Kamitani Lab/International Research Center for Infectious Diseases  Laboratory of Clinical Research on Infectious Diseases

Coronaviruses infect many different animals, including human, and cause them to have respiratory and gastrointestinal diseases. Newly emerged Middle East respiratory syndrome coronavirus (MERS-CoV) and severe acute respiratory syndrome coronavirus (SARS-CoV) infect respiratory tract and cause severe pneumonia disease. Our research group focuses on these coronaviruses and studies the molecular biology and host cell-virus interaction of these coronaviruses.


SARS-CoV is the etiological agent of a newly-emerged human respiratory disease that originated in southern China in 2002 and spread worldwide in the 2003 epidemic. After 10 years of the epidemic of SARS-CoV, novel coronavirus, MERS-CoV, has been reported in Middle East region. MERS-CoV spreads to North America, Europe, China, and Korea. No effective treatment against MERS-CoV. Our research group studies about non-structural protein 1 (nsp1), that is one of pathogenicity factor in Coronavirus. Nsp1 of SARS-CoV induces host protein synthesis suppression through binding to 40S ribosome complex. The nsp1 enhance viral replication through binding to viral RNA. Our research group utilizes a Bacterial Artificial chromosome (BAC)-based revers genetics system for these coronaviruses. Our group try to understand the mechanism of Coronaviruses replication and pathogenesis for development therapeutic targets against Coronaviruses using the BAC-based revers genetics system.

 

  • Fig. Gene expression control by SARS-CoV nsp1 |
    ①Nsp1 binds to 40S ribosome, and then induces translational shutoff. The nsp1-40S binding induces cleavage of mRNA.
    ②Nsp1 binds to viral mRNA, and then the interaction enhances viral replication.

Staff

  • Guest Prof.: Wataru Kamitani (Grad. Schoool of Medicine, Gunma University)

Website

Publications

  • (1) Middle East Respiratory Syndrome Coronavirus Spike Protein Is Not Activated Directly by Cellular Furin during Viral Entry into Target Cells. Matsuyama S., et al., J. Virol. (2018) 92(19). pii: e00683-18
    (2) MERS coronavirus nsp1 participates in an efficient propagation through a specific interaction with viral RNA. Terada Y., et al., Virology. (2017) 511:95-105.
    (3) Two-amino acids change in the nsp4 of SARS coronavirus abolishes viral replication. Sakai Y., et al., Virology. (2017) 510:165-174.
    (4) Severe Acute Respiratory Syndrome Coronavirus nsp1 Facilitates Efficient Propagation in Cells through a Specific Translational Shutoff of Host mRNA. Tanaka T., et al., J. Virol. (2012) 86(20):11128-37