1. Highly homologous simian T-cell leukemia virus type 1 genome in Japanese macaques: a large cohort study.
- Author
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Hiraga K, Kitamura T, Kuramitsu M, Murata M, Tezuka K, Okuma K, Hamaguchi I, Akari H, and Mizukami T
- Subjects
- Animals, Phylogeny, Cohort Studies, Deltaretrovirus Infections virology, Deltaretrovirus Infections veterinary, Deltaretrovirus Infections epidemiology, Japan, Humans, Sequence Analysis, DNA, Molecular Epidemiology, Genetic Variation, Simian T-lymphotropic virus 1 genetics, Simian T-lymphotropic virus 1 isolation & purification, Genome, Viral, Macaca fuscata genetics
- Abstract
Background: Simian T-cell leukemia virus type 1 (STLV-1) is a retrovirus closely related to human T-cell leukemia virus type 1 (HTLV-1), the causative agent of adult T-cell leukemia (ATL). It has been shown that Japanese macaques (Macaca fuscata, JMs) are one of the main hosts of STLV-1 and that a high percentage of JMs (up to 60%) are infected with STLV-1; however, the molecular epidemiology of STLV-1 in JMs has not been examined., Methods: In this study, we analyzed full-length STLV-1 genome sequences obtained from 5 independent troops including a total of 68 JMs., Results: The overall nucleotide heterogeneity was 4.7%, and the heterogeneity among the troops was 2.1%, irrespective of the formation of distinct subclusters in each troop. Moreover, the heterogeneity within each troop was extremely low (>99% genome homology) compared with cases of STLV-1 in African non-human primates as well as humans. It was previously reported that frequent G-to-A single-nucleotide variants (SNVs) occur in HTLV-1 proviral genomes in both ATL patients and HTLV-1 carriers, and that a G-to-A hypermutation is associated with the cellular antiviral restriction factor, Apobec3G. Surprisingly, these SNVs were scarcely observed in the STLV-1 genomes in JMs., Conclusions: Taken together, these results indicate that STLV-1 genomes in JMs are highly homologous, at least in part due to the lack of Apobec3G-dependent G-to-A hypermutation., (© 2024. The Author(s).)
- Published
- 2024
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