Viral infection varicella zoster

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. 

Antiviral Efficacy and Clinical Use. Vidarabine (Vira-A) was the first systemic agent used to treat herpesvirus infections, including CMV, herpes simplex virus, and varicella-zoster virus.42 In the past, this drug was administered by continuous intravenous infusion to treat severe systemic infections caused by these viruses, but systemic use of vidarabine has been replaced by safer and less toxic agents. Vidarabine is currently used primarily to treat local viral infections of the eye (e.g., herpes simplex keratoconjunctivitis) it is applied topically by ophthalmic ointment to treat these infections. 

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... 

Varicella-zoster virus is a member of the Herpesviridae femily. The viral contagion is transmitted via aerosolized water droplets or close physical contact with infected lesions. The primary infection results in varicella or chickenpox. The varicella infection can have potentially devastating ocular sequelae the most common is anterior uveitis followed by SPK. After the primary infection, latent infection occurs in multiple ganglia throughout the body. Herpes zoster is the resultant reactivation of the latent varicella-zoster virus and most often occurs in elderly and immunocompromised patients. Factors such as physical and emotional trauma, immunosuppressive medications, irradiation, cancer, tuberculosis, malaria, and syphilis are known to reactivate the virus. 

Impaired immune responses render the subject more liable to bacterial and viral infections. Treat all infection early and vigorously (using bactericidal drugs where practicable) use human gamma globulin to protect if there is exposure to virus infections, e.g. measles, varicella. For example, patients who have not had chickenpox and are receiving therapeutic (as opposed to replacement) doses of corticosteroid are at risk of severe chickenpox they should receive varicella-zoster immunoglobulin if there has been contact with the disease within the previous 3 months. 

Viral infections contracted during steroid therapy can be overwhelming because the immune response of the body may be largely suppressed. This is particularly relevant to immunosuppressed patients exposed to varicella/herpes zoster virus, which may cause fulminant illness they may need passive protection with varicella/zoster immimoglobulin, VZIG, as soon as practicable. Continuous use of prednisolone 20 mg/day (or the equivalent) is immunosuppressive. But a corticosteroid may sometimes be useful in therapy after the disease has begun (thyroiditis, encephalitis) and there has been time for the immune response to occur. It then acts by suppressing unwanted effects of immime responses and excessive inflammatory reaction. 

Severe viral infections/reactivation that have been reported in patients given ritnximab have inclnded fnl-minant hepatitis B (18), parvovims-indnced red cell aplasia (15), and fatal Varicella zoster infection (19). There was a high incidence of reactivation of cytomegalovirus and V. zoster virus when rituximab was combined with high-dose chemotherapy in high-risk patients with non-Hodgkin s lymphoma (20). 

A 19-month-old girl was immunized against Varicella at 15 months of age and later developed zoster infection (18). Viral cultures from various lesions isolated Varicella zoster virus. The Oka vaccine strain was revealed by polymerase chain reaction. 

Ocular antiviral chemotherapy in the horse is adapted from that used in herpes simplex virus (HSV) and varicella zoster keratitis in humans. The agents used are nucleotide analogs capable of inhibiting viral replication by competitive inhibition of the uptake of the nucleotide into the viral genome. These agents are virustatic and require an intact immune system to suppress or eliminate the virus from the eye. They probably do not eradicate any latent infection. The antiviral drugs available currently do not penetrate intact comeal epithelium and are poorly disseminated within the comeal stroma. The availability of these dmgs will vary in different countries and some may only be obtained from hospital pharmacies. 

Viral Hemagglutinins. The initial step in many viral infections is the binding of surface proteins (hemagglutinins) to mucosal cells. These binding proteins have been identified for most viruses, including rotaviruses (73), varicella zoster virus (74), Semliki Forest virus (75), adenoviruses (76), potato leafroll virus (77), and reovirus (78). 

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... 

Viral infections of the skin are very common and include verrucae (human paprUomavims [HPV]), herpes simplex (HSV), condyloma acuminatum (HPV), moUuscum contagiosum (poxvirus), and chicken pox (variceUa-zoster vims [VZV]). Acyclovir (ZOVIRAK), famciclovir (famvir), and vala-cyclovir (VALTREX) frequently are used systemicaUy to treat herpes simplex and varicella infections... 

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