Primary Varicella Research Articles

The epidemiology and economic impact of varicella-related hospitalizations in Turkey from 2008 to 2010: a nationwide survey during the pre-vaccine era (VARICOMP study)

Varicella can cause complications that are potentially serious and require hospitalization. Our current understanding of the causes and incidence of varicella-related hospitalization in Turkey is limited and sufficiently accurate epidemiological and economical information is lacking. The aim of this study was to estimate the annual incidence of varicella-related hospitalizations, describe the complications, and estimate the annual mortality and cost of varicella in children. VARICOMP is a multi-center study that was performed to provide epidemiological and economic data on hospitalization for varicella in children between 0 and 15years of age from October 2008 to September 2010 in Turkey. According to medical records from 27 health care centers in 14 cities (representing 49.3% of the childhood population in Turkey), 824 children (73% previously healthy) were hospitalized for varicella over the 2-year period. Most cases occurred in the spring and early summer months. Most cases were in children under 5years of age, and 29.5% were in children under 1year of age. The estimated incidence of varicella-related hospitalization was 5.29-6.89 per 100,000 in all children between 0-15years of age in Turkey, 21.7 to 28 per 100,000 children under 1year of age, 9.8-13.8 per 100,000 children under 5years of age, 3.96-6.52 per 100,000 children between 5 and 10years of age and 0.42 to 0.71 per 100,000 children between 10 and 15years of age. Among the 824 children, 212 (25.7%) were hospitalized because of primary varicella infection. The most common complications in children were secondary bacterial infection (23%), neurological (19.1%), and respiratory (17.5%) complications. Secondary bacterial infections (p < 0.001) and neurological complications (p < 0.001) were significantly more common in previously healthy children, whereas hematological complications (p < 0.001) were more commonly observed in children with underlying conditions. The median length of the hospital stay was 6days, and it was longer in children with underlying conditions (<0.001). The median cost of hospitalization per patient was $338 and was significantly higher in children with underlying conditions (p < 0.001). The estimated direct annual cost (not including the loss of parental work time and school absence) of varicella-related hospitalization in children under the age of 15years in Turkey was $856,190 to $1,407,006. According to our estimates, 882 to 1,450 children are hospitalized for varicella each year, reflecting a population-wide occurrence of 466-768 varicella cases per 100,000 children. In conclusion, this study confirms that varicella-related hospitalizations are not uncommon in children, and two thirds of these children are otherwise healthy. The annual cost of hospitalization for varicella reflects only a small part of the overall cost of this disease, as only a very few cases require hospital admission. The incidence of this disease was higher in children <1year of age, and there are no prevention strategies for these children other than population-wide vaccination. Universal vaccination is therefore the only realistic option for the prevention of severe complications and deaths. The surveillance of varicella-associated complications is essential for monitoring of the impact of varicella immunization.

Cardiac-Related Varicella Mortality in Childhood: A Literature Review With Clinical Experience

Among unvaccinated populations, primary varicella zoster virus (VZV) infection results in a minor childhood illness for the majority of individuals. Mortality is rare, and fatalities associated with cardiac complications are exceptional. In a population where routine VZV vaccination is not practised, we report a death in a previously healthy child secondary to VZV myocarditis. A literature review of cardiac-related VZV mortality in childhood is included. This identified a further 13 cases where death was associated with or attributable to, direct involvement of the myocardium or conducting system with what is frequently considered a benign childhood illness.

Varicella-related musculoskeletal complications in children

Eight children with post-varicella musculoskeletal complications were treated between 2001 and 2009. The complications that were observed were cellulitis (three children), pyomyositis (three children), osteomyelitis (two children) and gangrene (one child). On average, 8.8 days elapsed between primary varicella infection and complication. The most common presentation was pain. Before we started treating them, all children received antibiotics during interhospital transfers (average: 2.4). Interventions included drainage (eight), fasciatomy (one), arthrotomy (one), bone drilling (one), and amputation (one). Blood cultures were negative in all children. Two children had positive pus cultures for Staphylococcus aureus, one of them had a methicillin-resistant S. aureus infection. One of the four children who developed coagulopathy ended with significant morbidity. Varicella-related methicillin-resistant S. aureus osteomyelitis suggests a widening spectrum of these infections.

Varicella-zoster virus immunity in dermatological patients on systemic immunosuppressant treatment

Primary varicella infection is caused by varicella-zoster virus (VZV). It is a common childhood infection, which is usually benign but can occasionally cause morbidity and mortality. In immunosuppressed adults, atypical presentation and disseminated disease can occur with significant morbidity and mortality. A VZV vaccine is available. This study was designed to measure the prevalence of immunity to VZV and to determine the predictive value of a self-reported history of varicella infection in a population of dermatological patients receiving systemic immunosuppressant therapy. We sought to assess the need for routine serological testing for varicella-zoster immunity in this cohort. Serological testing for VZV immunity was done on 228 patients receiving systemic immunosuppressive treatment for a dermatological condition. Information regarding a history of previous primary VZV infection was obtained from each patient. Two hundred and twenty-eight patients had VZV serology performed. The mean age of the patients was 49·6 years. The prevalence of VZV seropositivity in this cohort was 98·7%. One hundred and two patients (44·7%) reported having a definite history of primary VZV. The sensitivity of a self-reported history of VZV infection was 45·3% with a specificity of 100%. The positive and negative predictive values of a self-reported history of VZV for serologically confirmed immunity were 100% and 2·3%, respectively. The prevalence of VZV IgG antibodies in our cohort of Irish dermatology patients receiving immunosuppressive therapy is 98·7%. A recalled history of varicella infection is a good predictor of serological immunity. This study has shown that there are VZV-susceptible individuals within our cohort. These patients did not have a clear history of previous infection. We recommend serological testing of patients without a clear history of infection prior to the commencement of immunosuppressive therapy and vaccination of patients with negative serology.

Exploring the Impact of Exposure to Primary Varicella in Children on Varicella-Zoster Virus Immunity of Parents

Varicella-zoster virus (VZV) causes both primary varicella, and through reactivation of the virus, herpes zoster. It is hypothesized that VZV-immune adults may reduce the probability of developing herpes zoster through exposure to varicella. In this study we examine the existence of immunological boosting in VZV-immune adults after close contact with primary varicella. We followed-up 18 parents with household exposure to primary varicella for 1 y. Fifteen age-matched healthy and 20 older volunteers served as control groups. Cellular (IFN-γ ELISPOT) and humoral responses were measured. Data analyses were performed by t-tests and linear mixed models. The young control group only showed higher cellular responses than the older control group and the exposed group 1 mo after exposure. The exposed group had a strong tendency toward higher cellular responses compared to the older control group, reaching significance 1 y post-exposure. The best fitting linear mixed model predicts a decline in cellular response of 50% between 1 wk and 1 mo post-exposure, followed by an increase to attain an 80% higher level at 1 y compared to the first week post-exposure. No significant results emerged based on the humoral response of the individual parents in the exposed group, despite a general tendency toward higher antibody concentrations in the exposed versus the control groups. No significant difference in humoral immunity was found between the control groups. One year after initial re-exposure to VZV, VZV-immune adults showed a rise in cellular response as assessed by IFN-γ ELISPOT, and steady-state levels for the humoral response.

Primary varicella zoster infection associated with fingolimod treatment

The therapy of relapsing-remitting multiple sclerosis (MS) has been revolutionized since the appearance of first-line disease-modifying drugs such as interferon-β and glatiramer acetate. These drugs are associated with moderate efficacy but no life-threatening risks. In contrast, new treatments, which have recently entered the MS scene, have been reported to display a superior efficacy with respect to relapse rate and progression of disability but also an unexpected risk of fatal adverse events.1,2 The oral drug sphingosine-1-phosphate-receptor modulator, fingolimod (FTY720), has been recently shown to have superior efficacy vs IM interferon-β 1a on clinical and MRI outcomes (TRANSFORMS study).3 However, 2 fatal viral infections occurred in patients who received fingolimod, including one case of primary varicella zoster (VZ). Recently, other adverse effects have been reported, mainly affecting the vascular system, such as a case of hemorrhagic focal …

A case of intracranial saccular aneurysm after primary varicella zoster virus infection

We report a case of intracranial saccular aneurysm that developed 3 years after post-varicella ischemic stroke. A 6-year-old girl without apparent immunologic defects presented with right hemiparesis and expressive aphasia 1 month after chickenpox. Her magnetic resonance imaging scans revealed left basal ganglia infarction because of left lenticulostriate artery occlusion. Although her neurologic symptoms improved gradually, segmental irregular narrowing remained in the A1 and M1 segments of the left anterior and middle cerebral arteries, respectively. Three years later, the follow-up magnetic resonance angiography indicated saccular aneurysm in the anterior communicating artery and the anti-VZV IgG antibody index in the cerebrospinal fluid was elevated. Subclinical reactivation of VZV and the segmental vascular narrowing might cause intracranial aneurysm, even in immunocompetent children.

A recalcitrant acrodermatitis continua of Hallopeau successfully treated with etanercept

Acrodermatitis continua of Hallopeau (ACH) is considered as a localized form of pustularpsoriasis that is usually refractory to the treatment. The condition is characterized by sterile pustules, onychodystrophy, anonychia, and osteolysis of distal phalanges. The authors report a case of recalcitrant ACH who previously failed to topical corticosteroid, methotrexate, acitretin, and phototherapy and rapidly responded to etanercept in combination with acitretin. The primary varicella infection occurred during the therapy. The patient was able to discontinue etanercept within four months after starting the treatment. The lesion was then under-controlled by acitretin and topical clobetasol ointment with an 8-month clinical remission.

Granulomatous skin lesions complicating Varicella infection in a patient with Rothmund-Thomson syndrome and immune deficiency: case report

Rothmund-Thomson syndrome (RTS)(OMIM 268400) is a rare autosomal recessive genodermatosis characterized by poikiloderma, small stature, skeletal and dental abnormalities, cataract and an increased risk of cancer. It is caused by mutations in RECQL4 at 8q24. Immune deficiency is not described as a classical feature of the disease. Here we report the appearance of granulomatous skin lesions complicating primary Varicella Zoster Virus infection in a toddler with Rothmund Thomson syndrome and immune deficiency. Although granulomatous disorders are sometimes seen after Herpes zoster, they are even more rare after Varicella primary infection. Granulomas have hitherto not been described in Rothmund-Thomson syndrome. With this report we aim to stress the importance of screening for immune deficiency in patients with Rothmund-Thomson syndrome.

Serious infections in patients with inflammatory bowel disease receiving anti‐tumor‐necrosis‐factor‐alpha therapy: An Australian and New Zealand experience

Anti-tumor-necrosis-factor-alpha (anti-TNF-α) medications are effective in inflammatory bowel disease (IBD), but have an increased risk of tuberculosis (TB) and serious infections. The aim of this study was to examine the Australian/New Zealand experience of serious infections and TB in IBD patients receiving anti-TNF-α therapy from 1999-2009. Serious infections, defined as 'requiring hospital admission' and TB cases in patients receiving, or within 3 months following, anti-TNF-α therapy were analyzed across Australia and New Zealand. Patient demographics, IBD medications, duration of anti-TNF-α therapy, and infection details were collected. A total of 5562 IBD patients were managed across the centers. Of these, 489 (16.8%) Crohn's disease and 137 (5.2%) ulcerative colitis patients received anti-TNF-α therapy. There were three cases of latent TB that received prophylaxis prior to anti-TNF-α therapy. No cases of active TB were reported. Fourteen (2.2%) serious infections occurred. Seven occurred in patients receiving anti-TNF-α therapy for less than 6 months, including two cases of primary Varicella zoster (VZV), two cases of Pneumocystis jiroveci pneumonia, two cases of Staphylococcus aureus bacteremia, and one severe flu-like illness. Six patients were taking additional immunosuppressive medications. The other seven infections occurred after 6 months (mean 32.6 ± 24.3 months) and included one case of primary VZV, one flu-like illness, and five bacterial infections. All infections resolved with treatment. TB is a very rare complication of anti-TNF-α therapy in Australia and New Zealand. Serious infections are uncommon but early opportunistic infections with Pneumocystis jiroveci pneumonia suggest a need for vigilance in patients on multiple immunosuppressive medications. VZV vaccination prior to immunosuppressive therapy should be considered in VZV-naïve patients.

Disseminated Cutaneous Varicella Zoster Virus Infections During Infliximab Therapy for Crohn’s Disease: Case Report of Two Pediatric Patients at One Institution

Infliximab is a monoclonal antibody against tumor necrosis factor-a (TNF-a) that has been approved for the treatment of rheumatoid arthritis and Crohn’s disease. It is used in steroid-sparing regimens for patients who have had an inadequate response to conventional therapy. There are a number of studies that have shown an increased risk of infections with bacteria, fungi, mycobacterium, and more recently, chronic viral infections in patients receiving TNF-a antagonists. We report 2 cases of pediatric patients on infliximab therapy for Crohn’s disease who presented with disseminated cutaneous varicella zoster and primary varicella infections. Despite prompt and appropriate antiviral therapy both patients continued to manifest clinical findings of varicella zoster virus (VZV) infection and ultimately required hospitalization.

Varicella and Herpes Zoster. Part 2: Therapy and Prevention

In Germany, five antiviral agents are approved for antiviral therapy in zoster patients (acyclovir, valacyclovir, famciclovir, brivudine, and foscarnet). They should be administered within 72 h after rash onset and can significantly shorten viral replication and reduce the complications. In 2004, the German Standing Committee on Vaccination (STIKO) at the Robert Koch Institute suggested the active immunization against varicella with a live attenuated varicella vaccine (Oka strain) for all children and young persons. The first dose is given between the ages of 11 and 14 months, the second at the earliest 4 weeks later. Passive immunization is indicated as postexposure prophylaxis in high-risk individuals within 72-96 h after exposure. High-risk individuals are pregnant women, immunocompromised patients, or newborns, whose mothers had a primary varicella infection 5 days before or 2 days after birth. The Shingles Prevention Study demonstrated that vaccination is the most effective strategy for prevention of herpes zoster and postherpetic neuralgia.

Advances in the understanding of the pathogenesis and epidemiology of herpes zoster

The primary varicella zoster virus (VZV) infection results in chickenpox (varicella), which is transmitted via the airborne route. VZV is highly infectious, but in the USA the incidence of varicella has been reduced by 76-87% as a result of the varicella vaccine. The virus establishes latency in the dorsal root ganglia during varicella and, when reactivated, travels along the sensory nerve axons to cause shingles (herpes zoster [HZ]). There are over 1 million cases of HZ in the USA each year, with an estimated lifetime attack rate of 30%. The incidence of HZ, which causes significant morbidity, increases with age and reaches approximately 10 cases per 1,000 patient-years by age 80. Cell-mediated immunity (CMI) is known to decline with age as part of immunosenescence, and decreased CMI is associated with reactivation of VZV. This article provides an overview of our emerging understanding of the epidemiology and pathogenesis of varicella and HZ, in addition to exploring the current theories on latency and reactivation. Understanding the risk factors for developing HZ and the complications associated with infection, particularly in older people, is important for prompt diagnosis and management of HZ in primary care, and they are therefore also reviewed.

779 PF-03491390 PAN-CASPASE INHIBITOR DECREASES LIVER INJURY AND FIBROSIS IN A MURINE MODEL OF NON-ALCOHOLIC STEATOHEPATITIS (NASH)

with 5% of patients who received the BAP placebo in the SOC arm. Lymphopenia was the most common reason for discontinuation of BAP. There were 2 deaths reported in the study (primary varicella and B-cell lymphoma) and these were considered related to study medication and a potential consequence of the lymphopenia. Conclusions: When combined with the SOC, BAP increased the rate of RVR and cEVR in genotype 1 patients; however, the drug did not confer an SVR advantage due in part to frequent safetyrelated dose reductions and discontinuations for both BAP and SOC. Further development of BAP has been halted because of the unfavourable benefit:risk ratio. Investigations are ongoing to explore the mechanism of BAP-related toxicity.

Varicella-zoster virus meningoencephalitis in an immunocompetent patient without a rash

Varicella-zoster virus (VZV) is an unusual cause of meningoencephalitis in the immunocompetent patient. Most cases of VZV-associated aseptic meningitis or encephalitis are associated with the skin rash of primary varicella, localized herpes zoster, or disseminated zoster. We report a case of VZV meningoencephalitis without a rash occurring in a normal host.

Early detection of Varicella-Zoster Virus (VZV)-specific T-cells before seroconversion in primary varicella infection: case report

Here we report the case of a 54-year old, immunocompetent German patient with primary varicella whose Varicella-Zoster Virus (VZV)-specific T-cell responses could be detected early in infection and before the onset of seroconversion. This case demonstrates that the detection of VZV-specific T-cells may under certain circumstances support the diagnosis of a primary varicella infection, as for example in cases of atypical or subclinical varicella or in the absence of detectable VZV DNA in plasma.

Oral Fingolimod or Intramuscular Interferon for Relapsing Multiple Sclerosis

Fingolimod (FTY720), a sphingosine-1-phosphate-receptor modulator that prevents lymphocyte egress from lymph nodes, showed clinical efficacy and improvement on imaging in a phase 2 study involving patients with multiple sclerosis. In this 12-month, double-blind, double-dummy study, we randomly assigned 1292 patients with relapsing-remitting multiple sclerosis who had a recent history of at least one relapse to receive either oral fingolimod at a daily dose of either 1.25 or 0.5 mg or intramuscular interferon beta-1a (an established therapy for multiple sclerosis) at a weekly dose of 30 microg. The primary end point was the annualized relapse rate. Key secondary end points were the number of new or enlarged lesions on T(2)-weighted magnetic resonance imaging (MRI) scans at 12 months and progression of disability that was sustained for at least 3 months. A total of 1153 patients (89%) completed the study. The annualized relapse rate was significantly lower in both groups receiving fingolimod--0.20 (95% confidence interval [CI], 0.16 to 0.26) in the 1.25-mg group and 0.16 (95% CI, 0.12 to 0.21) in the 0.5-mg group--than in the interferon group (0.33; 95% CI, 0.26 to 0.42; P<0.001 for both comparisons). MRI findings supported the primary results. No significant differences were seen among the study groups with respect to progression of disability. Two fatal infections occurred in the group that received the 1.25-mg dose of fingolimod: disseminated primary varicella zoster and herpes simplex encephalitis. Other adverse events among patients receiving fingolimod were nonfatal herpesvirus infections, bradycardia and atrioventricular block, hypertension, macular edema, skin cancer, and elevated liver-enzyme levels. This trial showed the superior efficacy of oral fingolimod with respect to relapse rates and MRI outcomes in patients with multiple sclerosis, as compared with intramuscular interferon beta-1a. Longer studies are needed to assess the safety and efficacy of treatment beyond 1 year. (ClinicalTrials.gov number, NCT00340834.)

Review article: chronic viral infection in the anti‐tumour necrosis factor therapy era in inflammatory bowel disease

Anti-tumour necrosis factor (TNF) therapy is now well established in the treatment of inflammatory bowel disease and the risk of opportunistic infection is recognized. However, specific considerations regarding screening, detection, prevention and treatment of chronic viral infections in the context of anti-TNF therapy in inflammatory bowel disease are not widely adopted in practice. To provide a detailed and comprehensive review of the relevance of chronic viral infections in the context of anti-TNF therapy in inflammatory bowel disease. Literature search was conducted using Medline, Pubmed and Embase using the terms viral infection, hepatitis, herpes, CMV, EBV, HPV, anti-TNF, infliximab, adalimumab, certolizumab pegol and etanercept. Hepatitis B and C and HIV had the largest literature associated and these have been summarized in Tables. Particular risks are associated with the use of anti-TNF drugs in patients with hepatitis B infection, in whom reactivation is common unless anti-viral prophylaxis is used. Reactivation of herpes zoster is the most common viral problem associated with anti-TNF treatment, and may be particularly severe. Primary varicella infection may present with atypical features in patients on anti-TNF. Appreciation of risks of chronic viral disease associated with anti-TNF therapy may permit early recognition, prophylaxis and treatment.

Varicella Zoster Virus (VZV) in Solid Organ Transplant Recipients

-herpesvirus family. VZV is presentworldwide and is highly infectious. Primary infection leadsto acute varicella or ‘chickenpox,’ usually from exposureeither through direct contact with a skin lesion or throughairborne spread from respiratory droplets (1,2). After initialinfection, VZV establishes lifelong latency in cranial nerveanddorsalrootganglia,andcanreactivateyearstodecadeslater as herpes zoster (HZ) or ‘shingles’ (3). More than90% of adults in the United States acquired the disease inchildhood, while the majority of children and young adultshave been vaccinated with the live virus vaccine (2,4).Primary varicella typically presents with fever, constitu-tional symptoms and a vesicular, pruritic, widely dissem-inated rash that primarily involves the trunk and face (5).Thesymptomsusuallyresolvewithin7–10days,butinrarecases primary varicella leads to more severe disease andvisceral invasion. Complications, such as hepatitis, pancre-atitis, pneumonitis and encephalitis are infrequent but canbelife-threatening;adultsandveryyoungchildrenaremorelikely to develop such complications from primary infection(6,7). Rates of hospitalization and mortality due to varicellahave dropped with the institution of routine childhood vari-cella vaccination (8,9).Nearly all patients with HZ develop an exanthem of vesic-ular lesions in a dermatomal distribution. The annual inci-dence of HZ in the general population is 1.5–3.0 cases per1000 persons (2), and is estimated to occur in up to 20%of individuals during their lifetime (10). Secondary compli-cations such as bacterial superinfection and postherpeticneuralgia (PHN), or chronic neuropathic pain at the site ofHZ, lead to increased morbidity (11).Over 90% of adult solid organ transplant (SOT) recipientswill be seropositive for VZV. Rates are lower in pediatrictransplants(12,13),butimmunitywillincreaseasuptakeofvaricella vaccine improves. Varicella is rare in adult SOT re-cipients,butcanbedevastating,withvisceralinvolvement,severe skin disease, and disseminated intravascular coag-ulation (14–19). HZ is a frequent infectious complication inSOT recipients with an incidence of approximately 8–11%during the first 4 years posttransplant (20–22). Invasive dis-ease and dissemination similar to that seen in primary VZVinfection are uncommon but have been reported in SOTand other immunocompromised populations, and level ofimmunosuppression may alter the risk of developing thesecomplications (17,23,24). Rates of PHN in SOT recipi-ents may also be higher than in immunocompetent popu-lations (22).

Immunogenicity of the Live Attenuated Varicella Vaccine Following Allogeneneic HCT.

Abstract 1137Poster Board I-159The live attenuated varicella vaccine (VARIVAX, Merck & Co., Inc) was licensed in 1995. Initial Advisory Committee on Immunization Practices [ACIP] recommended one dose of vaccine in children aged 12-18 months, catch-up vaccination of VZ seronegative children 19 months-12 years old, and vaccination of VZ seronegative older children and adults with close contact to persons at high risk for serious complications secondary to varicella. In 2006, due to breakthrough cases of varicella in recipients of a single dose of Varivax, the ACIP recommended 2 doses of vaccine in healthy children at 12-15 months and 4-6 years of age, a second dose in children, adolescents, and adults who previously received only one dose, and routine vaccination of all healthy persons 13 years or older without evidence of immunity. The ACIP also recommended Varivax in HIV-infected children and adults with circulating CD4+ T lymphocyte counts ≥ 200 cells/ul. There are no studies assessing Varivax following alloHCT. Nevertheless, up to 30% of children are VZ seronegative before transplant and many lose seroprotection following HCT. Due to the increased morbidity of primary varicella acquired later in life and the safety of Varivax in pediatric patients with ALL in remission on maintenance therapy, HIV infected children, and pediatric solid organ transplant recipients despite concomitant immunosuppression, this institution has instituted vaccination of VZ seronegative children following alloHCT. To reduce the potential risk of vaccination with a live attenuated vaccine, susceptible (VZ seronegative) patients had to be ≥ 2 years post HCT, off all immunosuppressive therapy, and similar to the ACIP recommendations in HIV-infected individuals have a circulating CD4 cell count >200 cells/ul. In addition, patients were required to have a PHA T cell proliferative response >75% of the lower limit of normal and demonstrate antibody response to >1 vaccine administered post HCT. To date, 34 patients have received Varivax following an HLA matched related (n=16), HLA mis-matched related (n=5) or unrelated (n=13) HCT. Patients were transplanted for acute leukemia (n=15), an immunodeficiency disorder (n=10), MDS/aplastic anemia (n=2), JMML (n=1), HLH (n=2), hemoglobinopathy (n=3), or Kostman's syndrome (n=1). Eleven of 34 patients received a T cell depleted graft. The median time to vaccination post HCT, age at HCT and age at vaccination were 4, 4, and 8.4 years, respectively. No patient had a serious adverse event. One of 34 patients developed a transient rash which resolved within 24 hours. Pre and post vaccine titers are currently available in 31 patients, 22 of whom responded (seroconverted) following Varivax. Four patients who failed to seroconvert were tested for development of T cell specific VZ response; three of the four responded. There was no significant difference in response between recipients of an unrelated or HLA matched related HCT. All 5 recipients of a TCD MM related HCT responded. These data suggest that Varivax is safe and immunogenic following HCT when given according to preset clinical and immunologic requirements. DisclosuresOff Label Use: Live attenuated varicella vaccine post HCT.