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Yoshihiro Kitamura

Researcher at Chinese Academy of Sciences

Publications -  26
Citations -  1548

Yoshihiro Kitamura is an academic researcher from Chinese Academy of Sciences. The author has contributed to research in topics: Virus & Homologous recombination. The author has an hindex of 14, co-authored 26 publications receiving 1400 citations. Previous affiliations of Yoshihiro Kitamura include University of Tokyo & International University of Health and Welfare.

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Emergence of Fatal PRRSV Variants: Unparalleled Outbreaks of Atypical PRRS in China and Molecular Dissection of the Unique Hallmark

TL;DR: This is the first comprehensive report documenting the 2006 epidemic of atypical PRRS outbreak in China and identifying the 30 amino-acid deletion in NSP2, a novel determining factor for virulence which may be implicated in the high pathogenicity of PRRSV, and will stimulate further study by using the infectious cDNA clone technique.
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Cyclophilin A interacts with influenza A virus M1 protein and impairs the early stage of the viral replication.

TL;DR: The mutagenesis results and immunofluorescence assays indicated that CypA interacted with the M1 protein and affected the early stage of the viral replication.
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Depletion of mitochondrial DNA in HIV-1-infected patients and its amelioration by antiretroviral therapy.

TL;DR: The decrease in mtDNA levels in PBMCs amongst HIV‐1‐infected patients and its amelioration by antiretroviral therapy may suggest the influence of direct effects on mitochondria or mtDNA by HIV‐ 1 infection.
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F gene recombination between genotype II and VII Newcastle disease virus.

TL;DR: Complete genome sequences analysis indicated that the N-terminal of SRZ03 F gene originated from a genotype II NDV strain, whereas the C-terminals of F gene and the rest of the genes originated fromA prevalent velogenic genotype VII NDV strains.
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Genetic analysis of double-strand break repair in Escherichia coli.

TL;DR: It is concluded that the RecBCD, Rec BCD-, and RecF pathways cannot promote conservative double-strand break repair as the RecE and lambda Red pathways can.