Taisuke Izumi

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Several members of the APOBEC3 family of cellular restriction factors provide intrinsic immunity to the host against viral infection. Specifically, APOBEC3DE, APOBEC3F, APOBEC3G, and APOBEC3H haplotypes II, V, and VII provide protection against HIV-1Δvif through hypermutation of the viral genome, inhibition of reverse transcription, and inhibition of viral(More)
A population protocol is one of distributed computing models for passively-mobile systems, where a number of agents change their states by pairwise interactions between two agents. In this paper, we investigate the solvability of the self-stabilizing leader election in population protocols without any kind of oracles. We identify the necessary and(More)
In the context of designing a scalable overlay network to support decentralized topic-based pub/sub communication, the Minimum Topic-Connected Overlay problem (Min-TCO in short) has been investigated: Given a set of t topics and a collection of n users together with the lists of topics they are interested in, the aim is to connect these users to a network(More)
We study the problem of Byzantine agreement in synchronous systems where malicious agents can move from one process to another and try to corrupt them. This model is known as mobile Byzantine faults. In a previous result [10], Garay has shown that n > 6t (n is the total number of processes, and t is the number of mobile faults) is sufficient to solve this(More)
Apolipoprotein B mRNA-editing enzyme catalytic polypeptide-like 3G (APOBEC3G, referred to here as A3G) is a potent antiretroviral host factor against human immunodeficiency virus type 1 (HIV-1). HIV-1 viral infectivity factor (Vif) counteracts A3G by promoting its degradation via the ubiquitin-proteasome pathway. Recent studies demonstrated that protein(More)
APOBEC3G (A3G) is an antiretroviral host factor that functions by deaminating dC to dU in retroviral cDNA. HIV-1 Vif protein counteracts A3G via a ubiquitin-proteasome pathway. In the case of a simple retrovirus such as the murine leukemia virus (MLV), it remains unclear why it can replicate in cells expressing APOBEC3 (A3) even though it doesn't possess(More)
Genomic hypermutation of RNA viruses, including human immunodeficiency virus type 1 (HIV-1), can be provoked by intrinsic and extrinsic pressures, which lead to the inhibition of viral replication and/or the progression of viral diversity. Human APOBEC3G was identified as an HIV-1 restriction factor, which edits nascent HIV-1 DNA by inducing G-to-A(More)
Several APOBEC3 proteins, particularly APOBEC3D, APOBEC3F, and APOBEC3G, induce G-to-A hypermutations in HIV-1 genome, and abrogate viral replication in experimental systems, but their relative contributions to controlling viral replication and viral genetic variation in vivo have not been elucidated. On the other hand, an HIV-1-encoded protein, Vif, can(More)