5 research outputs found

    Influenza Cases From Surveillance Acute Respiratory Infection in Indonesia, 2011

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    Background: Severe Acute Respiratory Infection (SARI) or pneumonia has a major contribution in the morbidity and mortality, however, Indonesia still has lack of its epidemiology. The aim of the study is to know the epidemiological pattern of influenza virus as the etiology of SARI cases. Methods:This analysis based on the sentinel surveillanceSARI conducted by Center for Biomedical and Basic Technology of Health (CBBTH) of Indonesia carried out at nine hospitals in nine provinces in 2011.Every patient who met the criteria of SARI was included in this study. Serum, throat and nasal swabs were taken and examined at the Virology laboratory CBBTH to determine the etiology. RT-PCR was used to detect type and subtype of influenza viruses from swabs.Results: Total number of SARI cases were 333. We found 6% cases were influenza positive by RT-PCR. The proportion of influenza A was 5% and influenza B 1% from total SARI cases. We detected that seasonal influenza A subtype H1N1pdm09was the dominant subtypes that circulating in Indonesia.Conclusion: We foundseasonal Influenza infection from SARI patients, however, it was only small number. Therefore, further detection of SARI cases is needed. (Health Science Indones 2014;1:7-11

    Deteksi Resistensi Oseltamivir Influenza a (H1N1pdm09) Dari Pasien Infeksi Saluran Pernafasan Akut Berat Di Indonesia Tahun 2014

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    Influenza viruses are classified into subtypes based on two surface antigens known as hemagglutinin (HA) and neuraminidase (NA). Antigenic changes of influenza virus can cause resistance to antiviral drugs which is already limited in variation. Resistance to the drugs used recently are due to antigenic drift by point mutation in a single amino acid at position 275 (H275Y). The purpose of this research is to identify the presence of influenza virus A (H1N1pdm09) that were resistant to oseltamivir from cases of severe acute respiratory infection (SARI)in Indonesia in 2014 by using a rapid detection test. Detection of oseltamivir resistance in NA gene is to identify the single nucleotide polimorphism (SNP) at position 275 (H275Y) using the real-time RT-PCR method from clinical specimens SARI case. A total of 870 specimens from six sentinel hospitals were collected and 15 of them positive H1N1pdm09. Of the 15 clinical specimens, H1N1pdm09 virus strains that have mutations H275Y were not found. Based on this finding, it can be concluded that during the year 2014, there is no influenza virus A (H1N1pdm09) resistant to oseltamivir from SARI cases specimen in six sentinel hospitals in Indonesia

    Interaction of Kaposi's Sarcoma-Associated Herpesvirus ORF59 with oriLyt Is Dependent on Binding with K-Rta â–¿

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    Kaposi's sarcoma-associated herpesvirus (KSHV)/human herpesvirus 8 (HHV-8) displays two distinct life stages, latency and lytic reactivation. Progression through the lytic cycle and replication of the viral genome constitute an essential step toward the production of infectious virus and human disease. KSHV K-RTA has been shown to be the major transactivator required for the initiation of lytic reactivation. In the transient-cotransfection replication assay, K-Rta is the only noncore protein required for DNA synthesis. K-Rta was shown to interact with both C/EBPα binding motifs and the R response elements (RRE) within oriLyt. It is postulated that K-Rta acts in part to facilitate the recruitment of replication factors to oriLyt. In order to define the role of K-Rta in the initiation of lytic DNA synthesis, we show an interaction with ORF59, the DNA polymerase processivity factor (PF), one of the eight virally encoded proteins necessary for origin-dependent DNA replication. Using the chromatin immunoprecipitation (ChIP) assay, both K-Rta and ORF59 interact with the RRE and C/EBPα binding motifs within oriLyt in cells harboring the KSHV bacterial artificial chromosome (BAC). A transient-transfection ChIP assay demonstrated that the interaction of ORF59 with oriLyt is dependent on binding with K-Rta and that ORF59 fails to bind to oriLyt in the absence of K-Rta. Also, using the cotransfection replication assay, overexpression of the interaction domain of K-Rta with ORF59 has a dominant negative effect on oriLyt amplification, suggesting that the interaction of K-Rta with ORF59 is essential for DNA synthesis and supporting the hypothesis that K-Rta facilitates the formation of a replication complex at oriLyt
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