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Article: Crimean-Congo hemorrhagic fever.

Masayuki, Saijo

Nihon rinsho. Japanese journal of clinical medicine

2019 Volume 74, Issue 12, Page(s) 2003–2007

Abstract: Crimean-Congo hemorrhagic fever (CCHF), caused by infection with CCHF virus (CCHFV), is viral hemorrhagic fever with high case fatality rate. CCHFV is classified to Family Bunyaviridae, Genus Nairovirus. CCHF is endemic to Africa, Eastern Europe, the ... ...

Abstract	Crimean-Congo hemorrhagic fever (CCHF), caused by infection with CCHF virus (CCHFV), is viral hemorrhagic fever with high case fatality rate. CCHFV is classified to Family Bunyaviridae, Genus Nairovirus. CCHF is endemic to Africa, Eastern Europe, the Middle East, central Asia, and southern Asia. CCHFV is maintained in nature in several spe- cies of ticks (Hyalomma and Ixodes species) and mammals. Humans are infected with CCHFV by tick-bite or direct contact with viremic animals such as sheep. The CCHF-endemic re- gions are relatively economically disadvantaged areas, therefore CCHF is considered to be one of the neglected infectious diseases. The pathophysiology has not yet been clarified fully. It is necessary to clarify the pathophysiology of CCHF and to develop specific antiviral drug- based therapy and vaccines, which might be effective in confering protection against CCHFV infections in the near future, because CCHF outbreaks continue to occur in the endemic re- gions.
MeSH term(s)	Antiviral Agents/therapeutic use ; Disease Outbreaks ; Hemorrhagic Fever Virus, Crimean-Congo ; Hemorrhagic Fever, Crimean/drug therapy ; Hemorrhagic Fever, Crimean/prevention & control ; Humans ; Viral Vaccines/therapeutic use
Chemical Substances	Antiviral Agents ; Viral Vaccines
Language	Japanese
Publishing date	2019-01-15
Publishing country	Japan
Document type	Journal Article
ZDB-ID	390903-7
ISSN	0047-1852
ISSN	0047-1852
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Animal models for Ebola and Marburg virus infections

MasayukiSaijo

Frontiers in Microbiology, Vol

2013 Volume 4

Abstract: Ebola and Marburg hemorrhagic fevers (EHF and MHF) are caused by the Filoviridae family, Ebolavirus and Marburgvirus (ebolavirus and marburgvirus), respectively. These severe diseases have high mortality rates in humans. Although EHF and MHF are endemic ... ...

Abstract	Ebola and Marburg hemorrhagic fevers (EHF and MHF) are caused by the Filoviridae family, Ebolavirus and Marburgvirus (ebolavirus and marburgvirus), respectively. These severe diseases have high mortality rates in humans. Although EHF and MHF are endemic to sub-Saharan Africa. A novel filovirus, Lloviu virus, which is genetically distinct from ebolavirus and marburgvirus, was recently discovered in Spain where filoviral hemorrhagic fever had never been reported. The virulence of this virus has not been determined. Ebolavirus and marburgvirus are classified as biosafety level-4 (BSL-4) pathogens and Category A agents, for which the US government requires preparedness in case of bioterrorism. Therefore, preventive measures against these viral hemorrhagic fevers should be prepared, not only in disease-endemic regions, but also in disease-free countries. Diagnostics, vaccines, and therapeutics need to be developed, and therefore the establishment of animal models for EHF and MHF is invaluable. Several animal models have been developed for EHF and MHF using nonhuman primates (NHPs) and rodents, which are crucial to understand pathophysiology and to develop diagnostics, vaccines, and therapeutics. Rhesus and cynomolgus macaques are representative models of filovirus infection as they exhibit remarkably similar symptoms to those observed in humans. However, the NHP models have practical and ethical problems that limit their experimental use. Furthermore, there are no inbred and genetically manipulated strains of NHP. Rodent models such as mouse, guinea pig, and hamster, have also been developed. However, these rodent models require adaptation of the virus to produce lethal disease and do not mirror all symptoms of human filovirus infection. This review article provides an outline of the clinical features of EHF and MHF in animals, including humans, and discusses how the animal models have been developed to study pathophysiology, vaccines, and therapeutics.
Keywords	Animal Models ; filovirus ; Ebola virus ; Marburg virus ; viral hemorrhagic fever ; Microbiology ; QR1-502 ; Science ; Q
Language	English
Publishing date	2013-09-01T00:00:00Z
Publisher	Frontiers Media S.A.
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: The nonstructural p17 protein of a fusogenic bat-borne reovirus regulates viral replication in virus species- and host-specific manners

Ryotaro Nouda / Takahiro Kawagishi / Yuta Kanai / Masayuki Shimojima / Masayuki Saijo / Yoshiharu Matsuura / Takeshi Kobayashi

PLoS Pathogens, Vol 18, Iss

2022 Volume 6

Abstract: Nelson Bay orthoreovirus (NBV), a member of the family Reoviridae, genus Orthoreovirus, is a bat-borne virus that causes respiratory diseases in humans. NBV encodes two unique nonstructural proteins, fusion-associated small transmembrane (FAST) protein ... ...

Abstract	Nelson Bay orthoreovirus (NBV), a member of the family Reoviridae, genus Orthoreovirus, is a bat-borne virus that causes respiratory diseases in humans. NBV encodes two unique nonstructural proteins, fusion-associated small transmembrane (FAST) protein and p17 protein, in the S1 gene segment. FAST induces cell–cell fusion between infected cells and neighboring cells and the fusogenic activity is required for efficient viral replication. However, the function of p17 in the virus cycle is not fully understood. Here, various p17 mutant viruses including p17-deficient viruses were generated by a reverse genetics system for NBV. The results demonstrated that p17 is not essential for viral replication and does not play an important role in viral pathogenesis. On the other hand, NBV p17 regulated viral replication in a bat cell line but not in other human and animal cell lines. Nuclear localization of p17 is associated with the regulation of NBV replication in bat cells. We also found that p17 dramatically enhances the cell–cell fusion activity of NBV FAST protein for efficient replication in bat cells. Furthermore, we found that a protein homologue of NBV p17 from another bat-borne orthoreovirus, but not those of avian orthoreovirus or baboon orthoreovirus, also supported efficient viral replication in bat cells using a p17-deficient virus-based complementation approach. These results provide critical insights into the functioning of the unique replication machinery of bat-borne viruses in their natural hosts. Author summary Bat-borne viruses including the severe acute respiratory syndrome coronavirus and Nipah virus generally cause highly pathogenic diseases in humans but not in their bat reservoirs. Nelson Bay orthoreovirus (NBV), a bat-borne virus associated with acute respiratory tract infections in humans, possesses two unique nonstructural proteins, FAST and p17. FAST enhances viral replication through its cell–cell fusion activity, while the function of p17 in the viral life cycle is poorly understood. In this ...
Keywords	Immunologic diseases. Allergy ; RC581-607 ; Biology (General) ; QH301-705.5
Subject code	570
Language	English
Publishing date	2022-06-01T00:00:00Z
Publisher	Public Library of Science (PLoS)
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: The nonstructural p17 protein of a fusogenic bat-borne reovirus regulates viral replication in virus species- and host-specific manners.

Ryotaro Nouda / Takahiro Kawagishi / Yuta Kanai / Masayuki Shimojima / Masayuki Saijo / Yoshiharu Matsuura / Takeshi Kobayashi

PLoS Pathogens, Vol 18, Iss 6, p e

2022 Volume 1010553

Abstract	Nelson Bay orthoreovirus (NBV), a member of the family Reoviridae, genus Orthoreovirus, is a bat-borne virus that causes respiratory diseases in humans. NBV encodes two unique nonstructural proteins, fusion-associated small transmembrane (FAST) protein and p17 protein, in the S1 gene segment. FAST induces cell-cell fusion between infected cells and neighboring cells and the fusogenic activity is required for efficient viral replication. However, the function of p17 in the virus cycle is not fully understood. Here, various p17 mutant viruses including p17-deficient viruses were generated by a reverse genetics system for NBV. The results demonstrated that p17 is not essential for viral replication and does not play an important role in viral pathogenesis. On the other hand, NBV p17 regulated viral replication in a bat cell line but not in other human and animal cell lines. Nuclear localization of p17 is associated with the regulation of NBV replication in bat cells. We also found that p17 dramatically enhances the cell-cell fusion activity of NBV FAST protein for efficient replication in bat cells. Furthermore, we found that a protein homologue of NBV p17 from another bat-borne orthoreovirus, but not those of avian orthoreovirus or baboon orthoreovirus, also supported efficient viral replication in bat cells using a p17-deficient virus-based complementation approach. These results provide critical insights into the functioning of the unique replication machinery of bat-borne viruses in their natural hosts.
Keywords	Immunologic diseases. Allergy ; RC581-607 ; Biology (General) ; QH301-705.5
Subject code	570
Language	English
Publishing date	2022-06-01T00:00:00Z
Publisher	Public Library of Science (PLoS)
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Case–Control Study of Long COVID, Sapporo, Japan

Toshiaki Asakura / Takashi Kimura / Isaku Kurotori / Katabami Kenichi / Miyuki Hori / Mariko Hosogawa / Masayuki Saijo / Kaori Nakanishi / Hiroyasu Iso / Akiko Tamakoshi

Emerging Infectious Diseases, Vol 29, Iss 5, Pp 956-

2023 Volume 966

Abstract: We conducted a cross-sectional survey among SARS-CoV-2–positive persons and negative controls in Sapporo, Japan, to clarify symptoms of long COVID. We collected responses from 8,018 participants, 3,694 case-patients and 3,672 controls. We calculated ... ...

Abstract	We conducted a cross-sectional survey among SARS-CoV-2–positive persons and negative controls in Sapporo, Japan, to clarify symptoms of long COVID. We collected responses from 8,018 participants, 3,694 case-patients and 3,672 controls. We calculated symptom prevalence for case-patients at 2–3, 4–6, 7–9, 10–12, and 13–18 months after illness onset. We used logistic regression, adjusted for age and sex, to estimate the odds ratio (OR) for each symptom and control reference. We calculated symptom prevalence by stratifying for disease severity, age, and sex. At 4–18 months from illness onset, ORs for anosmia, ageusia, dyspnea, alopecia, and brain fog were consistently >1, whereas ORs for common cold–like, gastrointestinal, and dermatologic symptoms were <1. Time trend ORs increased for diminished ability to concentrate, brain fog, sleep disturbance, eye symptoms, and tinnitus. Clinicians should focus on systemic, respiratory, and neuropsychiatric symptoms among long COVID patients.
Keywords	COVID-19 ; respiratory infections ; severe acute respiratory syndrome coronavirus 2 ; SARS-CoV-2 ; SARS ; coronavirus disease ; Medicine ; R ; Infectious and parasitic diseases ; RC109-216
Language	English
Publishing date	2023-05-01T00:00:00Z
Publisher	Centers for Disease Control and Prevention
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Macacine alphaherpesvirus 1 (B Virus) Infection in Humans, Japan, 2019

Souichi Yamada / Harutaka Katano / Yuko Sato / Tadaki Suzuki / Akihiko Uda / Keita Ishijima / Motoi Suzuki / Daigo Yamada / Shizuko Harada / Hitomi Kinoshita / Phu Hoang Anh Nguyen / Hideki Ebihara / Ken Maeda / Masayuki Saijo / Shuetsu Fukushi

Emerging Infectious Diseases, Vol 30, Iss 1, Pp 177-

2024 Volume 179

Abstract: Two human patients with Macacine alphaherpesvirus 1 infection were identified in Japan in 2019. Both patients had worked at the same company, which had a macaque facility. The rhesus-genotype B virus genome was detected in cerebrospinal fluid samples ... ...

Abstract	Two human patients with Macacine alphaherpesvirus 1 infection were identified in Japan in 2019. Both patients had worked at the same company, which had a macaque facility. The rhesus-genotype B virus genome was detected in cerebrospinal fluid samples from both patients.
Keywords	Macacine alphaherpesvirus 1 ; B virus ; viruses ; zoonoses ; Japan ; Medicine ; R ; Infectious and parasitic diseases ; RC109-216
Language	English
Publishing date	2024-01-01T00:00:00Z
Publisher	Centers for Disease Control and Prevention
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Co-infection with Severe Fever with Thrombocytopenia Syndrome Virus and Rickettsia japonica after Tick Bite, Japan

Tatsuya Fujikawa / Tomoki Yoshikawa / Takeshi Kurosu / Masayuki Shimojima / Masayuki Saijo / Kyoko Yokota

Emerging Infectious Diseases, Vol 27, Iss 4, Pp 1247-

2021 Volume 1249

Abstract: Severe fever with thrombocytopenia syndrome was diagnosed in a febrile woman in Japan after a tick bite. However, Rickettsia japonica DNA was retrospectively detected in the eschar specimen, suggesting co-infection from the bite. Establishment of the ... ...

Abstract	Severe fever with thrombocytopenia syndrome was diagnosed in a febrile woman in Japan after a tick bite. However, Rickettsia japonica DNA was retrospectively detected in the eschar specimen, suggesting co-infection from the bite. Establishment of the severe fever with thrombocytopenia syndrome virus infection might have overpowered the R. japonica infection.
Keywords	severe fever with thrombocytopenia syndrome ; severe fever with thrombocytopenia syndrome virus ; Japanese spotted fever ; tickborne infectious diseases ; co-infection ; rickettsia ; Medicine ; R ; Infectious and parasitic diseases ; RC109-216
Language	English
Publishing date	2021-04-01T00:00:00Z
Publisher	Centers for Disease Control and Prevention
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Inactivation of severe fever with thrombocytopenia syndrome virus for improved laboratory safety

Toshihiko Harada / Shuetsu Fukushi / Takeshi Kurosu / Tomoki Yoshikawa / Masayuki Shimojima / Kiyoshi Tanabayashi / Masayuki Saijo

Journal of Biosafety and Biosecurity, Vol 2, Iss 1, Pp 31-

2020 Volume 35

Abstract: Summary: Severe fever with thrombocytopenia syndrome (SFTS), a tick-borne infectious disease with high mortality, is diagnosed by the serological testing of serum samples from patients in the acute and convalescent phases and/or by direct detection of ... ...

Abstract	Summary: Severe fever with thrombocytopenia syndrome (SFTS), a tick-borne infectious disease with high mortality, is diagnosed by the serological testing of serum samples from patients in the acute and convalescent phases and/or by direct detection of the SFTS virus (SFTSV). Conventionally, heat and UV treatments have been used to inactivate the viruses present in serum samples before performing the serological assays. Here, we examined the inactivation conditions optimal for SFTSV-containing serum samples to ensure the safety of laboratory workers while maintaining the accuracy of serological assay results simultaneously. Heating human serum samples spiked with SFTSV to 60 °C for 30 min or exposing them to UV irradiation for 30 min, reduced the infectious virus titer below the limit of detection. SFTSV in sera from patients in the acute phase of SFTS was completely inactivated by heating to 60 °C for 30 min, followed by UV irradiation for 10 min. This inactivation procedure had minimal impact on the performance of SFTSV antibody detection tests. The data provided herein can serve as a guide for laboratory workers and researchers working with SFTS serological tests.
Keywords	Biosafety ; Inactivation ; Severe fever with thrombocytopenia syndrome (SFTSV) ; Serology ; Biology (General) ; QH301-705.5
Language	English
Publishing date	2020-03-01T00:00:00Z
Publisher	KeAi Communications Co., Ltd.
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Efficient functional screening of a cellular cDNA library to identify severe fever with thrombocytopenia syndrome virus entry factors

Masayuki Shimojima / Satoko Sugimoto / Satoshi Taniguchi / Tomoki Yoshikawa / Takeshi Kurosu / Masayuki Saijo

Scientific Reports, Vol 10, Iss 1, Pp 1-

2020 Volume 12

Abstract: Abstract The identification of host cell factors for virus entry is useful for the molecular explanation of viral tropisms and often leads to a more profound understanding of virus-induced diseases. Severe fever with thrombocytopenia syndrome (SFTS) is ... ...

Abstract	Abstract The identification of host cell factors for virus entry is useful for the molecular explanation of viral tropisms and often leads to a more profound understanding of virus-induced diseases. Severe fever with thrombocytopenia syndrome (SFTS) is an emerging infectious disease caused by SFTS virus. No countermeasures against the disease exist. In this report, we show an efficient method using virus-like particles for the functional screening of a cellular cDNA library to identify SFTS virus entry factors. Two variants encoding dendritic cell-specific ICAM-3 grabbing non-integrin related (DC-SIGNR), a calcium-dependent lectin known to enhance SFTS virus infection, were successfully identified from a human liver cDNA library. We will discuss applications for yet unidentified factor(s) for SFTS virus entry and for entry factor(s) for other viruses related to SFTS virus.
Keywords	Medicine ; R ; Science ; Q
Language	English
Publishing date	2020-04-01T00:00:00Z
Publisher	Nature Publishing Group
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Dengue virus infection induces selective expansion of Vγ4 and Vγ6TCR γδ T cells in the small intestine and a cytokine storm driving vascular leakage in mice.

Takeshi Kurosu / Daisuke Okuzaki / Yusuke Sakai / Mohamad Al Kadi / Supranee Phanthanawiboon / Yasusi Ami / Masayuki Shimojima / Tomoki Yoshikawa / Shuetsu Fukushi / Noriyo Nagata / Tadaki Suzuki / Daisuke Kamimura / Masaaki Murakami / Hideki Ebihara / Masayuki Saijo

PLoS Neglected Tropical Diseases, Vol 17, Iss 11, p e

2023 Volume 0011743

Abstract: Dengue is a major health problem in tropical and subtropical regions. Some patients develop a severe form of dengue, called dengue hemorrhagic fever, which can be fatal. Severe dengue is associated with a transient increase in vascular permeability. A ... ...

Abstract	Dengue is a major health problem in tropical and subtropical regions. Some patients develop a severe form of dengue, called dengue hemorrhagic fever, which can be fatal. Severe dengue is associated with a transient increase in vascular permeability. A cytokine storm is thought to be the cause of the vascular leakage. Although there are various research reports on the pathogenic mechanism, the complete pathological process remains poorly understood. We previously reported that dengue virus (DENV) type 3 P12/08 strain caused a lethal systemic infection and severe vascular leakage in interferon (IFN)-α/β and γ receptor knockout mice (IFN-α/β/γRKO mice), and that blockade of TNF-α signaling protected mice. Here, we performed transcriptome analysis of liver and small intestine samples collected chronologically from P12/08-infected IFN-α/β/γRKO mice in the presence/absence of blockade of TNF-α signaling and evaluated the cytokine and effector-level events. Blockade of TNF-α signaling mainly protected the small intestine but not the liver. Infection induced the selective expansion of IL-17A-producing Vγ4 and Vγ6 T cell receptor (TCR) γδ T cells in the small intestine, and IL-17A, together with TNF-α, played a critical role in the transition to severe disease via the induction of inflammatory cytokines such as TNF-α, IL-1β, and particularly the excess production of IL-6. Infection also induced the infiltration of neutrophils, as well as neutrophil collagenase/matrix metalloprotease 8 production. Blockade of IL-17A signaling reduced mortality and suppressed the expression of most of these cytokines, including TNF-α, indicating that IL-17A and TNF-α synergistically enhance cytokine expression. Blockade of IL-17A prevented nuclear translocation of NF-κB p65 in stroma-like cells and epithelial cells in the small intestine but only partially prevented recruitment of immune cells to the small intestine. This study provides an overall picture of the pathogenesis of infection in individual mice at the cytokine and effector ...
Keywords	Arctic medicine. Tropical medicine ; RC955-962 ; Public aspects of medicine ; RA1-1270
Subject code	570
Language	English
Publishing date	2023-11-01T00:00:00Z
Publisher	Public Library of Science (PLoS)
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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