VZV infection

Scrape VZV-infected Mewo cells into overlay medium when cytopathic effect is 60-80% (scraping ruptures syncytia and releases virus). 

Acute VZV infection leads to chickenpox, which is characterized by malaise, fever, and an extensive vesicular rash (Abendorth and Arvin, 2000). Chickenpox in the immunocompetent child is mostly benign and associated with lassitude and a temperature of 100-103 °F for 1-2 days. Other symptoms include malaise, itching, anorexia, weakness, and exhaustion, and these gradually resolve as the illness improves. The hallmark of chickenpox is the skin manifesta- 

Remove medium, rinse with PBS, and scrape VZV-infected MRC5 fibroblasts into PSGC (1/10 vol of overlay medium). 

In those with a history of VZV infection, VZV disease occurs in 30% of allogeneic HCT recipients.91 The appropriate duration of VZV prophylaxis is controversial.8 Although VZV infections are reduced by prophylactic acyclovir (800 mg twice daily), administered from 1 to 2 months until 1 year after HCT, the risk of VZV persists in those on continued immune suppression.91 

Foscarnet1 Intravenous Acyclovir-resistant HSV and VZV infections 40 mg/kg q8h until healed 

Patients who are HSV- or VZV-seronegative prior to HCT rarely develop primary HSV or VZV infection therefore, prophylactic antivirals are not warranted. Patients who are HSV-antibody-seropositive before HCT are at high risk for reactivation of their 

Three oral agents are licensed for the treatment of HSV and VZV infections acyclovir, valacyclovir, and famciclovir. They have similar mechanisms of action and similar indications for clinical use all are well tolerated. Acyclovir, licensed first, has been the most extensively studied in addition, it is the only anti-HSV agent available for intravenous use in the United States. Neither valacyclovir nor famciclovir have been fully evaluated in pediatric patients thus, they are not indicated for the treatment of varicella infection. 

VZV radiculopathy or myeloradiculopathy AIDS Acute Lumbosacral pain saddle anesthesia rapidly progressive flaccid paraparesis VZV infection Schwann ceU-endothelial cells infection 

AGENTS TO TREAT HERPES SIMPLEX VIRUS (HSV) VARICELLA-ZOSTER VIRUS (VZV) INFECTIONS 

Agents to Treat Herpes Simplex Virus (HSV) Varicella Zoster Virus (VZV) Infections 

Table 49-1 Agents to Treat or Prevent Herpes Simplex Virus (HSV) and Varicella-Zoster Virus (VZV) Infections.

Intravenous acyclovir is the treatment of choice for herpes simplex encephalitis, neonatal HSV infection, and serious HSV or VZV infections (Table 49-1). In immunocompromised patients with VZV infection, intravenous acyclovir reduces the incidence of cutaneous and visceral dissemination. 

Acyclovir-resistant VZV isolates uncommonly have been recovered from HIV-infected children and adults who may manifest chronic hyperkeratotic or verrucous lesions and sometimes meningoradiculitis. Intravenous foscarnet appears to be effective for acyclovir-resistant VZV infections. 

The bioavailability of penciclovir from orally administered famciclovir is 70% less than 20% is plasma protein-bound. A peak serum concentration of 2 vgJmL is achieved following a 250 mg oral dose. Penciclovir triphosphate has an intracellular half-life of 10 hours in HSV-1-infected cells, 20 hours in HSV-2-infected cells, and 7 hours in VZV-infected cells in vitro. Penciclovir is excreted primarily in the urine. 

THERAPEUTIC USES In immunocompetent persons, the clinical benefits of acyclovir and valacyclovir are greater in initial HS V infections than in recurrent ones, which typically are milder. These drugs are particularly useful in immunocompromised patients because these individuals experience more frequent and more severe HSV and VZV infections. Since VZV is less susceptible than HSV to acyclovir, higher doses must be used for treating varicella or zoster infections. Oral valacyclovir is as effective as oral acyclovir in HSV infections and more effective for treating herpes zoster. 

Aciclovir After oral application, only about 20% of the applied dose of this guanosine derivative is absorbed. Aciclovir is mainly eliminated via the kidneys (ca. 85% of the dose within 48 hours). Its half-life, which is approx. 3 hours, depends on renal function. The substance is employed especially in HSV and VZV infections. This agent inhibits DNA polymerase (i.e. replication) and effects a chain break. As a monotherapy in HBV infection, aciclovir only shows moderate efficacy. Side effects are rare. 

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 

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