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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)
We consider the parallel computing environment where m organizations provide machines and several jobs to be executed. While cooperation of organizations is required to minimize the global makespan, each organization also expects the faster completion of its own jobs primarily and thus it is not necessarily cooperative. To handle the situations, we(More)
APOBEC3G (apolipoprotein B mRNA-editing enzyme catalytic polypeptide-like 3G) was identified as an anti-HIV-1 (human immunodeficiency virus type 1) cellular factor in target CD4 T cells. It is a member of the APOBEC family of cytidine deaminases consisting of APOBEC1, APOBEC2, APOBEC3 (A to H), and AID (activation induced deaminase). During reverse(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)
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)
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)
OBJECTIVE The human APOBEC3 family of proteins potently restricts HIV-1 replication APOBEC3B, one of the family genes, is frequently deleted in human populations. Two previous studies reached inconsistent conclusions regarding the effects of APOBEC3B loss on HIV-1 acquisition and pathogenesis. Therefore, it was necessary to verify the effects of APOBEC3B on(More)