphorylation to a triphosphate with the aid of normal cell enzymes. Then, ACV triphosphate inhibits the herpes virus DNA... 

Vidarabine is a purine nucleoside analogue active against herpes viruses, influenza viruses, and some RNA viruses. Use of vidarabine for treatment of herpes simplex and varicella-zoster infections has largely been supplanted by acyclovir because of the superior efficacy, fewer adverse effects, and easier administration of the latter agent. Vidarabine has been associated with significant gastrointestinal, neurologic, and hematopoietic toxicities. Patients with renal insuffi-... 

Vaccinia immune globulin IV is a vaccinia-specific immunoglobulin G (IgG), which directly neutralizes vaccinia virus. It is indicated in treatment and/or modification of aberrant infections induced by vaccinia virus (including accidental implantation in eyes, mouth, or other areas where vaccinia infection would constitute a special hazard), eczema vaccinatum, progressive vaccinia, severe generalized vaccinia, and vaccinia infections in individuals who have skin conditions such as bums, impetigo, varicella-zoster, or poison ivy, or in individuals with eczematous skin lesions. Treat complications that include vaccinia keratitis with caution. 

Infection risk Virus infections can develop during treatment with TNF antagonists, as in a case of varicella zoster infection [113 ]. 

Viral infections that occur after transplantation are not limited to the lung. Herpes simplex infections are frequent early after the procedure, manifesting as oral vesicles or ulcerations. Less frequent is genital involvement by herpes simple virus, hepatitis or encephalitis. Herpes zoster and varicella reactivate in most patients, particularly if aciclovir prophylaxis is discontinued. Occasionally, severe cerebral arteritis or pneumonia caused by this virus may occur. CMV infection is frequent after transplantation and has to be regularly monitored by antigenemia and/or PCR for early treatment avoiding CMV disease. Epstein Barr virus (EBV) infection and EBV-associated lymphoproliferative disorders have also to be tested on a regular basis, especially in transplants with in... 

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