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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.