Morbillivirus Receptors and Tropism: Multiple Pathways for Infection

Sato, Hiroki; Yoneda, Misako; Honda, Tomoyuki; Kai, Chieko

Previously, we have found that infection with several SLAM (and presumably nectin-4) negative cell lines with morbillivirus was inhibited by soluble heparin, and that virus bound to immobilized heparin. These results suggest that ubiquitously expressed heparin-like glycosaminoglycans are involved in morbillivirus infection (Fujita et al., 2007; Terao-Muto et al., 2008) . More recently, we have also demonstrated a unique infection mechanism of MeV, in which viral particles incorporate cellular cyclophilin (Cyp)B on their surface and bind to cellular CD147, a receptor for CypA and B, independently of MeV-H (Watanabe et al., 2010) . It is known that CypA incorporated into HIV-1 particles translocates to the surfaces of virions (Misumi et al., 2002) , and that the interaction between CypA and CD147 enables HIV-1 to infect target cells via CD147, independently of the binding of gp120 and CD4 (Pushkarsky et al., 2001) . Additionally, severe acute respiratory syndrome coronavirus (SARS-CoV) is proposed to use CD147 as a receptor in the same manner as HIV-1 (Chen et al., 2005) . Unlike HIV-1 and SARS-CoV, MeV uses CypB instead of CypA for binding to CD147. This finding is the first among viruses belonging to the order Mononegavirales and shows a new infection mode of MeV, which is independent of H protein.