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Yoshio Koyanagi

Researcher at Kyoto University

Publications -  249
Citations -  15331

Yoshio Koyanagi is an academic researcher from Kyoto University. The author has contributed to research in topics: Virus & Viral replication. The author has an hindex of 57, co-authored 247 publications receiving 14514 citations. Previous affiliations of Yoshio Koyanagi include Yamaguchi University & Tokyo Medical and Dental University.

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NOD/SCID/gamma(c)(null) mouse: an excellent recipient mouse model for engraftment of human cells.

TL;DR: It is suggested that multiple immunological dysfunctions, including cytokine production capability, in addition to functional incompetence of T, B, and NK cells, may lead to the high engraftment levels of xenograft in NOD/SCID/gamma(c)(null) mice.
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Infection of HTLV-III/LAV in HTLV-I-carrying cells MT-2 and MT-4 and application in a plaque assay

TL;DR: Activities of HTLV-III were neutralized by the human antibodies against the virus when immunofluorescence and plaque assays were used, and the same results were obtained with the lymphadenopathy-associated virus (LAV1).
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Dual infection of the central nervous system by AIDS viruses with distinct cellular tropisms.

TL;DR: Results indicate that genetic variation of HIV in vivo may result in altered cell tropisms and possibly implicate strains of HIV with glial cell tropism in the pathogenesis of some neurologic disorders of AIDS.
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HIV-1 tropism for mononuclear phagocytes can be determined by regions of gp120 outside the CD4-binding domain.

TL;DR: It is proposed that at least one determinant for mononuclear phagocyte tropism involves target cell interactions with regions of gp120 distinct from the CD4-binding domain, and genetic mapping of the macrophage-tropic phenotype by construction of recombinant viruses indicates this region can be determined by a 157-amino-acid region of the gp120 glycoprotein of HIV-1JR–FL.
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Harnessing the CRISPR/Cas9 system to disrupt latent HIV-1 provirus

TL;DR: The potential of the CRISPR/Cas9 system to edit the HIV-1 genome and block its expression is shown and this system was also able to remove internal viral genes from the host cell chromosome.