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A polymorphism of the TIM-1 IgV domain: Implications for the susceptibility to filovirus infection

Kuroda, Makoto, Fujikura, Daisuke, Noyori, Osamu, Kajihara, Masahiro, Maruyama, Junki, Miyamoto, Hiroko, Yoshida, Reiko, Takada, Ayato
Biochemical and biophysical research communications 2014 v.455 pp. 223-228
Cercopithecus aethiops, Filoviridae, T-lymphocytes, amino acid substitution, amino acids, fever, genes, host range, humans, immunoglobulin A, kidneys, mortality, mucins, pathogenicity, vesicular stomatitis, viruses
Filoviruses, including Ebola and Marburg viruses, cause severe hemorrhagic fever in humans and nonhuman primates with mortality rates of up to 90%. Human T-cell immunoglobulin and mucin domain 1 (TIM-1) is one of the host proteins that have been shown to promote filovirus entry into cells. In this study, we cloned TIM-1 genes from three different African green monkey kidney cell lines (Vero E6, COS-1, and BSC-1) and found that TIM-1 of Vero E6 had a 23-amino acid deletion and 6 amino acid substitutions compared with those of COS-1 and BSC-1. Interestingly, Vero E6 TIM-1 had a greater ability to promote the infectivity of vesicular stomatitis viruses pseudotyped with filovirus glycoproteins than COS-1-derived TIM-1. We further found that the increased ability of Vero E6 TIM-1 to promote virus infectivity was most likely due to a single amino acid difference between these TIM-1s. These results suggest that a polymorphism of the TIM-1 molecules is one of the factors that influence cell susceptibility to filovirus infection, providing a new insight into the molecular basis for the filovirus host range.