Analysis of the entry mechanism of Crimean-Congo hemorrhagic fever virus, using a vesicular stomatitis virus pseudotyping system

• Published in: Archives of virology Vol. 161; no. 6; pp. 1447 - 1454
• Main Authors: Suda, Yuto, Fukushi, Shuetsu, Tani, Hideki, Murakami, Shin, Saijo, Masayuki, Horimoto, Taisuke, Shimojima, Masayuki
• Format: Journal Article
• Language: English
• Published: Vienna Springer Vienna 01.06.2016; Springer Nature B.V
• Subjects: Animals; Arachnids; Biomedical and Life Sciences; Biomedicine; Cell Adhesion Molecules - physiology; Chlorocebus aethiops; Crimean-Congo hemorrhagic fever; Crimean-Congo hemorrhagic fever orthonairovirus; Crimean-Congo hemorrhagic fever virus; Dengue fever; Fatalities; Glycoproteins; HEK293 Cells; Hemorrhagic Fever Virus, Crimean-Congo - genetics; Hemorrhagic Fever Virus, Crimean-Congo - pathogenicity; Hemorrhagic Fever Virus, Crimean-Congo - physiology; Hemorrhagic Fever, Crimean - etiology; Hemorrhagic Fever, Crimean - virology; Humans; Infections; Infectious Diseases; Jurkat Cells; Lectins; Lectins, C-Type - physiology; Medical Microbiology; mortality; neutralization; Original; Original Article; Plasmids; Proteins; Receptors, Cell Surface - physiology; RNA polymerase; Vero Cells; Vesicular stomatitis Indiana virus - genetics; Vesicular stomatitis Indiana virus - physiology; Vesicular stomatitis virus; Vesiculovirus; Viral Envelope Proteins - genetics; Viral Envelope Proteins - physiology; Viral infections; Virology; Virus Internalization; Viruses; Japan; Severe Fever With Thrombocytopenia Syndrome Virus; Pseudotype Virus; Rift Valley Fever Virus; Jurkat Cell; Vesicular Stomatitis Indiana Virus
• ISSN: 0304-8608; 1432-8798
• DOI: 10.1007/s00705-016-2803-1

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.