Crimean–Congo haemorrhagic fever virus uses LDLR to bind and enter host cells

Climate change and population densities accelerated transmission of highly pathogenic viruses to humans, including the Crimean–Congo haemorrhagic fever virus (CCHFV). Here we report that the Low Density Lipoprotein Receptor (LDLR) is a critical receptor for CCHFV cell entry, playing a vital role in...

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Vydáno v:	Nature microbiology Ročník 9; číslo 6; s. 1499 - 1512
Hlavní autoři:	Monteil, Vanessa M., Wright, Shane C., Dyczynski, Matheus, Kellner, Max J., Appelberg, Sofia, Platzer, Sebastian W., Ibrahim, Ahmed, Kwon, Hyesoo, Pittarokoilis, Ioannis, Mirandola, Mattia, Michlits, Georg, Devignot, Stephanie, Elder, Elizabeth, Abdurahman, Samir, Bereczky, Sándor, Bagci, Binnur, Youhanna, Sonia, Aastrup, Teodor, Lauschke, Volker M., Salata, Cristiano, Elaldi, Nazif, Weber, Friedemann, Monserrat, Nuria, Hawman, David W., Feldmann, Heinz, Horn, Moritz, Penninger, Josef M., Mirazimi, Ali
Médium:	Journal Article
Jazyk:	angličtina
Vydáno:	London Nature Publishing Group UK 01.06.2024 Nature Publishing Group
Témata:	13/1 13/31 14/63 631/326/596/2555 631/326/596/2557 64/60 96/10 Animals Apolipoprotein E Apolipoproteins E - genetics Apolipoproteins E - metabolism Biomedical and Life Sciences Biosensors Blood vessels Cell culture Climate change Crimean hemorrhagic fever Fever Glycoproteins Hemorrhagic Fever Virus, Crimean-Congo - genetics Hemorrhagic Fever Virus, Crimean-Congo - physiology Hemorrhagic Fever, Crimean - metabolism Hemorrhagic Fever, Crimean - virology Humans Infections Infectious Diseases LDLR protein Life Sciences Low density lipoprotein Low density lipoprotein receptors Medical Microbiology Mice Mice, Knockout Microbiology Organoids Parasitology Population density Receptor density Receptors, LDL - genetics Receptors, LDL - metabolism Receptors, Virus - metabolism Ticks - metabolism Ticks - virology Virology Virus Internalization Viruses
ISSN:	2058-5276, 2058-5276
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Abstract	Climate change and population densities accelerated transmission of highly pathogenic viruses to humans, including the Crimean–Congo haemorrhagic fever virus (CCHFV). Here we report that the Low Density Lipoprotein Receptor (LDLR) is a critical receptor for CCHFV cell entry, playing a vital role in CCHFV infection in cell culture and blood vessel organoids. The interaction between CCHFV and LDLR is highly specific, with other members of the LDLR protein family failing to bind to or neutralize the virus. Biosensor experiments demonstrate that LDLR specifically binds the surface glycoproteins of CCHFV. Importantly, mice lacking LDLR exhibit a delay in CCHFV-induced disease. Furthermore, we identified the presence of Apolipoprotein E (ApoE) on CCHFV particles. Our findings highlight the essential role of LDLR in CCHFV infection, irrespective of ApoE presence, when the virus is produced in tick cells. This discovery holds profound implications for the development of future therapies against CCHFV. Laboratory and clinical strains of Crimean–Congo haemorrhagic fever virus use LDLR to bind and enter host cells in blood vessel organoids and mice. Infection can also occur through ApoE, possibly present on virus particles.
AbstractList	Climate change and population densities accelerated transmission of highly pathogenic viruses to humans, including the Crimean-Congo haemorrhagic fever virus (CCHFV). Here we report that the Low Density Lipoprotein Receptor (LDLR) is a critical receptor for CCHFV cell entry, playing a vital role in CCHFV infection in cell culture and blood vessel organoids. The interaction between CCHFV and LDLR is highly specific, with other members of the LDLR protein family failing to bind to or neutralize the virus. Biosensor experiments demonstrate that LDLR specifically binds the surface glycoproteins of CCHFV. Importantly, mice lacking LDLR exhibit a delay in CCHFV-induced disease. Furthermore, we identified the presence of Apolipoprotein E (ApoE) on CCHFV particles. Our findings highlight the essential role of LDLR in CCHFV infection, irrespective of ApoE presence, when the virus is produced in tick cells. This discovery holds profound implications for the development of future therapies against CCHFV. Climate change and population densities accelerated transmission of highly pathogenic viruses to humans, including the Crimean–Congo haemorrhagic fever virus (CCHFV). Here we report that the Low Density Lipoprotein Receptor (LDLR) is a critical receptor for CCHFV cell entry, playing a vital role in CCHFV infection in cell culture and blood vessel organoids. The interaction between CCHFV and LDLR is highly specific, with other members of the LDLR protein family failing to bind to or neutralize the virus. Biosensor experiments demonstrate that LDLR specifically binds the surface glycoproteins of CCHFV. Importantly, mice lacking LDLR exhibit a delay in CCHFV-induced disease. Furthermore, we identified the presence of Apolipoprotein E (ApoE) on CCHFV particles. Our findings highlight the essential role of LDLR in CCHFV infection, irrespective of ApoE presence, when the virus is produced in tick cells. This discovery holds profound implications for the development of future therapies against CCHFV.Laboratory and clinical strains of Crimean–Congo haemorrhagic fever virus use LDLR to bind and enter host cells in blood vessel organoids and mice. Infection can also occur through ApoE, possibly present on virus particles. Climate change and population densities accelerated transmission of highly pathogenic viruses to humans, including the Crimean–Congo haemorrhagic fever virus (CCHFV). Here we report that the Low Density Lipoprotein Receptor (LDLR) is a critical receptor for CCHFV cell entry, playing a vital role in CCHFV infection in cell culture and blood vessel organoids. The interaction between CCHFV and LDLR is highly specific, with other members of the LDLR protein family failing to bind to or neutralize the virus. Biosensor experiments demonstrate that LDLR specifically binds the surface glycoproteins of CCHFV. Importantly, mice lacking LDLR exhibit a delay in CCHFV-induced disease. Furthermore, we identified the presence of Apolipoprotein E (ApoE) on CCHFV particles. Our findings highlight the essential role of LDLR in CCHFV infection, irrespective of ApoE presence, when the virus is produced in tick cells. This discovery holds profound implications for the development of future therapies against CCHFV. Laboratory and clinical strains of Crimean–Congo haemorrhagic fever virus use LDLR to bind and enter host cells in blood vessel organoids and mice. Infection can also occur through ApoE, possibly present on virus particles. Climate change and population densities accelerated transmission of highly pathogenic viruses to humans, including the Crimean-Congo haemorrhagic fever virus (CCHFV). Here we report that the Low Density Lipoprotein Receptor (LDLR) is a critical receptor for CCHFV cell entry, playing a vital role in CCHFV infection in cell culture and blood vessel organoids. The interaction between CCHFV and LDLR is highly specific, with other members of the LDLR protein family failing to bind to or neutralize the virus. Biosensor experiments demonstrate that LDLR specifically binds the surface glycoproteins of CCHFV. Importantly, mice lacking LDLR exhibit a delay in CCHFV-induced disease. Furthermore, we identified the presence of Apolipoprotein E (ApoE) on CCHFV particles. Our findings highlight the essential role of LDLR in CCHFV infection, irrespective of ApoE presence, when the virus is produced in tick cells. This discovery holds profound implications for the development of future therapies against CCHFV.Climate change and population densities accelerated transmission of highly pathogenic viruses to humans, including the Crimean-Congo haemorrhagic fever virus (CCHFV). Here we report that the Low Density Lipoprotein Receptor (LDLR) is a critical receptor for CCHFV cell entry, playing a vital role in CCHFV infection in cell culture and blood vessel organoids. The interaction between CCHFV and LDLR is highly specific, with other members of the LDLR protein family failing to bind to or neutralize the virus. Biosensor experiments demonstrate that LDLR specifically binds the surface glycoproteins of CCHFV. Importantly, mice lacking LDLR exhibit a delay in CCHFV-induced disease. Furthermore, we identified the presence of Apolipoprotein E (ApoE) on CCHFV particles. Our findings highlight the essential role of LDLR in CCHFV infection, irrespective of ApoE presence, when the virus is produced in tick cells. This discovery holds profound implications for the development of future therapies against CCHFV.
Author	Aastrup, Teodor Monteil, Vanessa M. Monserrat, Nuria Mirazimi, Ali Appelberg, Sofia Weber, Friedemann Kwon, Hyesoo Devignot, Stephanie Abdurahman, Samir Wright, Shane C. Dyczynski, Matheus Pittarokoilis, Ioannis Feldmann, Heinz Michlits, Georg Elder, Elizabeth Ibrahim, Ahmed Bagci, Binnur Youhanna, Sonia Kellner, Max J. Hawman, David W. Bereczky, Sándor Elaldi, Nazif Horn, Moritz Penninger, Josef M. Lauschke, Volker M. Salata, Cristiano Platzer, Sebastian W. Mirandola, Mattia
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organization: Public Health Agency of Sweden – sequence: 6 givenname: Sebastian W. orcidid: 0000-0002-2518-6273 surname: Platzer fullname: Platzer, Sebastian W. organization: IMBA, Institute of Molecular Biotechnology of the Austrian Academy of Science, Vienna Biocenter PhD Program, a Doctoral School of the University of Vienna and the Medical University of Vienna – sequence: 7 givenname: Ahmed surname: Ibrahim fullname: Ibrahim, Ahmed organization: Attana AB – sequence: 8 givenname: Hyesoo orcidid: 0000-0003-4637-4609 surname: Kwon fullname: Kwon, Hyesoo organization: Unit of Clinical Microbiology, Department of Laboratory Medicine, Karolinska Institute and Karolinska University Hospital, National Veterinary Institute – sequence: 9 givenname: Ioannis orcidid: 0009-0008-1510-487X surname: Pittarokoilis fullname: Pittarokoilis, Ioannis organization: Department of Physiology and Pharmacology, Karolinska Institutet – sequence: 10 givenname: Mattia surname: Mirandola fullname: Mirandola, 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Snippet	Climate change and population densities accelerated transmission of highly pathogenic viruses to humans, including the Crimean–Congo haemorrhagic fever virus... Climate change and population densities accelerated transmission of highly pathogenic viruses to humans, including the Crimean-Congo haemorrhagic fever virus...
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SubjectTerms	13/1 13/31 14/63 631/326/596/2555 631/326/596/2557 64/60 96/10 Animals Apolipoprotein E Apolipoproteins E - genetics Apolipoproteins E - metabolism Biomedical and Life Sciences Biosensors Blood vessels Cell culture Climate change Crimean hemorrhagic fever Fever Glycoproteins Hemorrhagic Fever Virus, Crimean-Congo - genetics Hemorrhagic Fever Virus, Crimean-Congo - physiology Hemorrhagic Fever, Crimean - metabolism Hemorrhagic Fever, Crimean - virology Humans Infections Infectious Diseases LDLR protein Life Sciences Low density lipoprotein Low density lipoprotein receptors Medical Microbiology Mice Mice, Knockout Microbiology Organoids Parasitology Population density Receptor density Receptors, LDL - genetics Receptors, LDL - metabolism Receptors, Virus - metabolism Ticks - metabolism Ticks - virology Virology Virus Internalization Viruses
Title	Crimean–Congo haemorrhagic fever virus uses LDLR to bind and enter host cells
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