Search

OBJECTIVE. Extremely preterm infants mount lower antibody responses than term infants to several vaccines. The objective of this study was to measure the immunogenicity of measles-mumps-rubella and varicella vaccines in [...]

Background. Two doses of live-attenuated varicella-zoster vaccine are recommended for human immunodeficiency virus 1 (HIV-1)-infected children with CD4% =15%. We determined the prevalence and persistence of antibody in immunized children with perinatal HIV (PHIV) and their association with number of vaccinations, combination antiretroviral therapy (cART), and HIV status. Methods. The Adolescent Master Protocol is an observational study of children with PHIV and perinatally HIV-exposed but uninfected (PHEU) children conducted at 15 US sites. In a cross-sectional analysis, we tested participants' most recent stored sera for varicella antibody using whole-cell and glycoprotein enzyme-linked immunosorbent assay. Seropositivity predictors were identified using multivariable logistic regression models and C statistics. Results. Samples were available for 432 children with PHIV and 221 PHEU children; 82% of children with PHIV and 97% of PHEU children were seropositive (P < .001). Seropositivity after 1 vaccine dose among children with PHIV and PHEU children was 100% at <3 years (both), 73% and 100% at 3-<7 years (P < .05), and 77% and 97% at ≥7 years (P < .01), respectively. Seropositivity among recipients of 2 vaccine doses was >94% at all intervals. Independent predictors of seropositivity among children with PHIV were receipt of 2 vaccine doses, receipt of 1 dose while on ≥3 months of cART, compared with none (adjusted odds ratio [aOR]: 14.0 and 2.8, respectively; P < .001 for overall dose effect), and in those vaccinated ≥3 years previously, duration of cART (aOR: 1.29 per year increase, P ≥ .02). Conclusions. Humoral immune responses to varicella vaccine are best achieved when children with PHIV receive their first dose ≥3 months after cART initiation and maintained by completion of the 2-dose series and long-term cART use. [ABSTRACT FROM AUTHOR]

Immunization with the vOka vaccine prevents varicella (chickenpox) in children and susceptible adults. The vOka vaccine strain comprises a mixture of genotypes and, despite attenuation, causes rashes in small numbers of recipients. Like wild-type virus, the vaccine establishes latency in neuronal tissue and can later reactivate to cause Herpes zoster (shingles). Using hybridization-based methodologies, we have purified and sequenced vOka directly from skin lesions. We show that alleles present in the vaccine can be recovered from the lesions and demonstrate the presence of a severe bottleneck between inoculation and lesion formation. Genotypes in any one lesion appear to be descended from one to three vaccine-genotypes with a low frequency of novel mutations. No single vOka haplotype and no novel mutations are consistently present in rashes, indicating that neither new mutations nor recombination with wild type are critical to the evolution of vOka rashes. Instead, alleles arising from attenuation (i.e., not derived from free-living virus) are present at lower frequencies in rash genotypes. We identify 11 loci at which the ancestral allele is selected for in vOka rash formation and show genotypes in rashes that have reactivated from latency cannot be distinguished from rashes occurring immediately after inoculation. We conclude that the vOka vaccine, although heterogeneous, has not evolved to form rashes through positive selection in the mode of a quasispecies, but rather alleles that were essentially neutral during the vaccine production have been selected against in the human subjects, allowing us to identify key loci for rash formation. [ABSTRACT FROM PUBLISHER]

Background. Sporadic cases of parotitis are generally assumed to be mumps, which often requires a resource-intensive public health response. This project surveyed the frequency of viruses detected among such cases.Methods. During 2009–2011, 8 jurisdictions throughout the United States investigated sporadic cases of parotitis. Epidemiologic information, serum, and buccal and oropharyngeal swabs were collected. Polymerase chain reaction methods were used to detect a panel of viruses. Anti–mumps virus immunoglobulin M (IgM) antibodies were detected using a variety of methods.Results. Of 101 specimens, 38 were positive for a single virus: Epstein-Barr virus (23), human herpesvirus (HHV)-6B (10), human parainfluenza virus (HPIV)-2 (3), HPIV-3 (1), and human bocavirus (1). Mumps virus, enteroviruses (including human parechovirus), HHV-6A, HPIV-1, and adenoviruses were not detected. Early specimen collection did not improve viral detection rate. Mumps IgM was detected in 17% of available specimens. Patients in whom a virus was detected were younger, but no difference was seen by sex or vaccination profile. No seasonal patterns were identified.Conclusions. Considering the timing of specimen collection, serology results, patient vaccination status, and time of year may be helpful in assessing the likelihood that a sporadic case of parotitis without laboratory confirmation is mumps. [ABSTRACT FROM PUBLISHER]

Background. Vaccine-strain herpes zoster (HZ) can occur after varicella vaccination. This study determined the number and proportion of HZ cases caused by vaccine-strain varicella zoster virus (VZV), assessed the positive predictive value of provider diagnosis of HZ, and computed HZ incidence rates in vaccinated and unvaccinated children. Methods. We used electronic medical records to identify all office visits with an HZ diagnosis for children aged <18 years in a managed care plan. Providers collected skin specimens and completed a questionnaire. Specimens were tested by polymerase chain reaction to identify wild-type or vaccine-strain VZV. Results. From May 2005 to September 2009, we enrolled 322 subjects. VZV was detected in 82% of specimens (84% wild-type, 15% vaccine-strain, 1% possible vaccine-wild-type recombinant). Among the 118 vaccinated subjects, VZV was detected in 70% (52% wild-type). The positive predictive value for provider diagnosis of 'definite HZ' was 93% for unvaccinated and 79% for vaccinated children. The incidence of laboratory-confirmed HZ was 48 per 100 000 person-years in vaccinated children (both wild-type and vaccine-strain) and 230 per 100 000 person-years in unvaccinated children (wild-type only). Conclusions. HZ incidence in vaccinated children was 79% lower than in unvaccinated children. Among vaccinated children, half of HZ cases were due to wild-type VZV. [ABSTRACT FROM AUTHOR]

Congenital cytomegalovirus (CMV) affects ∼1 of 150 births and is a leading cause of hearing loss and intellectual disability. It has been suggested that transmission may occur via contaminated surfaces. CMV AD169 in filtered human saliva, applied to environmental surfaces, was recovered at various time points. Samples were evaluated by culture and real-time polymerase chain reaction. CMV was found viable on metal and wood to 1 hour, glass and plastic to 3 hours, and rubber, cloth, and cracker to 6 hours. CMV was cultured from 83 of 90 wet and 5 of 40 dry surfaces. CMV was more likely to be isolated from wet, highly absorbent surfaces at earlier time points. [ABSTRACT FROM AUTHOR]

Analysis of 36 individuals over age 60 years who were immunized with Zostavax revealed varicella zoster virus (VZV) DNA in swabs of skin inoculation sites obtained immediately after immunization in 18 (50%) of 36 subjects (copy number per nanogram of total DNA, 28 to 2.1 × 106) and in saliva collected over 28 days in 21 (58%) of 36 subjects (copy number, 20 to 248). Genotypic analysis of DNA extracted from 9 random saliva samples identified vaccine virus in all instances. In some immunized individuals over age 60, vaccine virus DNA is shed in saliva up to 4 weeks. [ABSTRACT FROM PUBLISHER]

Objective: To demonstrate varicella zoster virus (VZV) infection in an asymptomatic extracranial (temporal) artery in a patient with ischemic optic neuropathy produced by VZV vasculopathy in whom the pathological changes were mistakenly identified as giant cell arteritis. Design: Case report. Setting: Teaching hospital, pathology and virology laboratory. Patient: An 80-year-old man with left ophthalmic distribution zoster who developed left ischemic optic neuropathy. Intervention: An ipsilateral temporal artery biopsy revealed inflammation that wasmistakenly identified as giant cell arteritis. The patient was initially treated with steroids but his condition did not improve. When the diagnosis of VZV vasculopathy was confirmed virologically and the patient was treated with intravenous acyclovir, his vision improved. Results: Pathological and virological studies provided proof of VZV vasculopathy in the asymptomatic temporal artery. Varicella zoster virus antigen was abundant in arterial adventitia and scattered throughout the media. With intravenous antiviral therapy, the patient's vision improved. Conclusion: Although in previously studied patients who died of chronic VZV vasculopathy after 10 to 12 months, VZV antigen was present exclusively in the intima, collective analyses of chronic cases and the asymptomatic VZV-infected temporal artery suggest that virus enters arteries through the adventitia and spreads transmurally to the intima. [ABSTRACT FROM AUTHOR]

Background. Since the introduction of live attenuated varicella zoster virus (VZV) vaccine in 1995 there has been a significant reduction in varicella incidence and its associated complications, but the impact on VZV-associated central nervous system (CNS) disease has not been assessed. Methods. In this descriptive study we evaluated patients referred to the California Encephalitis Project from 1998 to 2009 with VZV PCR-positive cerebrospinal fluid (CSF). Epidemiological, clinical, and laboratory data were collected using a standardized case form. Specimens were genotyped using multi-single nucleotide polymorphism (SNP) analysis. Results. Twenty-six specimens were genotyped from patients 12-85 years of age (median, 46 years). Clinical presentations included meningitis (50%), encephalitis (42%), and acute disseminated encephalomyelitis (ADEM) (8%). Only 11 patients (42%) had a concomitant herpes zoster rash. Genotype analysis identified 20 European Group (Clade1, Clade 3) strains; 4 Asian (Clade 2) strains, and 2 Mosaic Group (Clade 4, Clade VI) strains. One specimen was recognized as vaccine strain by identifying vaccine-associated SNPs. Conclusions. VZV continues to be associated with CNS disease, with meningitis being the most frequent clinical presentation. CNS VZV disease often presented without accompanying zoster rash. Sequencing data revealed multiple genotypes, including 1 vaccine strain detected in the CSF of a young patient with meningitis. [ABSTRACT FROM AUTHOR]