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VZV Infection (vzv + infection)
Selected AbstractsHerpetic Folliculitis is Usually a Consequence of Varicella Zoster Virus InfectionJOURNAL OF CUTANEOUS PATHOLOGY, Issue 1 2005J Blair Skin biopsies of 8 patients diagnosed with herpetic folliculitis by light microscopy were retrieved from the files of the UCSF Dermatopathology Service. Clinical and microscopical features were reviewed and tabulated, and PCR analysis was employed to seek DNA sequences specific for herpes simplex virus (HSV) and varicella zoster virus (VZV). The study group included 4 women and 4 men, ages 15 to 54. Five patients (62%) were immunosuppressed, with underlying conditions including HIV infection, leukemia, rheumatoid arthritis, and lupus erythematosus with polyarteritis nodosa. Microscopically, herpetic cytopathic changes involved the isthmus in 7/8 cases (87%), and involved the sebaceous apparatus in 4/8 cases (50%). Herpetic viropathic changes were not found within eccrine epithelium. A moderate to dense perifollicular infiltrate, comprised mostly of lymphocytes, was evident in 7/8 cases (87%). After PCR expansion of genetic material extracted from the original paraffin blocks, VZV-specific DNA sequences were detected in 8/8 cases. We conclude that herpetic folliculitis is a consequence of VZV infection. Because follicular herpetic infection is often accompanied by a dense perifollicular lymphoid infiltrate, the microscopical presentation can simulate inflammatory skin diseases such as lupus erythematosus. Level sections may be required for a specific diagnosis to be made. [source] Genotypes of varicella-zoster virus wild-type strains in GermanyJOURNAL OF MEDICAL VIROLOGY, Issue 6 2008A. Sauerbrei Abstract Surveillance of varicella-zoster virus (VZV) genotypes is indicated in Germany after implementation of universal varicella vaccination. This article reports genotyping data of 77 VZV strains obtained from 54 patients with varicella, 1 newborn with congenital varicella syndrome, 2 fetuses with intrauterine VZV infection and 20 cases with zoster. Fragments of the open reading frames (ORF) 1, 21, 22, 37, 50, 54, and 60 were analyzed by sequencing. In addition, the PstI polymorphism of the ORF 38 was characterized. Thirty strains, 22 from varicella and 8 from zoster, had the genetic markers of genotype E2, 2 of them carried new single nucleotide polymorphisms (SNP). Twenty-nine VZV isolates, 17 from varicella, and 12 from zoster, could be analyzed as E1 strains, 6 of them as E1 variants containing individual SNPs. Finally, 17 strains taken from primary VZV infection were classified as genotype M1, 13 of which belonged to the M1 subtype 1, 3 to the M1 subtype 2, and 1 to the M1 subtype 3. One strain was regarded as potential E2/J recombinant. In conclusion, VZV genotypes E2, E1, and M1 can be found in nearly equal incidence in varicella in Germany. The most frequent group is attributed to the genotype E2. Genotype M1 strains can only be detected after primary VZV infection and not in zoster cases. The possible recombinant could not be classified definitely by the scattered SNP method used and, therefore, has to be confirmed by full-genome sequencing studies. J. Med. Virol. 80:1123,1130, 2008. © 2008 Wiley-Liss, Inc. [source] Use of a rodent model to show that varicella-zoster virus ORF61 is dispensable for establishment of latency,JOURNAL OF MEDICAL VIROLOGY, Issue S1 2003Hitoshi Sato Abstract Varicella-zoster virus (VZV) results in a latent infection in humans after primary infection. Latency has also been established in guinea pigs and rats after inoculation with the virus. It was found that infection of cotton rats with the Oka vaccine strain of VZV results in a latent infection. To begin to identify which genes are required for latency, we infected cotton rats with VZV strain Oka that is deleted for ORF61. ORF61 protein transactivates certain VZV promoters and enhances the infectivity of viral DNA in transient transfections. Deletion of ORF61 results in abnormal syncytia and impairs the growth of VZV in vitro. Inoculation of cotton rats with ORF61-deleted Oka virus resulted in latent VZV infection in the nervous system similar to that seen for animals infected with parental virus. Thus, the cotton rat can be used to study the ability of mutants in the Oka vaccine strain of VZV to establish latent infection. J. Med. Virol. 70:S79,S81, 2003. © 2003 Wiley-Liss, Inc. [source] Modelling the impact of vaccination on the epidemiology of varicella zoster virus in AustraliaAUSTRALIAN AND NEW ZEALAND JOURNAL OF PUBLIC HEALTH, Issue 6 2005Heather F. Gidding Objective: To model the impact of universal varicella vaccination in Australia. Methods: The results of an Australia-wide serosurvey for varicella zoster virus (VZV) immunity were used to parameterise realistic, age-structured deterministic models (RAS) developed by Brisson and colleagues. We examined the impact of a vaccination program for one-year-olds alone, and with a catch-up campaign for 11 -year-olds, on the incidence of varicella and zoster, using Australia's population structure. Morbidity was then determined by calculating the number of hospital in-patient days. Results: Infant vaccination is predicted to reduce the incidence of varicella. However, zoster incidence is expected to increase initially, assuming exposure to varicella boosts immunity to zoster. Accumulated morbidity from both varicella and zoster is predicted to remain above that expected without vaccination for the first 70 years of an infant program (assuming 90% coverage with boosting for 20 years). However, after 70 years the net health savings from vaccination are predicted to increase substantially. Conclusions and Implications: Infant vaccination is expected to be a successful long-term commitment to reducing morbidity associated with VZV infection in Australia. [source] Clinical efficacy of prophylactic strategy of long-term low-dose acyclovir for Varicella-Zoster virus infection after allogeneic peripheral blood stem cell transplantation,CLINICAL TRANSPLANTATION, Issue 6 2008Dong Hwan Kim Abstract:, Varicella-Zoster virus infection (VZV) has a high incidence post-allogeneic peripheral blood stem cell transplant (PBSCT). However, data regarding long-term acyclovir prophylaxis for VZV prevention are limited. We evaluated the clinical efficacy of long-term low-dose acyclovir prophylaxis for VZV infection after allogeneic PBSCT at the Princess Margaret Hospital (PMH), Canada and the Kyungpook National University Hospital (KNUH), Korea. The acyclovir prophylaxis regimen at PMH was acyclovir 400 mg/d orally until engraftment, and at KNUH was acyclovir 800 mg/d orally until immunosuppression discontinuation. Long-term acyclovir prophylaxis was given to 26/193 (14%) patients in the PMH group and 73/79 (92%) patients in the KNUH group. In the PMH group, 42 cases (22%) developed VZV infection, while six cases (8%) had VZV infection in the KNUH group (p = 0.005). With a median of 26.5 months of follow-up, the incidences of VZV infection at one and two yr were 15.8% and 20.7% in the PMH group, and 2.5% and 5.8% in the KNUH group, respectively (p = 0.001). By controlling the other potential risk factors for VZV infection in multivariate analysis, the use of long-term acyclovir was the only protective factor for VZV infection after allogeneic PBSCT (p = 0.04, hazard ratio = 0.296). Long-term use of acyclovir appears to be protective for VZV infection after allogeneic PBSCT, especially during the period of immunosuppressive therapy. [source] | ||||||||||