No description available.

Objetivo: Determinar si la presentación del herpes zoster en el hospital Dos de Mayo muestra variación estacional. Materiales y Métodos: Se estudiaron casos de herpes zoster atendidos en el hospital Nacional Dos de Mayo de Lima-Perú entre los años 2002 a 2006. Se determinaron las distribuciones de casos según mes y estación para cada año de estudio, y se aplicaron pruebas estadísticas para analizar significación de los valores obtenidos. Resultados: Se incluyeron 816 casos. La distribución mensual mostró predominio de casos en los meses de verano, aunque sin observarse una clara tendencia estacional. La distribución de casos acumulados según estación fue: 233 (28,6%) en el verano, 205 (25,1%) en otoño, 190 (23,3%) en invierno y 188 (23,0%) en primavera. Aunque la frecuencia de casos en verano fue superior al de las otras estaciones, no se evidenció que la diferencia fuera de significación estadística. Conclusiones: Los resultados del estudio no demuestran que los casos de herpes zoster en el hospital Dos de Mayo presenten variación estacional. / -- Objective: To assess whether cases of herpes zoster at hospital Dos de Mayo exhibit a seasonal presentation. Materials and Methods: Cases of herpes zoster attended at hospital Nacional Dos de Mayo in Lima-Perú from 2002 and 2006 were studied. Cases were distributed according to the months and the seasons for each year, and statistical analysis was performed. Results: A total of 816 cases were included. Monthly distribution of cases showed predominance during summer months without a clear seasonal trend. Distribution of accumulated cases according to season was as follows: 233 (28,6%) in summer, 205 (25,1%) in fall, 190 (23,3%) in winter and 188 (23,0%) in spring. Whereas increased frequency was detected in summer, no statistically significance was disclosed. Conclusions: Results failed to show a seasonal variation for cases of herpes zoster at hospital Dos de Mayo.

Human herpes virus type 8 (HHV-8) is strongly implicated as the etiological agent of Kaposi’s sarcoma (KS). The incidence of KS in South Africa is increasing in parallel with the HIV-1 epidemic. Molecular and serological prevalence of HHV-8 in HIV-1 infected individuals with and without KS was investigated. DNA fragments from ORF26 (capsid, 330BAM233) and ORF75 (tegument) regions were used to determine the prevalence of HHV-8 DNA in peripheral blood mononuclear cells (PBMC) from 429 HIV-1 infected individuals, 95 of whom had histologically confirmed KS. Of those without KS, 14 (4.2%) were PGR positive for HHV-8 DNA. In the individuals with KS, the proportion of HHV-8 DNA positive PBMC samples was 11 times higher (46/95,48%). Similarly, an immunofluorescence assay showed that 78% of KS patients had antibodies to HHV-8 compared to 16% of KS negative individuals. Among the KS group, 93% of PCRpositive samples were also HHV-8 antibody positive compared to only 66% of PCR negative samples indicating that viremia is associated with good antibody responses. Matched lymph node and PBMC samples were available for 8 patients. HHV-8 DNA was more frequently detected in the lymph node (3/8) than in the blood (1/8), suggesting that the lymph nodes are a reser / o r for HHV-8. These data confirm the association between HHV-8 and KS and suggest that there is a high background prevalence of HHV-8 infection in HIV-1 infected individuals in South Africa. The ORP 75 gene of 40 HHV-8 strains was sequenced and the phylogenetic relationships between South African and already published sequences were investigated. The majority (n=29) of strains overlapped with the published A and B subgroups and were termed A/B variants.Three strains were classified as subgroup C while 8 sequences did not cluster with any of the previously classified subgroups and were termed novel (N) group. The DNA distance of this novel group differed from the A, B and C subgroups by 4.7%, 3.8% and 4,5% respectively although within the N group there was only 0.4% variation. The addition of this group significantly increased the number of subgroup-specific polymorphisms from 17 to 47 over a 804 bp region. There was sufficient inter-subgroup genetic diversity that single strand conformational polymorphisms (SSCP) could be used to rapidly identify them. Thus, based on the analysis of the ORF75 gene, a unique HHV-8 sub-group is present in South Africa which accounts for 20% of circulating strains. Further studies are required to determine the extent of evolutionary phytogeny, distribution and pathogenic potential of this novel group.

During herpes simplex virus 1 (HSV-1) replication, newly constructed capsids escape the nucleus to undergo maturation in the cytoplasm via a process termed nuclear egress. Capsids perform nuclear egress through localized disruption of the nuclear lamina, envelopment of the inner nuclear membrane to create a perinuclear enveloped virion, and de-envelopment of the outer nuclear membrane for capsid release into the cytoplasm. Critical virial factors for this process are viral proteins pUL31 and pUL34 that interact to form heterodimers. These heterodimers form larger hexameric arrays to drive membrane budding. Through the characterization of phenotypes of UL34 point mutants, we are able to further study the underlying mechanisms of nuclear lamina disruption and nuclear budding. One such mutant, UL34(Q163A), results in impaired virus production, cell-cell spread, and an inability to disrupt lamin A/C networks. Selection for extragenic suppression of UL34(Q163A) yielded the UL31(R229L) mutation, that partially rescued the growth and spread defects of UL34(Q163A), but was unable to regain the ability to disrupt lamin A/C networks. Through this study we concluded that disruption of lamin A/C networks was not required for efficient HSV-1 replication. In order to understand the underlying mechanisms of membrane budding, the previously characterized UL34(CL13) double mutant, which results in a 100-fold reduction in virus production, a severe impairment in cell-cell spread, and an accumulation of capsid-less perinuclear vesicles was further studied. Characterization of the single mutations of UL34(CL13), UL34(R158A) and UL34(R161A) revealed that neither single mutation was responsible for spread or growth defect, but that either single mutation resulted in a promiscuous budding phenotype. Through this study, we concluded that although individual steps of the nuclear egress pathway are tightly regulated, alteration of the regulation at a single step does not grossly impact HSV-1 replication.

Marek's disease virus (MDV), the etiologic agent of Marek's disease, is a potent oncogenic herpesvirus. MDV is highly contagious and elicits a rapid onset of malignant T-cell lymphomas in chickens within several weeks after infection. The MDV genome encodes an oncoprotein, Meq, which shares resemblance with the Jun/Fos family of bZIP transcription factors. Similar to c-Jun, the leucine zipper region of Meq allows the formation of homo- and heterodimers. Meq homo- and heterodimers have different DNA binding affinities and transcriptional activity; therefore, they may differentially regulate transcription of viral and cellular genes. Previous in vitro data has suggested that Meq homodimers may be involved in regulating viral latency/reactivation, while Meq/c-Jun heterodimers are involved in transformation. Therefore, this research investigates the role of Meq homodimers and Meq-Jun heterodimers in the pathogenicity of MDV, by generating chimeric meq genes, which contain the leucine zipper region of the yeast transcription factor GCN4 (meqGCN) or leucine zipper region of c-Fos (meqFos). Thus producing Meq proteins that exclusively homodimerize (MeqGCN) or heterodimerize with Jun family members (MeqFos). Recombinant viruses (rMd5-MeqGCN and rMd5- MeqFos) containing the chimeric genes meqGCN or meqFos, respectively, in place of parental meq were generated with overlapping cosmid clones of Md5, a very virulent MDV strain. The chimeric genes were evaluated in vitro and retained DNA binding and transactivation/repressive functions, however, selected cells expressing MeqGCN and MeqFos had reduced colony formation in soft agar. Both the rMd5-MeqGCN and rMd5- MeqFos viruses replicated in vitro and in vivo, but rMd5-MeqGCN was unable to transform T-cells in infected chickens, while rMd5-MeqFos induced preneoplastic nerve lesions in 50% of infected birds. However, a third virus rMd5-MeqFos/GCN, which contains one copy of each meqGCN and meqFos, induced preneoplastic nerve lesions in 60% of infected chickens and neoplastic lesions in 20% of infected chickens. These data provide the first in vivo evidence that both Meq homodimers and heterodimers are necessary for MDV induced transformation.

Objetivo: Determinar si la presentación del herpes zoster en el hospital Dos de Mayo muestra variación estacional. Materiales y Métodos: Se estudiaron casos de herpes zoster atendidos en el hospital Nacional Dos de Mayo de Lima-Perú entre los años 2002 a 2006. Se determinaron las distribuciones de casos según mes y estación para cada año de estudio, y se aplicaron pruebas estadísticas para analizar significación de los valores obtenidos. Resultados: Se incluyeron 816 casos. La distribución mensual mostró predominio de casos en los meses de verano, aunque sin observarse una clara tendencia estacional. La distribución de casos acumulados según estación fue: 233 (28,6%) en el verano, 205 (25,1%) en otoño, 190 (23,3%) en invierno y 188 (23,0%) en primavera. Aunque la frecuencia de casos en verano fue superior al de las otras estaciones, no se evidenció que la diferencia fuera de significación estadística. Conclusiones: Los resultados del estudio no demuestran que los casos de herpes zoster en el hospital Dos de Mayo presenten variación estacional. / Objective: To assess whether cases of herpes zoster at hospital Dos de Mayo exhibit a seasonal presentation. Materials and Methods: Cases of herpes zoster attended at hospital Nacional Dos de Mayo in Lima-Perú from 2002 and 2006 were studied. Cases were distributed according to the months and the seasons for each year, and statistical analysis was performed. Results: A total of 816 cases were included. Monthly distribution of cases showed predominance during summer months without a clear seasonal trend. Distribution of accumulated cases according to season was as follows: 233 (28,6%) in summer, 205 (25,1%) in fall, 190 (23,3%) in winter and 188 (23,0%) in spring. Whereas increased frequency was detected in summer, no statistically significance was disclosed. Conclusions: Results failed to show a seasonal variation for cases of herpes zoster at hospital Dos de Mayo.

No description available.

Thesis (PhD)--University of South Australia, 2000

Thesis (PhD)--University of South Australia, 2000

In 1995 and again in 1998, millions of pilchards (Sardinops sagax neopilchardus) were found dead or dying off the coast of Australia and also in New Zealand. The epizootics moved progressively, at a rapid speed against the prevailing currents. A previously unrecognised herpesvirus, Pilchard herpesvirus (PHV), was identified as the causative agent. Until recently, rapid and sensitive methods to detect PHV were not available and based on a previously identified and conserved 373 bp region of the genome, polymerase chain reaction (PCR), in situ hybridisation and real-time PCR methods were developed for the specific detection of PHV in formaldehyde-fixed and frozen tissues of pilchards. Real-time PCR was shown to have greater sensitivity than a conventional PCR and in situ hybridisation for the detection of PHV infection. The PCR assay and sequence analysis of the amplification products was used to compare the 373 bp region of the genome from strains obtained during the 1995 and 1998 epidemics. Significant differences between the strains were not detected. Additional sequence data was obtained adjacent to the 373 bp of known PHV sequence, which did not match any sequence in any of the genetic databases, and this will be invaluable for further study of the pilchard herpesvirus and the development of improved detection methods. The molecular-based methods of virus detection developed were applied to a reexamination of virus in paraffin-embedded tissues taken from fish during an attempt to transmit the virus to wild caught pilchards in 1999. The results obtained confirmed previously equivocal results that transmission of PHV to wild caught pilchards was achieved, although this experiment failed to demonstrate that transmission of the virus resulted in severe lesions typical of those seen in the epizootics. Using formaldehyde-fixed samples from fish collected during the 1998 PHV epizootic, virus was detected in fish collected 4 days prior to the occurrence of the epizootic even though the fish then appeared clinically normal, during the epizootic, and 8 days after mortalities had ceased. An investigation of wild pilchards collected from 4 Australian pilchard subpopulations using real-time PCR demonstrated that PHV was present in the gills of 13.75% of 800 fish sampled, indicating that the virus is now endemic in the Australian pilchard population. Variation in the prevalence of PHV infection in the 4 subpopulations was detected, higher in western and southern populations than in populations from the east coast. The endemic nature of PHV infection in the pilchard population explains why there have been no further epizootics with mass mortalities since 1998.