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Varicella-Zoster Virus Diseases
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Epidemiology

Approximately 95% of adults (aged ≥21 years) born in the United States have had primary varicella-zoster virus (VZV) infection, known as varicella (or chickenpox). Reactivation of latent VZV results in herpes zoster (or shingles). A person's lifetime risk for herpes zoster is 15%-20%, with the highest incidence occurring in the elderly and immunocompromised persons. The incidence of herpes zoster is >15-fold higher for HIV-infected adults than for age-matched controls (764Buchbinder SP, Katz MH, Hessol N, et al. Herpes zoster and human immunodeficiency virus infection. J Infect Dis 1992;166:1153-6.). Herpes zoster can occur in HIV-infected adults at any CD4+ count, but frequency of disease is highest with CD4+ counts of <200 cells/µL and is not reduced by ART (765Engels EA, Rosenberg PS, Biggar RJ. Zoster incidence in human immunodeficiency virus-infected hemophiliacs and homosexual men, 1984-1997. J Infect Dis 1999;180:1784-9., 766Vanhems P, Voisin L, Gayet-Ageron A, et al. The incidence of herpes zoster is less likely than other opportunistic infections to be reduced by highly active antiretroviral therapy. J Acquir Immune Def Syndr 2005;38:111-3., 767Gebo KA, Kalyani R, Moore RD, Polydefkis MJ. The incidence of, risk factors for, and sequelae of herpes zoster among HIV patients in the highly active antiretroviral therapy era. J Acquir Immune Defic Syndr 2005;40:169-74.).

Clinical Manifestations

The varicella rash first appears on the head, then on the trunk, and finally on the extremities, evolving through stages of vesicles, pustules, and crusts. The rash is characterized by rapid evolution of lesions during the initial 8-12 hours and by successive crops of new lesions. New vesicle formation continues for 2-4 days, accompanied by pruritus, fever, headache, malaise, and anorexia. Varicella can cause substantial morbidity in HIV-seropositive adolescents and adults. Visceral dissemination, especially VZV pneumonitis, is well documented (768Wallace MR, Hooper DG, Pyne JM, et al. Varicella immunity and clinical disease in HIV-infected adults. South Med J 1994;87:74-6.). Because most HIV-infected adults in the United States are VZV seropositive, varicella is an uncommon occurrence in this population.

Herpes zoster manifests as a painful cutaneous eruption in a dermatomal distribution, often preceded by prodromal pain. The most common sites for herpes zoster are the thoracic dermatomes (40%-50% of cases), followed by cranial nerve (20%-25%), cervical (15%-20%), lumbar (15%), and sacral (5%) dermatomes. Skin changes begin with an erythematous maculopapular rash, followed by the appearance of clear vesicles and accompanied by pain (which might be severe). New vesicle formation typically continues for 3-5 days, followed by lesion pustulation and scabbing. Crusts typically persist for 2-3 weeks and cutaneous dissemination might be as high as 25% to 50%. About 20%-30% of HIV-infected patients have one or more subsequent episodes of herpes zoster, which might involve the same or different dermatomes. The probability of a recurrence of herpes zoster within 1 year of the index episode is approximately 10% (767Gebo KA, Kalyani R, Moore RD, Polydefkis MJ. The incidence of, risk factors for, and sequelae of herpes zoster among HIV patients in the highly active antiretroviral therapy era. J Acquir Immune Defic Syndr 2005;40:169-74., 769Gnann JW, Crumpacker CS, Lalezari JP. Sorivudine versus acyclovir for treatment of dermatomal herpes zoster in human immunodeficiency virus-infected patients: results from a randomized, controlled clinical trial. Antimicrob Agents Chemother 1998;42:1139-45.). Approximately 10%-15% of HIV-seropositive patients report post-herpetic neuralgia (PHN) as a complication following herpes zoster (767Gebo KA, Kalyani R, Moore RD, Polydefkis MJ. The incidence of, risk factors for, and sequelae of herpes zoster among HIV patients in the highly active antiretroviral therapy era. J Acquir Immune Defic Syndr 2005;40:169-74., 770Harrison RA, Soong S, Weiss HL, Gnann JWJ, Whitley RJ. A mixed model for factors predictive of pain in AIDS patients with herpes zoster. J Pain Symptom Manage 1999;17:410-7.).

Most herpes zoster-related complications, including herpes zoster dissemination, occur in patients with CD4+ counts of <200 cells/µL (771Veenstra J, van Praag RM, Krol A, et al. Complications of varicella zoster virus reactivation in HIV-infected homosexual men. AIDS 1996;10:393-9.). The CNS is the primary target organ for herpes zoster dissemination in patients coinfected with HIV. Various VZV-related neurologic syndromes occur in HIV-infected patients, including CNS vasculitis, multifocal leukoencephalitis, ventriculitis, myelitis and myeloradiculitis, optic neuritis, cranial nerve palsies and focal brain-stem lesions, and aseptic meningitis.

ARN and progressive outer retinal necrosis (PORN) are variants of necrotizing retinopathy caused by VZV. Although ARN can occur in both immunocompetent and immunocompromised patients, PORN occurs almost exclusively in AIDS patients with CD4+ count <100 cells/µL (772Engstrom RE, Jr., Holland GN, Margolis TP, et al. The progressive outer retinal necrosis syndrome: a variant of necrotizing herpetic retinopathy in patients with AIDS. Ophthalmology 1994;101:1488-502.). In contrast to ARN, PORN is characterized by minimal inflammation in the aqueous and vitreous humor, absence of retinal vasculitis, and multiple discrete peripheral lesions in the outer retinal layer (773Ormerod LD, Larkin JA, Margo CA, et al. Rapidly progressive herpetic retinal necrosis: a blinding disease characteristic of advanced AIDS. Clin Infect Dis 1998;26:34-45.). PORN lesions rapidly coalesce, causing full-thickness retinal necrosis and subsequent retinal detachment (774Yin PD, Kurup SK, Fischer SH, et al. Progressive outer retinal necrosis in the era of highly active antiretroviral therapy: successful management with intravitreal injections and monitoring with quantitative PCR. J Clin Virol 2007;38:254-9.). Both ARN and PORN are associated with high rates of visual loss.

Diagnosis

Varicella and herpes zoster are distinctive in appearance and can usually be diagnosed clinically. Varicella can be diagnosed retrospectively by documenting seroconversion. When lesions are atypical or the diagnosis is uncertain, swabs from a fresh lesion or tissue biopsies can be submitted for viral culture, direct fluorescent antigen testing, or PCR. Histopathology and PCR can aid with diagnosis of VZV infections of visceral organs (e.g., encephalitis, retinitis, and pneumonitis).

Preventing Exposure

HIV-infected persons who are susceptible to VZV (i.e., those who have not been vaccinated, have no history of varicella or herpes zoster, or are seronegative for VZV) should avoid exposure to persons with chickenpox or herpes zoster (AII). VZV-susceptible household contacts of susceptible HIV-infected persons should be vaccinated to prevent acquisition of chickenpox and potential transmission of VZV to their susceptible HIV-infected contacts (BIII).

Preventing Disease
Postexposure Prophylaxis

For prophylaxis against chickenpox, HIV-infected children and adults who are susceptible to VZV should receive varicella-zoster immune globulin (VariZIG) as soon as possible (but within 96 hours) after close contact with a person who has active varicella or herpes zoster (AIII). As of June 2007, VariZIG can be obtained only under a treatment IND; contact FFF Enterprises, 800-843-7477. The duration of protection should last at least for 3 weeks. Patients receiving monthly high-dose immune globulin intravenous (IGIV) (>400 mg/kg) are likely to be protected and probably do not require VariZIG if the last dose of IGIV was administered <3 weeks before exposure. Risk for VZV transmission is higher from exposure to a patient with chickenpox than from exposure to localized herpes zoster.

Among VZV-susceptible immunocompetent children, post-exposure varicella vaccination has been shown to reduce the risk for chickenpox developing in children and is more effective than pre-emptive therapy with acyclovir. Post-exposure varicella vaccination (for patients with CD4+ counts of >200 cells/µL) or short-term post-exposure administration of acyclovir may be considered for preventing chickenpox among susceptible HIV-infected adolescents or adults, but has not been studied in this population (CIII).

Long-term-drug prophylaxis for prevention of primary VZV infection in HIV-infected persons is not recommended (DIII).

Vaccination

The live attenuated varicella vaccine has been documented to be safe and immunogenic in HIV-infected children aged ≥8 years with CD4+ counts ≥200 cells/µL (CD4+ percentage is ≥15%) (775Levin MJ, Gershon AA, Weinberg A, Song LY, Fentin T, Team. Administration of live varicella vaccine to HIV-infected children with current or past significant depression of CD4+ T cells. J Infect Dis 2006;194:247-55.) and is recommended for those children (776CDC. Prevention of varicella: recommendations of the Advisory Committee on Immunization Practices (ACIP). MMWR 2007;56(No. RR-4).). No studies have evaluated the vaccine in HIV-infected adolescents or adults, but varicella vaccination (two doses, administered 3 months apart) may be considered in HIV-seropositive/VZV-seronegative persons ≥8 years old with CD4+ counts ≥200 cells/µL (CIII). If vaccination results in disease because of vaccine virus, therapy with acyclovir is recommended (AIII). Administration of varicella vaccine to more severely immunocompromised HIV-infected patients is not recommended (DIII). Because of the high prevalence of VZV seropositivity in adults, use of varicella vaccine in this population will be infrequent. Routine serologic testing to determine the VZV serologic status of HIV-infected adults is not recommended.

Treatment of Disease

No controlled prospective studies of antiviral therapy for chickenpox in HIV-infected adults have been reported. For uncomplicated varicella, recommended treatment options are oral acyclovir (20 mg/kg body weight up to a maximum dose of 800 mg five times daily), valacyclovir (1 g PO tid), or famciclovir (500 mg PO tid) for 5-7 days (AII). IV acyclovir for 7-10 days is the recommended initial treatment for HIV-infected patients with severe chickenpox (AIII) (768Wallace MR, Hooper DG, Pyne JM, et al. Varicella immunity and clinical disease in HIV-infected adults. South Med J 1994;87:74-6., 777Prober CG, Kirk LE, Keeney RE. Acyclovir therapy of chickenpox in immunosuppressed children-a collaborative study. J Pediatr 1982;101:622-5., 778Arvin AM. Antiviral therapy for varicella and herpes zoster. Semin Pediatr Infect Dis 2002;13:12-21.). If no evidence of visceral involvement with VZV is available, switching to oral antiviral therapy after the patient has defervesced may be permissible (AIII) (779Carcao MD, Lau RC, Gupta A, et al. Sequential use of intravenous and oral acyclovir in the therapy of varicella in immunocompromised children. Pediatr Infect Dis J 1998;17:626-31.).

Prompt antiviral therapy should be instituted in all immunosuppressed herpes zoster patients within 1 week of rash onset or any time before full crusting of lesions. The recommended treatment options for acute localized dermatomal herpes zoster in HIV-infected patients are oral valacyclovir, famciclovir, or acyclovir for 7-10 days (AII), although longer durations of therapy should be considered if lesions resolve slowly. Valacyclovir or famciclovir are preferred because of their improved pharmacokinetic properties and simplified dosing schedule. If cutaneous lesions are extensive or if visceral involvement is suspected, IV acyclovir should be initiated and continued until clinical improvement is evident (AII) (780Balfour HH, Jr., Bean B, Laskin OL, et al. Acyclovir halts progression of herpes zoster in immunocompromised patients. N Engl J Med 1983;308:1448-53.). A switch from IV acyclovir to oral antiviral therapy (to complete a 10-14 day treatment course) is reasonable when formation of new cutaneous lesions has ceased and the signs and symptoms of visceral VZV infection are improving (AIII). Because of the absence of data to support benefit in this population, adjunctive corticosteroid therapy for herpes zoster is not recommended (DIII).

Optimal antiviral therapy for PORN remains undefined (774Yin PD, Kurup SK, Fischer SH, et al. Progressive outer retinal necrosis in the era of highly active antiretroviral therapy: successful management with intravitreal injections and monitoring with quantitative PCR. J Clin Virol 2007;38:254-9., 781Austin RB. Progressive outer retinal necrosis syndrome: a comprehensive review of its clinical presentation, relationship to immune system status, and management. Clin Eye Vis Care 2007;12:119-29.). Prognosis for visual preservation in involved eyes is poor despite aggressive antiviral therapy. A treatment regimen recommended by certain specialists is a combination of IV ganciclovir and foscarnet, plus intravitreal injections of ganciclovir and/or foscarnet (AIII). Optimization of ART in HIV-infected patients with PORN is also recommended (AIII). Anecdotal reports have described success with IV cidofovir. ARN appears to be more responsive to antiviral therapy; one recommended treatment is high-dose IV acyclovir (10 mg/kg every 8 hours for 10-14 days), followed by prolonged oral valacyclovir (1 gram tid for 6 weeks) (AIII). Involvement of an experienced ophthalmologist in management of patients with VZV retinitis is strongly recommended (AIII).

The incidence of herpes zoster in HIV-infected adults does not appear to be affected by ART therapy. Optimization of ART is recommended in patients with VZV infections (e.g., PORN) (AIII) that are difficult to treat.

Monitoring and Adverse Events, Including Immune Reconstitution Inflammatory Syndrome (IRIS)

For monitoring and adverse event recommendations related to anti-herpesvirus drugs, see preceding sections on HSV and CMV. Providers should be aware of the increased incidence of herpes zoster after initiation of ART. Such episodes should be treated as other episodes of herpes zoster.

Immune reconstitution following initiation of ART might be associated with an increased frequenty of VZV reactivation (782Martinez E, Gatell J, Morn Y, et al. High incidence of herpes zoster in patients with AIDS soon after therapy with protease inhibitors. Clin Infect Dis 1998;27:1510-3., 783Domingo P, Torres OH, Ris J, Vazquez G. Herpes zoster as an immune reconstitution disease after initiation of combination antiretroviral therapy in patients with human immunodeficiency virus type-1 infection. Am J Med 2001;110:605-9.). Between 4 and 16 weeks after beginning ART, the risk for herpes zoster increases two- to fourfold from baseline. During the 6 months after the start of combination ART, the incidence of herpes zoster exceeds 90 episodes per 1,000 person years. The percentage of CD8+ lymphocytes at baseline and the magnitude of their increase at 1 month after initiation of drug therapy are strongly associated with an increased risk for herpes zoster. The clinical presentation and natural history of herpes zoster in the setting of immune reconstitution do not differ from those observed in other HIV-infected patients.

Management of Treatment Failure

Treatment failure caused by resistance of VZV to acyclovir (and related drugs) should be suspected if lesions do not improve within 10 days of initiation of therapy or if they have an atypical (e.g., verrucous) appearance. A viral culture should be obtained, and if VZV is isolated, susceptibility testing performed to establish antiviral drug susceptibility or resistance and to document the need for alternative therapy. Among patients with suspected or proven acyclovir-resistant VZV infections, treatment with IV foscarnet is recommended (AII) (784Breton G, Fillet AM, Katlama C, Bricaire F, Caumes E. Acyclovir-resistant herpes zoster in human immunodeficiency virus-infected patients: results of foscarnet therapy. Clin Infect Dis 1998;27:1525-7.).

Preventing Recurrence

No intervention has been recognized as preventing the recurrence of herpes zoster among HIV-infected persons. An attenuated virus vaccine for prevention of herpes zoster has been approved for use in immunocompetent persons aged ≥60 years, but data regarding its use in HIV-infected persons are lacking. Prospective clinical trials to evaluate the safety and immunogenicity of herpes zoster vaccine in HIV-seropositive subjects are planned. Administration of herpes zoster vaccine to HIV-infected persons is not recommended (DIII).

Special Considerations During Pregnancy

HIV-infected pregnant women who are susceptible to VZV and have close contact to a person with active varicella or herpes zoster should receive VariZIG as soon as possible (within 96 hours) after exposure to VZV (AIII). If oral acyclovir is used for post-exposure prophylaxis, VZV serology should be performed so that the drug can be discontinued if the patient is seropositive for VZV (CIII). Pregnant women should not receive varicella vaccine (EIII).

Specific risks among HIV-infected women with varicella during pregnancy have not been reported. For HIV-seronegative women with chickenpox, the risk for transmitting VZV to the infant resulting in congenital varicella syndrome is 0.4% when infection occurs at or before 12 weeks of gestation, 2.2% with infection at 13-20 weeks, and is negligible after 20 weeks (785Pastuszak AL, Levy M, Schick B, et al. Outcome after maternal varicella infection in the first 20 weeks of pregnancy. N Engl J Med 1994;330:901-5.). Women with varicella during the first half of pregnancy should be counseled about the risks and offered detailed ultrasound surveillance for findings indicative of fetal congenital varicella syndrome (785Pastuszak AL, Levy M, Schick B, et al. Outcome after maternal varicella infection in the first 20 weeks of pregnancy. N Engl J Med 1994;330:901-5.). Administration of varicella-zoster immune globulin does not alter the risk for congenital varicella syndrome. Infants born to women who have chickenpox from 5 days before until 2 days after delivery should receive VariZIG to reduce the severity and mortality of neonatal varicella acquired during maternal viremia (AIII) (783Domingo P, Torres OH, Ris J, Vazquez G. Herpes zoster as an immune reconstitution disease after initiation of combination antiretroviral therapy in patients with human immunodeficiency virus type-1 infection. Am J Med 2001;110:605-9.).

Oral acyclovir or valacyclovir are the preferred treatments for HIV-infected pregnant women who have uncomplicated chickenpox during pregnancy (BIII). Pregnant women who have severe varicella or who exhibit signs or symptoms of VZV pneumonitis should be hospitalized and treated with IV acyclovir (10 mg/kg every 8 hours) (AII).

No controlled studies of antiviral therapy of herpes zoster during pregnancy have been reported. Recommended therapy for uncomplicated shingles in pregnant HIV-infected women is oral acyclovir or valacyclovir (BIII).

Prophylaxis to prevent first episode of opportunistic disease: Varicella zoster virus (VZV) infection
IndicationFirst choiceAlternative
Abbreviations: IM = intramuscular; SQ = subcutaneous
Pre-exposure prevention:
Patients with CD4+ count >200 cells/L who have not been vaccinated, have no history of varicella or herpes zoster, or who are seronegative for VZV (CIII)

Note: routine VZV serologic testing in HIV-infected adults is not recommended

Post-exposure -- close contact with a person who has active varicella or herpes zoster:
For susceptible patients (those who have no history of vaccination or of either condition, or are known to be VZV seronegative) (AIII)
Pre-exposure prevention:
Primary varicella vaccination (Varivax), 2 doses (0.5 mL SQ) administered 3 months apart (CIII)

If vaccination results in disease because of vaccine virus, treatment with acyclovir is recommended (AIII)

Post-exposure therapy: Varicella-zoster immune globulin (VariZIG) 125 IU per 10 kg (maximum of 625 IU) IM, administered within 96 hours after exposure to a person with active varicella or herpes zoster (AIII)

Note: As of June 2007, VariZIG can be obtained only under a treatment IND (1-800-843-7477, FFF Enterprises)
transparent gifgrey bulletVZV-susceptible household contacts of susceptible HIV-infected persons should be vaccinated to prevent potential transmission of VZV to their HIV-infected contacts (BIII)
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Alternative post-exposure therapy:
transparent gifgrey bulletPost exposure varicella vaccine (Varivax) 0.5 mL SQ x 2 doses, 3 months apart if CD4+ count >200 cells/µL (CIII); or
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transparent gifgrey bulletPre-emptive acyclovir 800 mg PO 5x/day for 5 days (CIII)
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transparent gifgrey bulletThese two alternatives have not been studied in the HIV population
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Drug therapy for treatment and chronic maintenance therapy of AIDS-associated opportunistic infections in adults and adolescents: Varicella zoster virus (VZV) disease
Preferred therapy, duration of therapy, chronic maintenanceAlternative therapyOther options/issues
Varicella (chickenpox) Uncomplicated cases
transparent gifgrey bulletAcyclovir (20 mg/kg body weight up to a maximum of 800 mg PO 5x daily), valacyclovir 1,000 mg PO tid, or famciclovir 500 mg PO tid x 5-7 days (AII)
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Severe or complicated cases
transparent gifgrey bulletAcyclovir 10-15 mg/kg IV q8h x 7-10 days (AIII)
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transparent gifgrey bulletMay switch to oral acyclovir, famciclovir, or valacyclovir after defervescence if no evidence of visceral involvement is evident (AIII)
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Herpes zoster (shingles)

Acute localized dermatomal
transparent gifgrey bulletValacyclovir 1g tid or famciclovir 500 mg tid, or acyclovir 800 mg PO 5x daily x 7-10 days (AII), longer duration should be considered if lesions are slow to resolve
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Extensive cutaneous lesion or visceral involvement
transparent gifgrey bulletAcyclovir 10-15 mg/kg IV q8h until clinical improvement is evident (AII)
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transparent gifgrey bulletSwitch to oral therapy (valacyclovir 1,000 mg tid or famciclovir 500 mg tid, or acyclovir 800 mg PO 5x daily) after clinical improvement is evident, to complete a 10-14 day course (AIII)
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Progressive outer retinal necrosis (PORN)
transparent gifgrey bulletGanciclovir 5 mg/kg IV q12h, plus foscarnet 90 mg/kg IV q12h, plus ganciclovir 2 mg/0.05mL intravitreal twice weekly, and/or foscarnet 1.2 mg/0.05mL intravitreal twice weekly (AIII)
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transparent gifgrey bulletOptimization of ART (AIII)
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Acute retinal necrosis (ARN)
transparent gifgrey bulletAcyclovir 10 mg/kg IV q8h x 10-14 days, followed by valacyclovir 1,000 mg PO tid x 6 weeks (AIII)
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Infection caused by acyclovir-resistant VZV
transparent gifgrey bulletFoscarnet 90 mg/kg IV q12h (AII)
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Involvement of an experienced ophthalmologist with management of VZV retinitis is strongly recommended (AIII)

Corticosteroid therapy for herpes zoster is not recommended (DIII)

References

764. Buchbinder SP, Katz MH, Hessol N, et al. Herpes zoster and human immunodeficiency virus infection. J Infect Dis 1992;166:1153-6.
765. Engels EA, Rosenberg PS, Biggar RJ. Zoster incidence in human immunodeficiency virus-infected hemophiliacs and homosexual men, 1984-1997. J Infect Dis 1999;180:1784-9.
766. Vanhems P, Voisin L, Gayet-Ageron A, et al. The incidence of herpes zoster is less likely than other opportunistic infections to be reduced by highly active antiretroviral therapy. J Acquir Immune Def Syndr 2005;38:111-3.
767. Gebo KA, Kalyani R, Moore RD, Polydefkis MJ. The incidence of, risk factors for, and sequelae of herpes zoster among HIV patients in the highly active antiretroviral therapy era. J Acquir Immune Defic Syndr 2005;40:169-74.
768. Wallace MR, Hooper DG, Pyne JM, et al. Varicella immunity and clinical disease in HIV-infected adults. South Med J 1994;87:74-6.
769. Gnann JW, Crumpacker CS, Lalezari JP. Sorivudine versus acyclovir for treatment of dermatomal herpes zoster in human immunodeficiency virus-infected patients: results from a randomized, controlled clinical trial. Antimicrob Agents Chemother 1998;42:1139-45.
770. Harrison RA, Soong S, Weiss HL, Gnann JWJ, Whitley RJ. A mixed model for factors predictive of pain in AIDS patients with herpes zoster. J Pain Symptom Manage 1999;17:410-7.
771. Veenstra J, van Praag RM, Krol A, et al. Complications of varicella zoster virus reactivation in HIV-infected homosexual men. AIDS 1996;10:393-9.
772. Engstrom RE, Jr., Holland GN, Margolis TP, et al. The progressive outer retinal necrosis syndrome: a variant of necrotizing herpetic retinopathy in patients with AIDS. Ophthalmology 1994;101:1488-502.
773. Ormerod LD, Larkin JA, Margo CA, et al. Rapidly progressive herpetic retinal necrosis: a blinding disease characteristic of advanced AIDS. Clin Infect Dis 1998;26:34-45.
774. Yin PD, Kurup SK, Fischer SH, et al. Progressive outer retinal necrosis in the era of highly active antiretroviral therapy: successful management with intravitreal injections and monitoring with quantitative PCR. J Clin Virol 2007;38:254-9.
775. Levin MJ, Gershon AA, Weinberg A, Song LY, Fentin T, Team. Administration of live varicella vaccine to HIV-infected children with current or past significant depression of CD4+ T cells. J Infect Dis 2006;194:247-55.
776. CDC. Prevention of varicella: recommendations of the Advisory Committee on Immunization Practices (ACIP). MMWR 2007;56(No. RR-4).
777. Prober CG, Kirk LE, Keeney RE. Acyclovir therapy of chickenpox in immunosuppressed children-a collaborative study. J Pediatr 1982;101:622-5.
778. Arvin AM. Antiviral therapy for varicella and herpes zoster. Semin Pediatr Infect Dis 2002;13:12-21.
779. Carcao MD, Lau RC, Gupta A, et al. Sequential use of intravenous and oral acyclovir in the therapy of varicella in immunocompromised children. Pediatr Infect Dis J 1998;17:626-31.
780. Balfour HH, Jr., Bean B, Laskin OL, et al. Acyclovir halts progression of herpes zoster in immunocompromised patients. N Engl J Med 1983;308:1448-53.
781. Austin RB. Progressive outer retinal necrosis syndrome: a comprehensive review of its clinical presentation, relationship to immune system status, and management. Clin Eye Vis Care 2007;12:119-29.
782. Martinez E, Gatell J, Morn Y, et al. High incidence of herpes zoster in patients with AIDS soon after therapy with protease inhibitors. Clin Infect Dis 1998;27:1510-3.
783. Domingo P, Torres OH, Ris J, Vazquez G. Herpes zoster as an immune reconstitution disease after initiation of combination antiretroviral therapy in patients with human immunodeficiency virus type-1 infection. Am J Med 2001;110:605-9.
784. Breton G, Fillet AM, Katlama C, Bricaire F, Caumes E. Acyclovir-resistant herpes zoster in human immunodeficiency virus-infected patients: results of foscarnet therapy. Clin Infect Dis 1998;27:1525-7.
785. Pastuszak AL, Levy M, Schick B, et al. Outcome after maternal varicella infection in the first 20 weeks of pregnancy. N Engl J Med 1994;330:901-5.
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