The Experts below are selected from a list of 138 Experts worldwide ranked by ideXlab platform
Michael R Holbrook - One of the best experts on this subject based on the ideXlab platform.
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A Critical Determinant of Neurological Disease Associated with Highly Pathogenic Tick-Borne Flavivirus in Mice
Journal of Virology, 2014Co-Authors: Kentaro Yoshii, Michael R Holbrook, Hiroaki Kariwa, Manabu Igarashi, Yuji Sunden, Kana Yokozawa, Ikuo TakashimaAbstract:Tick-borne encephalitis virus (TBEV) and Omsk Hemorrhagic Fever virus (OHFV) are highly pathogenic tick-borne flaviviruses; TBEV causes neurological disease in humans, while OHFV causes a disease typically identified with Hemorrhagic Fever. Although TBEV and OHFV are closely related genetically, the viral determinants responsible for these distinct disease phenotypes have not been identified. In this study, chimeric viruses incorporating components of TBEV and OHFV were generated using infectious clone technology, and their pathological characteristics were analyzed in a mouse model to identify virus-specific determinants of disease. We found that only four amino acids near the C terminus of the NS5 protein were primarily responsible for the development of neurological disease. Mutation of these four amino acids had no effect on viral replication or histopathological features, including inflammatory responses, in mice. These findings suggest a critical role for NS5 in stimulating neuronal dysfunction and degeneration following TBEV infection and provide new insights into the molecular mechanisms underlying the pathogenesis of tick-borne flaviviruses. IMPORTANCE Tick-borne encephalitis virus (TBEV) and Omsk Hemorrhagic Fever virus (OHFV) belong to the tick-borne encephalitis serocomplex, genus Flavivirus, family Flaviviridae. Although TBEV causes neurological disease in humans while OHFV causes a disease typically identified with Hemorrhagic Fever. In this study, we investigated the viral determinants responsible for the different disease phenotypes using reverse genetics technology. We identified a cluster of only four amino acids in nonstructural protein 5 primarily involved in the development of neurological disease in a mouse model. Moreover, the effect of these four amino acids was independent of viral replication property and did not affect the formation of virus-induced lesions in the brain directly. These data suggest that these amino acids may be involved in the induction of neuronal dysfunction and degeneration in virus-infected neurons, ultimately leading to the neurological disease phenotype. These findings provide new insight into the molecular mechanisms of tick-borne flavivirus pathogenesis.
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construction of an infectious cdna clone for Omsk Hemorrhagic Fever virus and characterization of mutations in ns2a and ns5
Virus Research, 2011Co-Authors: Michael R Holbrook, Kentaro Yoshii, Hiroaki Kariwa, Manabu Igarashi, Ikuo TakashimaAbstract:Abstract Omsk Hemorrhagic Fever virus (OHFV) is a member of the tick-borne encephalitis serocomplex of flaviviruses, and causes Hemorrhagic disease in humans. In this study, an infectious cDNA of OHFV was constructed to investigate the molecular mechanisms involved in OHFV pathogenesis for the first time. Our cDNA clone was capable of producing infectious virus which is genetically identical to the parental Guriev strain, and the recombinant virus showed similar biological properties to the parental virus including growth kinetics and virulence characteristics. While characterizing the cDNAs, fortuitous mutations at NS2A position 46 and NS5 position 836 were found to affect viral production. By using a viral replicon expressing luciferase, it was shown that both of the mutations produced a defect in RNA replication and that the NS5 mutation induced a temperature-sensitive phenotype, indicating the importance of these residues in RNA replication. This infectious cDNA will be a useful tool to study the replication and pathogenesis of OHFV.
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comparative analysis of immune responses to russian spring summer encephalitis and Omsk Hemorrhagic Fever viruses in mouse models
Virology, 2010Co-Authors: Bersabeh Tigabu, Michael R Holbrook, Terry L JuelichAbstract:Omsk Hemorrhagic Fever virus (OHFV) and Russian spring-summer encephalitis virus (RSSEV) are tick-borne flaviviruses that have close homology but different pathology and disease outcomes. Previously, we reported that C57BL/6 and BALB/c mice were excellent models to study the pathology and clinical signs of human RSSEV and OHFV infection. In the study described here, we found that RSSEV infection induced robust release of proinflammatory cytokines (IL-1α, IL-1β, IL-6 and TNF-α) and chemokines (MCP-1, MIP-1β, RANTES and KC) in the brain at 9 and 11dpi, together with moderate to low Th1 and Th2 cytokines. In contrast, OHFV infection stimulated an early and prominent induction of IL-1α, TNF-α, IL-12p70, MCP-1, MIP-1α and MIP-1β in the spleen of infected mice. Collectively our data suggest that a differential host response to infection may lead to the alternate disease outcomes seen following OHFV or RSSEV infection.
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Tick-borne flaviviruses.
Clinics in Laboratory Medicine, 2010Co-Authors: P. Rocco Lasala, Michael R HolbrookAbstract:Many of the human and zoonotic diseases caused by arthropod-borne flaviviruses have long been recognized—some were known centuries before the introduction of germ theory (eg, louping ill), while others helped to solidify its establishment (eg, yellow Fever). As such, their inclusion in an edition of emerging infections might seem suspect without further considering the remarkable increases in tick-borne flaviviral disease incidence throughout the past 2 decades. Hence, a compelling case is made for their status as ‘‘re’’-emerging entities. By contrast, other agents (eg, Alkhurma Hemorrhagic Fever virus, deer tick virus) have been characterized only very recently and do represent emerging pathogens in the truest sense of the word. While enhanced clinical awareness and improvements in laboratory diagnostic methods have contributed to this rising incidence, one must not fail to recognize that the transmission of tick-borne viruses, like other vector-borne agents, is impacted by a very broad set of factors, both natural (eg, climate and ecology) and man-made (eg, human mobility and agricultural patterns). As our encroachment into areas of virus endemicity intensifies, and as changes in global economic and environmental conditions continue to promote the expansion of tick populations, we will undoubtedly continue to observe attendant increases in rates of disease attributable to these vector-borne pathogens. This article focuses on a few of the major tick-borne flaviviral diseases. Specifically, diseases caused by tick-borne encephalitis virus (TBEV), louping ill virus (LIV), Powassan virus (POWV), Kyasanur Forest disease virus (KFDV) and Omsk Hemorrhagic Fever virus (OHFV), as well as their subtypes, are discussed. MICROBIOLOGY
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Clinical evaluation of highly pathogenic tick-borne flavivirus infection in the mouse model.
Journal of Medical Virology, 2009Co-Authors: Bersabeh Tigabu, Terry L Juelich, Joseph Bertrand, Michael R HolbrookAbstract:The objective of this study was to evaluate the feasibility of using clinical parameters to demonstrate disease progression and differentiate between Omsk Hemorrhagic Fever virus (OHFV) and Russian spring-summer encephalitis virus (RSSEV) infection in the mouse model. Adult C57BL/6 and balb/c mice were infected with either OHFV or RSSEV by footpad inoculation and their temperature, body weight, clinical signs complete blood count, and blood chemistries were evaluated for up to 15 days post-infection (dpi). Clinical evaluation showed that OHFV infection seriously affects balb/c mice, which had shorter average survival times (ASTs) than other groups. On the contrary, RSSEV infection of C57BL/6 mice was more severe than in balb/c mice. During these studies, the development of Fever was not observed and the body weight of OHFV infected balb/c and C57BL/6 mice began to decline sharply starting from day 7 and 8, respectively, which correlated with disease onset. Peak increase of globulin and neutrophils was demonstrated after 9 dpi in OHFV infected mice; however, the lymphocyte number was not affected. Viremia was undetectable in these animals with either virus infection, but virus was found in most organs tested. These results indicate marked differences in the clinical signs, pathology, and immune response of mice infected with either OHFV or RSSEV and further validate the use of this mouse model system to evaluate human disease. J. Med. Virol. 81:1261–1269, 2009. © 2009 Wiley-Liss, Inc.
Alan D T Barrett - One of the best experts on this subject based on the ideXlab platform.
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structure of the envelope protein domain iii of Omsk Hemorrhagic Fever virus
Virology, 2006Co-Authors: David E Volk, Leonard Chavez, David W C Beasley, Alan D T Barrett, Michael R Holbrook, David G GorensteinAbstract:We have solved the NMR solution structure of domain III from the Omsk Hemorrhagic Fever virus envelope protein and report the first sequencing of the Guriev strain of this virus. Important structural differences between tick-borne flaviviruses, such as OHFV and TBE, and mosquito-borne flaviviruses, such as West Nile virus, are discussed.
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an animal model for the tickborne flavivirus Omsk Hemorrhagic Fever virus
The Journal of Infectious Diseases, 2005Co-Authors: Michael R Holbrook, Judith F Aronson, Gerald A Campbell, Steven J M Jones, Heinz Feldmann, Alan D T BarrettAbstract:The tickborne encephalitis (TBE) serocomplex of flaviviruses consists primarily of virusesthatcauseneurologic disease; these viruses include Omsk Hemorrhagic Fever virus (OHFV), a virus that is genetically related to other TBE serocomplex viruses but that circulates in an ecologicallydistinctnicheandcausesmarkedlydifferent human disease. The objective of this study was to examine a potential small-animal model for OHFV and to compare the pathology of infection with that of the neurotropic tickborne flavivirus, Powassan virus (POWV). POWV-infected BALB/c mice demonstrated typical arboviralencephalitis,characterizedbyparesisandparalysis before death, and viral infection of the cerebrum, characterized by inflammation and necrosis. In contrast, lethal OHFV infection did not cause paralysis or significant infection of the cerebrum but showed marked involvement of the cerebellum. Distinct pathological results in the spleens suggest that the immune response in OHFV-infected mice is different from that in POWV-infected mice. This study demonstrates a clear pathological difference between OHFV-infected mice and POWV-infected mice and supports the use of the BALB/c mouse as a disease model for OHFV.
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An Animal Model for the Tickborne Flavivirus—Omsk Hemorrhagic Fever Virus
The Journal of Infectious Diseases, 2004Co-Authors: Michael R Holbrook, Judith F Aronson, Gerald A Campbell, Steven J M Jones, Heinz Feldmann, Alan D T BarrettAbstract:The tickborne encephalitis (TBE) serocomplex of flaviviruses consists primarily of virusesthatcauseneurologic disease; these viruses include Omsk Hemorrhagic Fever virus (OHFV), a virus that is genetically related to other TBE serocomplex viruses but that circulates in an ecologicallydistinctnicheandcausesmarkedlydifferent human disease. The objective of this study was to examine a potential small-animal model for OHFV and to compare the pathology of infection with that of the neurotropic tickborne flavivirus, Powassan virus (POWV). POWV-infected BALB/c mice demonstrated typical arboviralencephalitis,characterizedbyparesisandparalysis before death, and viral infection of the cerebrum, characterized by inflammation and necrosis. In contrast, lethal OHFV infection did not cause paralysis or significant infection of the cerebrum but showed marked involvement of the cerebellum. Distinct pathological results in the spleens suggest that the immune response in OHFV-infected mice is different from that in POWV-infected mice. This study demonstrates a clear pathological difference between OHFV-infected mice and POWV-infected mice and supports the use of the BALB/c mouse as a disease model for OHFV.
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Solution Structure and Structural Dynamics of Envelope Protein Domain III of Mosquito- and Tick-Borne Flaviviruses†
Biochemistry, 2004Co-Authors: Shaoning Yu, Michael R Holbrook, Reneeta Basu, Alan D T BarrettAbstract:The mosquito-borne West Nile (WNV) and dengue 2 (DEN2V) viruses and tick-borne Langat (LGTV) and Omsk Hemorrhagic Fever (OHFV) viruses are arthropod-borne flaviviruses (family Flaviviridae, genus Flavivirus). These viruses are quite similar at both the nucleotide and amino acid level, yet they are very divergent in their biological properties and in the diseases they cause. The objective of this study was to examine the putative receptor-binding domains of the flaviviruses, the envelope (E) protein domain III (D3), which assume very similar structures either as part of the whole envelope protein or as individual entities, and to define the biophysical properties that distinguish among these viruses. Circular dichroism and Fourier transform infrared spectroscopy were employed to monitor the solution structure of these proteins. While the spectroscopic results found that the D3 from each of these viruses is composed of either β-sheets or β-turns, which is consistent with X-ray crystal data for tick-borne en...
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analysis of the complete genome of the tick borne flavivirus Omsk Hemorrhagic Fever virus
Virology, 2003Co-Authors: Li Li, Alan D T Barrett, Heinz Feldmann, Daryl Dick, Robert E Shope, Michael R HolbrookAbstract:Abstract Omsk Hemorrhagic Fever virus (OHF) is a tick-borne flavivirus endemic to Western Siberia. This virus is the only known tick-borne flavivirus to cause Hemorrhagic disease in humans in the absence of encephalitis. OHF virus circulates within a small, defined niche in which other tick-borne complex flaviviruses are also present. The objectives of this study were to genetically classify OHF virus based on its complete genome and to identify genetic determinants that might be involved in tissue tropism and viral replication leading to the disease state caused by this virus. The OHF virus genome was sequenced and phylogenetic analysis demonstrated that OHF virus falls within the tick-borne encephalitis serocomplex of flaviviruses, yet is distinct from other members of the complex, including those closely associated geographically. OHF is also distinct from Alkhurma (ALK) and Kyasanur forest disease (KFD) viruses, both of which cause disease that includes Hemorrhagic and encephalitic manifestations. Several amino acid residues were found to be distinct among OHF, KFD, and ALK viruses; these residues include E-76, which is closely associated with the viral envelope protein fusion peptide. In addition, variation between the viral 5′-untranslated region of OHF and other tick-borne flaviviruses suggests potential variability in viral replication. These data demonstrate that OHF is a unique virus among the tick-borne flaviviruses and also provide insight to viral biodiversity and tropism.
Kentaro Yoshii - One of the best experts on this subject based on the ideXlab platform.
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trans complementation of replication defective Omsk Hemorrhagic Fever virus for antiviral study
Virologica Sinica, 2019Co-Authors: Qiuyan Zhang, Kentaro Yoshii, Na Li, Chenglin Deng, Zherui Zhang, Xiaodan Li, Hanqing Ye, Bo ZhangAbstract:Omsk Hemorrhagic Fever virus (OHFV) is a tick-borne flavivirus classified as a biosafety level-4 (BSL4) pathogen. Studies of OHFV are restricted to be conducted within BSL4 laboratories. Currently, no commercial vaccines or antiviral drugs are available against OHFV infection. In this study, we recovered a replication-deficient OHFV with an NS1 deletion (OHFV-ΔNS1) and reporter virus replacing NS1 with the Gaussia luciferase (Gluc) (OHFV-ΔNS1-Gluc). Both the defective OHFV-ΔNS1 and OHFV-ΔNS1-Gluc virus could only replicate efficiently in the BHK21 cell line expressing NS1 (BHK21NS1) but not in naive BHK21 cells. The Gluc reporter gene of OHFV-ΔNS1-Gluc virus was maintained stably after serial passaging of BHK21NS1 cells and was used to surrogate the replication of OHFV. Using NITD008, OHFV-ΔNS1-Gluc virus was validated for antiviral screening, and high-throughput screening parameters were optimized in a 96-well plate format with a calculated Z′ value above 0.5. The OHFV-ΔNS1-Gluc reporter virus is a powerful tool for antiviral screening as well as viral replication and pathogenesis studies in BSL2 laboratories.
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A Critical Determinant of Neurological Disease Associated with Highly Pathogenic Tick-Borne Flavivirus in Mice
Journal of Virology, 2014Co-Authors: Kentaro Yoshii, Michael R Holbrook, Hiroaki Kariwa, Manabu Igarashi, Yuji Sunden, Kana Yokozawa, Ikuo TakashimaAbstract:Tick-borne encephalitis virus (TBEV) and Omsk Hemorrhagic Fever virus (OHFV) are highly pathogenic tick-borne flaviviruses; TBEV causes neurological disease in humans, while OHFV causes a disease typically identified with Hemorrhagic Fever. Although TBEV and OHFV are closely related genetically, the viral determinants responsible for these distinct disease phenotypes have not been identified. In this study, chimeric viruses incorporating components of TBEV and OHFV were generated using infectious clone technology, and their pathological characteristics were analyzed in a mouse model to identify virus-specific determinants of disease. We found that only four amino acids near the C terminus of the NS5 protein were primarily responsible for the development of neurological disease. Mutation of these four amino acids had no effect on viral replication or histopathological features, including inflammatory responses, in mice. These findings suggest a critical role for NS5 in stimulating neuronal dysfunction and degeneration following TBEV infection and provide new insights into the molecular mechanisms underlying the pathogenesis of tick-borne flaviviruses. IMPORTANCE Tick-borne encephalitis virus (TBEV) and Omsk Hemorrhagic Fever virus (OHFV) belong to the tick-borne encephalitis serocomplex, genus Flavivirus, family Flaviviridae. Although TBEV causes neurological disease in humans while OHFV causes a disease typically identified with Hemorrhagic Fever. In this study, we investigated the viral determinants responsible for the different disease phenotypes using reverse genetics technology. We identified a cluster of only four amino acids in nonstructural protein 5 primarily involved in the development of neurological disease in a mouse model. Moreover, the effect of these four amino acids was independent of viral replication property and did not affect the formation of virus-induced lesions in the brain directly. These data suggest that these amino acids may be involved in the induction of neuronal dysfunction and degeneration in virus-infected neurons, ultimately leading to the neurological disease phenotype. These findings provide new insight into the molecular mechanisms of tick-borne flavivirus pathogenesis.
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evaluation of the european tick borne encephalitis vaccine against Omsk Hemorrhagic Fever virus
Microbiology and Immunology, 2014Co-Authors: Kentaro Yoshii, Nozyechi N Chidumayo, Hiroaki KariwaAbstract:This study focused on the antigenic cross-reactivity between tick-borne encephalitis virus (TBEV) and Omsk Hemorrhagic Fever virus (OHFV) to assess the efficacy of the commercial TBE vaccine against OHFV infection. Neutralization tests performed on sera from OHFV- and TBEV-infected mice showed that neutralizing antibodies are cross-protective. The geometric mean titers of antibodies against TBEV and OHFV from TBEV-infected mice were similar. However, the titers of anti-TBEV antibodies in OHFV-infected mice were significantly lower than those of anti-OHFV antibodies in the same animals. In mouse vaccination and challenge tests, the TBE vaccine provided 100% protection against OHFV infection. Eighty-six percent of vaccinees seroconverted against OHFV following complete vaccination, and the geometric mean titers of neutralizing antibodies against OHFV were comparable to those against TBEV. These data suggest that the TBE vaccine can prevent OHFV infection.
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construction of an infectious cdna clone for Omsk Hemorrhagic Fever virus and characterization of mutations in ns2a and ns5
Virus Research, 2011Co-Authors: Michael R Holbrook, Kentaro Yoshii, Hiroaki Kariwa, Manabu Igarashi, Ikuo TakashimaAbstract:Abstract Omsk Hemorrhagic Fever virus (OHFV) is a member of the tick-borne encephalitis serocomplex of flaviviruses, and causes Hemorrhagic disease in humans. In this study, an infectious cDNA of OHFV was constructed to investigate the molecular mechanisms involved in OHFV pathogenesis for the first time. Our cDNA clone was capable of producing infectious virus which is genetically identical to the parental Guriev strain, and the recombinant virus showed similar biological properties to the parental virus including growth kinetics and virulence characteristics. While characterizing the cDNAs, fortuitous mutations at NS2A position 46 and NS5 position 836 were found to affect viral production. By using a viral replicon expressing luciferase, it was shown that both of the mutations produced a defect in RNA replication and that the NS5 mutation induced a temperature-sensitive phenotype, indicating the importance of these residues in RNA replication. This infectious cDNA will be a useful tool to study the replication and pathogenesis of OHFV.
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Sub-genomic replicon and virus-like particles of Omsk Hemorrhagic Fever virus
Archives of Virology, 2009Co-Authors: Kentaro Yoshii, Michael R HolbrookAbstract:Omsk Hemorrhagic Fever virus (OHFV) is a member of the tick-borne encephalitis serocomplex of flaviviruses, and causes Hemorrhagic disease in humans. To investigate the molecular mechanisms involved in OHFV pathogenesis, we constructed several subgenomic OHFV replicons containing large deletions in the structural region. Replicon RNA was introduced into BHK cells by transfection and the production of viral proteins was monitored by IFA. GFP and luciferase genes were inserted into the OHFV replicon, and these reporter genes were expressed in cells harboring replicating replicon RNA. OHFV replicons were packaged into single-round infectious virus-like particles (VLPs) by sequential transfection with replicon RNA and a plasmid expressing the viral structural proteins. Reporter genes were expressed in cells infected with VLPs, and the infection was inhibited by neutralizing antibodies. These replicon and VLP systems will be useful tools for investigating the molecular mechanism of OHFV pathogenicity.
Heinz Feldmann - One of the best experts on this subject based on the ideXlab platform.
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an animal model for the tickborne flavivirus Omsk Hemorrhagic Fever virus
The Journal of Infectious Diseases, 2005Co-Authors: Michael R Holbrook, Judith F Aronson, Gerald A Campbell, Steven J M Jones, Heinz Feldmann, Alan D T BarrettAbstract:The tickborne encephalitis (TBE) serocomplex of flaviviruses consists primarily of virusesthatcauseneurologic disease; these viruses include Omsk Hemorrhagic Fever virus (OHFV), a virus that is genetically related to other TBE serocomplex viruses but that circulates in an ecologicallydistinctnicheandcausesmarkedlydifferent human disease. The objective of this study was to examine a potential small-animal model for OHFV and to compare the pathology of infection with that of the neurotropic tickborne flavivirus, Powassan virus (POWV). POWV-infected BALB/c mice demonstrated typical arboviralencephalitis,characterizedbyparesisandparalysis before death, and viral infection of the cerebrum, characterized by inflammation and necrosis. In contrast, lethal OHFV infection did not cause paralysis or significant infection of the cerebrum but showed marked involvement of the cerebellum. Distinct pathological results in the spleens suggest that the immune response in OHFV-infected mice is different from that in POWV-infected mice. This study demonstrates a clear pathological difference between OHFV-infected mice and POWV-infected mice and supports the use of the BALB/c mouse as a disease model for OHFV.
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An Animal Model for the Tickborne Flavivirus—Omsk Hemorrhagic Fever Virus
The Journal of Infectious Diseases, 2004Co-Authors: Michael R Holbrook, Judith F Aronson, Gerald A Campbell, Steven J M Jones, Heinz Feldmann, Alan D T BarrettAbstract:The tickborne encephalitis (TBE) serocomplex of flaviviruses consists primarily of virusesthatcauseneurologic disease; these viruses include Omsk Hemorrhagic Fever virus (OHFV), a virus that is genetically related to other TBE serocomplex viruses but that circulates in an ecologicallydistinctnicheandcausesmarkedlydifferent human disease. The objective of this study was to examine a potential small-animal model for OHFV and to compare the pathology of infection with that of the neurotropic tickborne flavivirus, Powassan virus (POWV). POWV-infected BALB/c mice demonstrated typical arboviralencephalitis,characterizedbyparesisandparalysis before death, and viral infection of the cerebrum, characterized by inflammation and necrosis. In contrast, lethal OHFV infection did not cause paralysis or significant infection of the cerebrum but showed marked involvement of the cerebellum. Distinct pathological results in the spleens suggest that the immune response in OHFV-infected mice is different from that in POWV-infected mice. This study demonstrates a clear pathological difference between OHFV-infected mice and POWV-infected mice and supports the use of the BALB/c mouse as a disease model for OHFV.
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analysis of the complete genome of the tick borne flavivirus Omsk Hemorrhagic Fever virus
Virology, 2003Co-Authors: Li Li, Alan D T Barrett, Heinz Feldmann, Daryl Dick, Robert E Shope, Michael R HolbrookAbstract:Abstract Omsk Hemorrhagic Fever virus (OHF) is a tick-borne flavivirus endemic to Western Siberia. This virus is the only known tick-borne flavivirus to cause Hemorrhagic disease in humans in the absence of encephalitis. OHF virus circulates within a small, defined niche in which other tick-borne complex flaviviruses are also present. The objectives of this study were to genetically classify OHF virus based on its complete genome and to identify genetic determinants that might be involved in tissue tropism and viral replication leading to the disease state caused by this virus. The OHF virus genome was sequenced and phylogenetic analysis demonstrated that OHF virus falls within the tick-borne encephalitis serocomplex of flaviviruses, yet is distinct from other members of the complex, including those closely associated geographically. OHF is also distinct from Alkhurma (ALK) and Kyasanur forest disease (KFD) viruses, both of which cause disease that includes Hemorrhagic and encephalitic manifestations. Several amino acid residues were found to be distinct among OHF, KFD, and ALK viruses; these residues include E-76, which is closely associated with the viral envelope protein fusion peptide. In addition, variation between the viral 5′-untranslated region of OHF and other tick-borne flaviviruses suggests potential variability in viral replication. These data demonstrate that OHF is a unique virus among the tick-borne flaviviruses and also provide insight to viral biodiversity and tropism.
David G Gorenstein - One of the best experts on this subject based on the ideXlab platform.
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structure of the envelope protein domain iii of Omsk Hemorrhagic Fever virus
Virology, 2006Co-Authors: David E Volk, Leonard Chavez, David W C Beasley, Alan D T Barrett, Michael R Holbrook, David G GorensteinAbstract:We have solved the NMR solution structure of domain III from the Omsk Hemorrhagic Fever virus envelope protein and report the first sequencing of the Guriev strain of this virus. Important structural differences between tick-borne flaviviruses, such as OHFV and TBE, and mosquito-borne flaviviruses, such as West Nile virus, are discussed.
