Analysis of the entry mechanism of Crimean-Congo hemorrhagic fever virus, using a vesicular stomatitis virus pseudotyping system
| Autor: | Hideki Tani, Shuetsu Fukushi, Taisuke Horimoto, Masayuki Saijo, Masayuki Shimojima, Yuto Suda, Shin Murakami |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2016 |
| Předmět: |
0301 basic medicine
viruses 030106 microbiology Jurkat Cell Receptors Cell Surface Vesicular stomatitis Indiana virus Virus 03 medical and health sciences Jurkat Cells Viral Envelope Proteins Viral entry Virology Severe Fever With Thrombocytopenia Syndrome Virus Chlorocebus aethiops Animals Humans Lectins C-Type Vero Cells biology General Medicine Virus Internalization biology.organism_classification Pseudotype Virus Titer 030104 developmental biology HEK293 Cells Vesicular stomatitis virus Hemorrhagic Fever Virus Crimean-Congo Pseudotyping Vero cell Rift Valley Fever Virus Original Article Hemorrhagic Fever Crimean Cell Adhesion Molecules Crimean Congo hemorrhagic fever virus |
| Zdroj: | Archives of Virology |
| ISSN: | 1432-8798 0304-8608 |
| Popis: | Crimean-Congo hemorrhagic fever (CCHF) is a tick-borne disease causing severe hemorrhagic symptoms with a nearly 30 % case-fatality rate in humans. The experimental use of CCHF virus (CCHFV), which causes CCHF, requires high-biosafety-level (BSL) containment. In contrast, pseudotyping of various viral glycoproteins (GPs) onto vesicular stomatitis virus (VSV) can be used in facilities with lower BSL containment, and this has facilitated studies on the viral entry mechanism and the measurement of neutralizing activity, especially for highly pathogenic viruses. In the present study, we generated high titers of pseudotyped VSV bearing the CCHFV envelope GP and analyzed the mechanisms involved in CCHFV infection. A partial deletion of the CCHFV GP cytoplasmic domain increased the titer of the pseudotyped VSV, the entry mechanism of which was dependent on the CCHFV envelope GP. Using the pseudotype virus, DC-SIGN (a calcium-dependent [C-type] lectin cell-surface molecule) was revealed to enhance viral infection and act as an entry factor for CCHFV. |
| Databáze: | OpenAIRE |
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