scholarly journals Dobrava Virus RNA Load in Patients Who Have Hemorrhagic Fever with Renal Syndrome

2008 ◽  
Vol 197 (5) ◽  
pp. 681-685 ◽  
Author(s):  
Ana Saksida ◽  
Darja Duh ◽  
Misa Korva ◽  
Tatjana Avsic‐Zupanc
Keyword(s):  
Hemorrhagic Fever ◽  
Dobrava Virus ◽  
Virus Rna

scholarly journals Dobrava Virus Carried by the Yellow-Necked Field Mouse Apodemus flavicollis, Causing Hemorrhagic Fever with Renal Syndrome in Romania

2014 ◽  
Vol 14 (5) ◽  
pp. 358-364 ◽  
Author(s):  
Raluca Ioana Panculescu-Gatej ◽  
Anca Sirbu ◽  
Sorin Dinu ◽  
Maria Waldstrom ◽  
Paul Heyman ◽  
...  
Keyword(s):  
Hemorrhagic Fever ◽  
Field Mouse ◽  
Apodemus Flavicollis ◽  
Dobrava Virus

scholarly journals Persistence of Crimean-Congo Hemorrhagic Fever Virus RNA

2020 ◽  
Vol 26 (2) ◽  
pp. 385-387
Author(s):  
Leholonolo Mathengtheng ◽  
Dominique Goedhals ◽  
Phillip A. Bester ◽  
Jacqueline Goedhals ◽  
Felicity J. Burt
Keyword(s):  
Hemorrhagic Fever ◽  
Fever Virus ◽  
Crimean Congo Hemorrhagic Fever ◽  
Hemorrhagic Fever Virus ◽  
Virus Rna

scholarly journals Dobrava virus: a mortal agent of hemorrhagic fever with renal syndrome

2013 ◽  
Vol 7 (10) ◽  
pp. 767-768
Author(s):  
Selçuk Kaya
Keyword(s):  
Full Text ◽  
Hemorrhagic Fever ◽  
Dobrava Virus

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Belgrade Virus, a Cause of Hemorrhagic Fever with Renal Syndrome in the Balkans, is Closely Related to Dobrava Virus of Field Mice

1993 ◽  
Vol 168 (3) ◽  
pp. 750-753 ◽  
Author(s):  
A. M. Taller ◽  
S.-Y. Xiao ◽  
M. S. Godec ◽  
A. Gligic ◽  
T. Avsic-Zupanc ◽  
...  
Keyword(s):  
Hemorrhagic Fever ◽  
The Balkans ◽  
Dobrava Virus ◽  
Field Mice

scholarly journals Hantaan Virus RNA Load in Patients Having Hemorrhagic Fever With Renal Syndrome: Correlation With Disease Severity

2012 ◽  
Vol 207 (9) ◽  
pp. 1457-1461 ◽  
Author(s):  
Jing Yi ◽  
Zhuwei Xu ◽  
Ran Zhuang ◽  
Jiuping Wang ◽  
Yusi Zhang ◽  
...  
Keyword(s):  
Disease Severity ◽  
Hemorrhagic Fever ◽  
Hantaan Virus ◽  
Virus Rna

scholarly journals HLA-Associated Hemorrhagic Fever with Renal Syndrome Disease Progression in Slovenian Patients

2011 ◽  
Vol 18 (9) ◽  
pp. 1435-1440 ◽  
Author(s):  
Miša Korva ◽  
Ana Saksida ◽  
Sabina Kunilo ◽  
Blanka Vidan Jeras ◽  
Tatjana Avšič-Županc
Keyword(s):  
Strong Association ◽  
Hemorrhagic Fever ◽  
Class Ii ◽  
Protective Role ◽  
Severe Form ◽  
Slovenian Population ◽  
Dobrava Virus ◽  
Histocompatibility Complex ◽  
Severity Of The Disease ◽  
Hla Molecules

ABSTRACTMajor histocompatibility complex (MHC) class I and class II genes regulate the balance between appropriate aggressive responses and invading pathogens while minimizing the destruction of host tissue. Several studies have shown that in hemorrhagic fever with renal syndrome (HFRS) patients, the disease outcome is determined by a complex interaction between the virus and immunopathologic and human genetic factors. In Slovenia, the severity of the disease caused by Puumala virus (PUUV) is significantly lower than that of HFRS due to Dobrava virus (DOBV). We have determined 23 different HLA-B and 12 different HLA-DRB1 types in Slovenian HFRS patients. Comparison of HLA frequencies between healthy individuals and HFRS patients showed no strong association with the susceptibility for hantaviral infection. Significant associations were recognized when the patient group was separated according to the virus responsible for the infection. DOBV-infected patients have a significantly higher frequency of HLA-B*35 than PUUV-infected patients. For HLA class II genes, the biggest difference between the PUUV- and DOBV-infected groups of patients was in HLA-DRB1*13, where this phenotype was more frequent in PUUV-infected patients, especially in the severe form of the disease. HLA-B*07 could play a protective role in PUUV-caused HFRS in the Slovenian population. Our study shows diverse associations of HLA molecules with DOBV- and PUUV-induced HFRS, and therefore, we presume that different hantaviruses are presented differently through the same HLA molecules and that this might lead to either a more severe or a milder form of the disease. In line with this idea, we have noticed that HLA-B*35 might be a genetic risk factor for DOBV infection in the Slovenian population.

scholarly journals Crimean-Congo Hemorrhagic Fever Virus-Encoded Ovarian Tumor Protease Activity Is Dispensable for Virus RNA Polymerase Function

2009 ◽  
Vol 84 (1) ◽  
pp. 216-226 ◽  
Author(s):  
Éric Bergeron ◽  
César G. Albariño ◽  
Marina L. Khristova ◽  
Stuart T. Nichol
Keyword(s):  
Protease Activity ◽  
Ovarian Tumor ◽  
Antiviral Drug ◽  
Hemorrhagic Fever ◽  
Fever Virus ◽  
Crimean Congo Hemorrhagic Fever ◽  
L Protein ◽  
Hemorrhagic Fever Virus ◽  
Virus Rna ◽  
N Terminus

ABSTRACT Crimean-Congo hemorrhagic fever virus (CCHFV) is a tick-borne virus (genus Nairovirus, family Bunyaviridae) associated with high case fatality disease outbreaks in regions of Africa, Europe, and Asia. The CCHFV genome consists of three negative-strand RNA segments, S, M, and L. The unusually large virus L polymerase protein and the need for biosafety level 4 (BSL-4) containment conditions for work with infectious virus have hampered the study of CCHFV replication. The L protein has an ovarian tumor (OTU) protease domain located in the N terminus, which has led to speculation that the protein may be autoproteolytically cleaved to generate the active virus L polymerase and additional functions. We report the successful development of efficient CCHFV helper virus-independent S, M, and L segment minigenome systems for analysis of virus RNA and protein features involved in replication. The virus RNA segment S, M, and L untranslated regions were found to be similar in support of replication of the respective minigenomes. In addition, the OTU domain located in the N terminus of the expressed virus L protein was shown to be a functional protease. However, no evidence of L protein autoproteolytic processing was found, and the OTU protease activity was dispensable for virus RNA replication. Finally, physiologically relevant doses of ribavirin inhibited CCHFV minigenome replication. These results demonstrated the utility of the minigenome system for use in BSL-2 laboratory settings to analyze CCHFV biology and in antiviral drug discovery programs for this important public health and bioterrorism threat.

scholarly journals Molecular Diagnostics of Hemorrhagic Fever with Renal Syndrome during a Dobrava Virus Infection Outbreak in the European Part of Russia

2009 ◽  
Vol 47 (12) ◽  
pp. 4029-4036 ◽  
Author(s):  
T. K. Dzagurova ◽  
B. Klempa ◽  
E. A. Tkachenko ◽  
G. P. Slyusareva ◽  
V. G. Morozov ◽  
...  
Keyword(s):  
Virus Infection ◽  
Molecular Diagnostics ◽  
Hemorrhagic Fever ◽  
European Part ◽  
Dobrava Virus ◽  
European Part Of Russia

scholarly journals DEMAM BERDARAH DENGUE (DBD) DAN NS1 ANTIGEN UNTUK DETEKSI DINI INFEKSI AKUT VIRUS DENGUE

2012 ◽  
Vol 6 (1) ◽  
Author(s):  
Meddy Setiawan
Keyword(s):  
Polymerase Chain Reaction ◽  
Aedes Albopictus ◽  
Gold Standard ◽  
Dengue Shock Syndrome ◽  
Hemorrhagic Fever ◽  
Rt Pcr ◽  
Chain Reaction ◽  
Virus Rna ◽  
Ns1 Antigen ◽  
Polymerase Chain

Demam Berdarah Dengue (DBD) atau Dengue Hemorrhagic Fever (DHF) disebabkan oleh infeksi virus dengue. Virus dengue merupakan virus RNA yang termasuk ke dalam famili flaviviridae , genus flavivirus dan ada 4 serotipe yang berbeda yaitu DEN1, DEN 2, DEN 3, dan DEN 4. Keempat serotipe terdapat di Indonesi a dengan dominasi DEN 3 dan DEN 2.   Dengue ini merupakan penyakit arbovirus endemik yang saat ini telah menjangkiti lebih dari 100 negara, baik  yang terletak di dae rah tropik maupun su btropik. WHO memperkirakan sekitar 50-100 juta ka sus infeksi virus dengue terjadi setiap tahun, menghasilkan 250.000-500.000 kasus demam berdarah dengue dan  24.000 kematian setiap tah unnya. Virus dengue ini dapat ditularkan melalui gigitan nyamuk Aedes aegyp ti dan Aedes albopictus sebagai vektornya dengan masa inkubasi ra ta-rata 4-6 hari. Infeksi virus dangue dapat menyebabkan manifestasi kilinis yang bervariasi mulai dari asimtomatik sampai manifestasi klinis  yang berat yang mengakibatka n kematian. Demam dengue atau dengue fever merupakan manifestasi klinis yang ringan, sedangkan DBD/DHF dan  Dengue Shock Syndrome (DSS) merupakan manifestasi klinis  yang berat.  Berbagai teori yang menjelaskan patogenesis DBD dan DSS banyak bermunculan dan saling kontroversi. Pada saat ini teori yang banyak dianut adalah teori Antibody Dependent Enhancement (ADE). Menurut teori ini, infeksi sekunder yang disebabkan oleh virus dengue dengan serotipe yang berbeda dengan infeksi primer akan menimbul kan antibodi heterologous yang dibentuk pada infeksi pertama namun tidak bisa mengeliminasi virus dengue pada infeksi sekunder (bersifat subnetralisasi) bahkan antibodi tersebut bersifat opsonis asi sehingga sel target menjadi lebih mudah di infeksi oleh virus dan  menyebabkan manifestasi klinis yang lebih berat.  Saat ini telah tersedia berbagai teknik pemeriksaan untuk mendeteksi infeksi virus dengue yaitu  pemeriksaan kultur dan isolasi  virus, RT-PCR (Reverse Transcription Polymerase Chain Reaction), serologi (anti dengue lgG dan lgM) dan juga pemeriksaan hematologi rutin. Kultur virus atau PCR saat ini dianggap sebagai gold standard untuk mendeteksi virus dengue, namun memiliki keterbatasan dalam hal biaya dan teknis pengerjaannya. Pemeriksaan  serologi anti dengue lgG dan lgM yang dike rjakan secara rutin di laboratorium juga  memiliki ketrbatasan yaitu tidak dapat mendeteksi infeksi dengan lebih aw al.  Saat ini telah dikembangkan suatu pemeriksaan baru terhadap antigen non struktural-1 dengue (NS1) yang  dapat mendeteksi infeksi virus dengue dengan  lebih awal bahkan pada hari pertama ons et demam.

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