Tokushima University / Educator and Researcher Directory --- Doi, Naoya

Personal Web Page

https://researchmap.jp/6g6g (researchmap)

Field of Study

○	Life sciences [Virology]

Subject of Study

Book / Paper

Book:

1.	Takaaki Koma, Naoya Doi, Le Quoc Bao, Tomoyuki Kondo, Akio Adachi and Masako Nomaguchi : HIV-1 Replication and Pathogenicity: Lessons from Macaque-Tropic HIV-1 Derivatives, IntechOpen, London, Sep. 2023.

Academic Paper (Judged Full Paper):

1.	Takaaki Koma, Naoya Doi, Bao Quoc Le, Tomoyuki Kondo, Mitsuki Ishizue, Chiaki Tokaji, Chizuko Tsukada, Akio Adachi and Masako Nomaguchi : Involvement of a Rarely Used Splicing SD2b Site in the Regulation of HIV-1 mRNA Production as Revealed by a Growth-Adaptive Mutation., Viruses, Vol.15, No.12, 2424, 2023. (Summary) We have previously reported an HIV-1 mutant designated NL-Y226tac that expresses Vif at an ultra-low level, being replication-defective in high-APOBEC3G cells, such as H9. It carries a synonymous mutation within the splicing SA1 site relative to its parental clone. In order to determine whether a certain mutant(s) emerges during multi-infection cycles, we maintained H9 cells infected with a relatively low or high input of NL-Y226tac for extended time periods. Unexpectedly, we reproducibly identified a g5061a mutation in the SD2b site in the two independent long-term culture experiments that partially increases Vif expression and replication ability. Importantly, the adaptive mutation g5061a was demonstrated to enhance mRNA production by activation of the SA1 site mediated through increasing usage of a rarely used SD2b site. In the long-term culture initiated by a high virus input, we additionally found a Y226Fttc mutation at the original Y226tac site in SA1 that fully restores Vif expression and replication ability. As expected, the adaptive mutation Y226Fttc enhances mRNA production through increasing the splicing site usage of SA1. Our results here revealed the importance of the SD2b nucleotide sequence in producing mRNA involved in the HIV-1 adaptation and of mutual antagonism between Vif and APOBEC3 proteins in HIV-1 adaptation/evolution and survival. (Keyword) RNA, Messenger / HIV-1 / Cell Line / vif Gene Products, Human Immunodeficiency Virus / Virus Replication / Cytidine Deaminase / Mutation (Link to Publication Site) ● Publication site (DOI): 10.3390/v15122424 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 38140666 ● Search Scopus @ Elsevier (PMID): 38140666 ● Search Scopus @ Elsevier (DOI): 10.3390/v15122424 (DOI: 10.3390/v15122424, PubMed: 38140666)
2.	Takaaki Koma, Tokifumi Odaka, Sung-il Lee, Naoya Doi, Tomoyuki Kondo, Kazu Okuma, Jun-Ichi Fujisawa, Akio Adachi and Masako Nomaguchi : Humanized mice generated by intra-bone marrow injection of CD133-positive hematopoietic stem cells: application to HIV-1 research, Frontiers in Virology, Vol.3, 2023. (Link to Publication Site) ● Publication site (DOI): 10.3389/fviro.2023.1192184 (Link to Search Site for Scientific Articles) ● Search Scopus @ Elsevier (DOI): 10.3389/fviro.2023.1192184 (DOI: 10.3389/fviro.2023.1192184)
3.	Takaaki Koma, Naoya Doi, Akihiro Suzuki, Kentaro Nagamatsu, Takeshi Yasui, Koji Yasutomo, Akio Adachi, Takeo Minamikawa and Masako Nomaguchi : Major target for UV-induced complete loss of HIV-1 infectivity: A model study of single-stranded RNA enveloped viruses, Frontiers in Virology, Vol.2, 994842, 2022. (Link to Publication Site) ● Publication site (DOI): 10.3389/fviro.2022.994842 (Link to Search Site for Scientific Articles) ● Search Scopus @ Elsevier (DOI): 10.3389/fviro.2022.994842 (DOI: 10.3389/fviro.2022.994842)
4.	Takaaki Koma, Naoya Doi, Mai Takemoto, Kyosuke Watanabe, Hideki Yamamoto, Satoshi Nakashima, Akio Adachi and Masako Nomaguchi : The Expression Level of HIV-1 Vif Is Optimized by Nucleotide Changes in the Genomic SA1D2prox Region during the Viral Adaptation Process., Viruses, Vol.13, No.10, 2021. (Summary) HIV-1 Vif plays an essential role in viral replication by antagonizing anti-viral cellular restriction factors, a family of APOBEC3 proteins. We have previously shown that naturally-occurring single-nucleotide mutations in the SA1D2prox region, which surrounds the splicing acceptor 1 and splicing donor 2 sites of the HIV-1 genome, dramatically alter the Vif expression level, resulting in variants with low or excessive Vif expression. In this study, we investigated how these HIV-1 variants with poor replication ability adapt and evolve under the pressure of APOBEC3 proteins. Adapted clones obtained through adaptation experiments exhibited an altered replication ability and Vif expression level compared to each parental clone. While various mutations were present throughout the viral genome, all replication-competent adapted clones with altered Vif expression levels were found to bear them within SA1D2prox, without exception. Indeed, the mutations identified within SA1D2prox were responsible for changes in the Vif expression levels and altered the splicing pattern. Moreover, for samples collected from HIV-1-infected patients, we showed that the nucleotide sequences of SA1D2prox can be chronologically changed and concomitantly affect the Vif expression levels. Taken together, these results demonstrated the importance of the SA1D2prox nucleotide sequence for modulating the Vif expression level during HIV-1 replication and adaptation. (Tokushima University Institutional Repository) ● Metadata: 116870 (Link to Publication Site) ● Publication site (DOI): 10.3390/v13102079 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 34696508 ● Search Scopus @ Elsevier (PMID): 34696508 ● Search Scopus @ Elsevier (DOI): 10.3390/v13102079 (Tokushima University Institutional Repository: 116870, DOI: 10.3390/v13102079, PubMed: 34696508)
5.	Takaaki Koma, Masaru Yokoyama, Osamu Kotani, Naoya Doi, Nina Nakanishi, Hayato Okubo, Shun Adachi, Akio Adachi, Hironori Sato and Masako Nomaguchi : Species-specific valid ternary interactions of HIV-1 Env-gp120, CD4, and CCR5 as revealed by an adaptive single-amino acid substitution at the V3 loop tip., Journal of Virology, 2021. (Summary) Understanding molecular bases for viral entry into cells leads to the elucidation of one of major viral survival strategies, and thus to the development of new effective antiviral measures. As experimentally shown recently, HIV-1 is highly mutable and adaptable in growth-restrictive cells such as those of macaque origin. HIV-1 initiates its infection by sequential interactions of Env-gp120 with two cell surface receptors, CD4 and CCR5. A recent epoch-making structural study has disclosed that CD4-induced conformation of gp120 is stabilized upon binding of CCR5 to the CD4-gp120 complex, whereas its biological significance remains totally unknown. Here, from a series of mutations found in our extensive studies, we identified a single-amino acid adaptive mutation at the V3 loop tip of Env-gp120 critical for its interaction with both CD4 and CCR5 in a host cell species-specific way. This remarkable finding would certainly provoke and accelerate studies to precisely clarify the HIV-1 entry mechanism. (Tokushima University Institutional Repository) ● Metadata: 116583 (Link to Publication Site) ● Publication site (DOI): 10.1128/JVI.02177-20 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 33883222 ● Search Scopus @ Elsevier (PMID): 33883222 ● Search Scopus @ Elsevier (DOI): 10.1128/JVI.02177-20 (Tokushima University Institutional Repository: 116583, DOI: 10.1128/JVI.02177-20, PubMed: 33883222)
6.	Naoya Doi, Takaaki Koma, Akio Adachi and Masako Nomaguchi : Expression Level of HIV-1 Vif Can Be Fluctuated by Natural Nucleotide Variations in the vif-Coding and Regulatory SA1D2prox Sequences of the Proviral Genome., Frontiers in Microbiology, Vol.10, 2019. (Tokushima University Institutional Repository) ● Metadata: 114460 (Link to Publication Site) ● Publication site (DOI): 10.3389/fmicb.2019.02758 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 31849897 ● Search Scopus @ Elsevier (PMID): 31849897 ● Search Scopus @ Elsevier (DOI): 10.3389/fmicb.2019.02758 (Tokushima University Institutional Repository: 114460, DOI: 10.3389/fmicb.2019.02758, PubMed: 31849897)
7.	Naoya Doi, Takaaki Koma, Akio Adachi and Masako Nomaguchi : Role for Gag-CA Interdomain Linker in Primate Lentiviral Replication., Frontiers in Microbiology, Vol.10, 2019. (Summary) -modulator to optimize the Gag-related viral replication process. We also have noted, during the course of conducting the research project, that HIV-1 and SIVmac, belonging to distinct primate lentiviral lineages, share a similarly biologically active linker region with each other. In this brief article, we summarize and report the results obtained by mutational studies that are relevant to the functional significance of the interdomain linker of HIV/SIV Gag-CA. Based on this investigation, we discuss about the future directions of the research in this line. (Tokushima University Institutional Repository) ● Metadata: 114459 (Link to Publication Site) ● Publication site (DOI): 10.3389/fmicb.2019.01831 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 31440231 ● Search Scopus @ Elsevier (PMID): 31440231 ● Search Scopus @ Elsevier (DOI): 10.3389/fmicb.2019.01831 (Tokushima University Institutional Repository: 114459, DOI: 10.3389/fmicb.2019.01831, PubMed: 31440231)
8.	Takaaki Koma, Osamu Kotani, Kei Miyakawa, Akihide Ryo, Masaru Yokoyama, Naoya Doi, Akio Adachi, Hironori Sato and Masako Nomaguchi : Allosteric regulation of HIV-1 capsid structure for Gag assembly, virion production, and viral infectivity by a disordered interdomain linker., Journal of Virology, 2019. (Summary) HIV-1 particle production and infection are highly ordered processes. Viral Gag proteins play a central role in the assembly and disassembly of viral molecules. Of these, capsid protein (CA) is a major contributor to the Gag-Gag interactions. CA consists of two structured domains, i.e., N-terminal (NTD) and C-terminal (CTD) domains, connected by an unstructured domain named interdomain linker. While multiple regions in the NTD and CTD domains are reported to play roles in virion morphogenesis and infectivity, the roles of the linker region in Gag assembly and virus particle formation remain elusive. In this report, we show by biological and molecular analyses that the linker region functions as an intramolecular modulator to tune Gag assembly, virion production, and viral infectivity. Our study thus illustrates a hitherto unrecognized mechanism, an allosteric regulation of CA structure by the disordered protein element, for HIV-1 replication. (Link to Publication Site) ● Publication site (DOI): 10.1128/JVI.00381-19 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 31189701 ● Search Scopus @ Elsevier (PMID): 31189701 ● Search Scopus @ Elsevier (DOI): 10.1128/JVI.00381-19 (DOI: 10.1128/JVI.00381-19, PubMed: 31189701)
9.	Naoya Doi, Masaru Yokoyama, Takaaki Koma, Osamu Kotani, Hironori Sato, Akio Adachi and Masako Nomaguchi : Concomitant Enhancement of HIV-1 Replication Potential and Neutralization-Resistance in Concert With Three Adaptive Mutations in Env V1/C2/C4 Domains., Frontiers in Microbiology, Vol.10, 2019. (Summary) adapts its Env to macaque cells with strongly replication-restrictive nature for HIV-1. While a single and two mutations gave a significantly enhanced replication phenotype in a macaque cell line and also in human cell lines that stably express either human CD4 or macaque CD4, the virus simultaneously carrying the three adaptive mutations always grew best. Entry kinetics of parental and triple mutant viruses were similar, whereas the mutant was significantly more readily inhibited for its infectivity by soluble CD4 than parental virus. Furthermore, molecular dynamics simulations of the Env ectodomain (gp120 and gp41 ectodomain) bound with CD4 suggest that the three mutations increase binding affinity of Env for CD4 in solution. Thus, it is quite likely that the affinity for CD4 of the mutant Env is enhanced relative to the parental Env. Neutralization sensitivity of the triple mutant to CD4 binding site antibodies was not significantly different from that of parental virus, whereas the mutant exhibited a considerably higher resistance against neutralization by a CD4-induced epitope antibody and Env trimer-targeting V1/V2 antibodies. These results suggest that the three adaptive mutations cooperatively promote viral growth via increased CD4 affinity, and also that they enhance viral resistance to several neutralization antibodies by changing the Env-trimer conformation. In total, we have verified here an HIV-1 adaptation pathway in host cells and individuals involving Env derived from a lab-adapted and highly neutralization-sensitive clone. (Tokushima University Institutional Repository) ● Metadata: 114458 (Link to Publication Site) ● Publication site (DOI): 10.3389/fmicb.2019.00002 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30705669 ● Summary page in Scopus @ Elsevier: 2-s2.0-85064397079 (Tokushima University Institutional Repository: 114458, DOI: 10.3389/fmicb.2019.00002, PubMed: 30705669, Elsevier: Scopus)
10.	Naoya Doi, Tomoyuki Miura, Hiromi Mori, Hiromi Sakawaki, Takaaki Koma, Akio Adachi and Masako Nomaguchi : CXCR4- and CCR5-Tropic HIV-1 Clones Are Both Tractable to Grow in Rhesus Macaques., Frontiers in Microbiology, Vol.9, 2018. (Summary) genetic manipulations and viral cell-adaptations, we have successfully generated a series of HIV-1 derivatives with CXCR4-tropism or CCR5-tropism that grow in macaque cells to various degrees. Of these viruses, those with best replicative potentials can grow comparably with a pathogenic SIVmac in macaque cells by counteracting major restriction factors TRIM5, APOBEC3, and tetherin proteins. In this study, rhesus macaques were challenged with CXCR4-tropic (MN4/LSDQgtu) or CCR5-tropic (gtu + A4CI1) virus. The two viruses were found to productively infect rhesus macaques, being rhesus macaque-tropic HIV-1 (HIV-1rmt). However, plasma viral RNA was reduced to be an undetectable level in infected macaques at 5-6 weeks post-infection and thereafter. While replicated similarly well in rhesus peripheral blood mononuclear cells, MN4/LSDQgtu grew much better than gtu + A4CI1 in the animals. To the best of our knowledge, this is the first report demonstrating that HIV-1 derivatives (variants) grow in rhesus macaques. These viruses certainly constitute firm bases for generating HIV-1rmt clones pathogenic for rhesus monkeys, albeit they grow more poorly than pathogenic SIVmac and SHIV clones reported to date. (Tokushima University Institutional Repository) ● Metadata: 114457 (Link to Publication Site) ● Publication site (DOI): 10.3389/fmicb.2018.02510 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30405570 ● Search Scopus @ Elsevier (PMID): 30405570 ● Search Scopus @ Elsevier (DOI): 10.3389/fmicb.2018.02510 (Tokushima University Institutional Repository: 114457, DOI: 10.3389/fmicb.2018.02510, PubMed: 30405570)
11.	Shoko Nakanishi, Sakimi Watanabe, Naoya Doi, Takaaki Koma, Akio Adachi and Masako Nomaguchi : Virological characterization of HIV-1 CA-NTD mutants constructed in a virus-lineage reflected manner., The Journal of Medical Investigation : JMI, Vol.65, No.1.2, 110-115, 2018. (Summary) Capsid (CA) protein is a major virion-constituent of all retroviruses including human immunodeficiency virus type 1 (HIV-1), and is essential for early and late phases in viral replication cycle through interaction with numerous cellular factors. In particular, N-terminal domain (NTD) of HIV-1 CA has been frequently and well reported to bind to various host cell proteins that considerably affect viral replication potential. In this study, in order to better define biological bases of the CA-NTD for HIV-1 replication, we performed an extensive mutational analysis in an unprecedented manner. By aligning CA-NTD sequences derived from representative infectious molecular clones of HIV-1, HIV-2, and simian immunodeficiency virus isolated from the rhesus macaque (SIVmac), a number of amino acids specific to HIV-1 were selected, and were replaced with those from SIVmac at the corresponding sites. Mutant viruses thus generated were then examined for multi-cycle infectivity, single-cycle infectivity, and ability to produce progeny virions. While some CA-NTD mutations affected viral replication ability to varying degrees, those in helix 7 abolished viral growth potential without exception. These results highlight functional importance of non-conserved amino acids in helix 7, and give new insights into functionality of HIV-1 CA-NTD. J. Med. Invest. 65:110-115, February, 2018. (Tokushima University Institutional Repository) ● Metadata: 111440 (Link to Publication Site) ● Publication site (DOI): 10.2152/jmi.65.110 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29593179 ● Search Scopus @ Elsevier (PMID): 29593179 ● Search Scopus @ Elsevier (DOI): 10.2152/jmi.65.110 (Tokushima University Institutional Repository: 111440, DOI: 10.2152/jmi.65.110, PubMed: 29593179)
12.	Masako Nomaguchi, Naoya Doi, Tomoya Yoshida, Takaaki Koma, Shun Adachi, Hirotaka Ode, Yasumasa Iwatani, Masaru Yokoyama, Hironori Sato and Akio Adachi : mRNA Is Modulated by Natural Nucleotide Variations and SLSA1 RNA Structure in SA1D2prox Genomic Region., Frontiers in Microbiology, Vol.8, No.2542, 2017. (Summary) mRNA level. (Tokushima University Institutional Repository) ● Metadata: 114455 (Link to Publication Site) ● Publication site (DOI): 10.3389/fmicb.2017.02542 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29326677 ● Summary page in Scopus @ Elsevier: 2-s2.0-85038265027 (Tokushima University Institutional Repository: 114455, DOI: 10.3389/fmicb.2017.02542, PubMed: 29326677, Elsevier: Scopus)
13.	Masako Nomaguchi, Naoya Doi, Takaaki Koma and Akio Adachi : Complete Genome Sequences of Human Immunodeficiency Type 1 Viruses Genetically Engineered To Be Tropic for Rhesus Macaques., Genome Announcements, Vol.5, No.39, 2017. (Summary) We have constructed two human immunodeficiency type 1 (HIV-1) derivatives, CXCR4 tropic and CCR5 tropic, that replicate in rhesus macaques. They are genetically engineered to be resistant to macaque restriction factors against HIV-1, including TRIM5, APOBEC3, and tetherin proteins. The two HIV-1 variants described here are fundamental clones aiming for rhesus infection studies of HIV-1. (Tokushima University Institutional Repository) ● Metadata: 115106 (Link to Publication Site) ● Publication site (DOI): 10.1128/genomeA.01063-17 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28963223 ● Search Scopus @ Elsevier (PMID): 28963223 ● Search Scopus @ Elsevier (DOI): 10.1128/genomeA.01063-17 (Tokushima University Institutional Repository: 115106, DOI: 10.1128/genomeA.01063-17, PubMed: 28963223)
14.	Naoya Doi, Yosuke Sakai, Akio Adachi and Masako Nomaguchi : Generation and characterization of new CCR5-tropic HIV-1rmt clones, The Journal of Medical Investigation : JMI, Vol.64, No.3,4, 272-279, 2017. (Summary) To develop effective non-human primate models for coping with numerous HIV-1/AIDS studies, rhesus macaque-tropic HIV-1 (HIV-1rmt) clones with a variety of biological properties are required. Such clones, if available, are powerful tools to experimentally elucidate HIV-1 replication and pathogenicity in host individuals, and also to develop anti-HIV-1 drugs/vaccines. However, only limited numbers of HIV-1rmt clones have been currently reported. In the present study, we generated new HIV-1rmt clones carrying various CCR5-tropic env (envelope) genes by standard recombinant DNA and intracellular homologous recombination techniques. Resultant virus clones contain the env sequences derived from an AIDS-inducible laboratory or two clinically isolated viral strains. We further constructed their variant clones bearing N160K, S304G, or G310R mutation in Env that potentially can change the viruses to better grow. Newly generated clones were analyzed for their virological properties such as Env expression, single-cycle infectivity, and multi-cycle replication ability. Out of a number of new clones examined, two were found to grow better in macaque cells than the previously constructed clone used for comparison. Our study described here constitutes the initial and essential step towards obtaining CCR5-tropic HIV-1rmt clones useful for various basic and clinical research projects on infected individuals. J. Med. Invest. 64: 272-279, August, 2017. (Keyword) Animals / Cells, Cultured / HIV-1 / Humans / Macaca mulatta / Receptors, CCR5 / Virus Replication / env Gene Products, Human Immunodeficiency Virus (Tokushima University Institutional Repository) ● Metadata: 111132 (Link to Publication Site) ● Publication site (DOI): 10.2152/jmi.64.272 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28954995 ● Search Scopus @ Elsevier (PMID): 28954995 ● Search Scopus @ Elsevier (DOI): 10.2152/jmi.64.272 (Tokushima University Institutional Repository: 111132, DOI: 10.2152/jmi.64.272, PubMed: 28954995)

Review, Commentary:

1.	Takaaki Koma, Shun Adachi, Naoya Doi, Akio Adachi and Masako Nomaguchi : Toward Understanding Molecular Bases for Biological Diversification of Human Coronaviruses: Present Status and Future Perspectives., Frontiers in Microbiology, Vol.11, Aug. 2020. (Summary) replication for various accessory proteins encoded by the variable 3' one-third portion of the CoV genome mostly remain to be determined. Importantly, the genomic sequences/structures closely linked to the high CoV recombination are poorly investigated and elucidated. Also, determinants for adaptation and pathogenicity have not been systematically investigated. We summarize here these research situations. Among conceivable projects, we are especially interested in the underlying molecular mechanism by which the observed CoV diversification is generated. Finally, as virologists, we discuss how we handle the present difficulties and propose possible research directions in the medium or long term. (Tokushima University Institutional Repository) ● Metadata: 115602 (Link to Publication Site) ● Publication site (DOI): 10.3389/fmicb.2020.02016 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32983025 ● Search Scopus @ Elsevier (PMID): 32983025 ● Search Scopus @ Elsevier (DOI): 10.3389/fmicb.2020.02016 (Tokushima University Institutional Repository: 115602, DOI: 10.3389/fmicb.2020.02016, PubMed: 32983025)
2.	Masako Nomaguchi, Naoya Doi, Takaaki Koma and Akio Adachi : HIV-1 mutates to adapt in fluxing environments., Microbes and Infection, Oct. 2018. (Summary) Human immunodeficiency virus type 1 (HIV-1) is specifically adapted for replication, persistence, transmission, and survival in humans. HIV-1 is highly mutable in nature, and well responds to a variety of environmental pressures by altering its genome sequences. In this review, we have described experimental evidence that demonstrates this phantasmagoric property of HIV-1. (Link to Publication Site) ● Publication site (DOI): 10.1016/j.micinf.2017.08.003 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28859896 ● Search Scopus @ Elsevier (PMID): 28859896 ● Search Scopus @ Elsevier (DOI): 10.1016/j.micinf.2017.08.003 (DOI: 10.1016/j.micinf.2017.08.003, PubMed: 28859896)

Proceeding of International Conference:

1.	Noriaki Minakawa, Noriko Saito-Tarashima, Takaaki Koma, NAOTO Hinotani, YOSHIDA Keigo, OGASA Moka, AKIHO Murai, INOUE Shuya, Tomoyuki Kondo, Naoya Doi, Koichi Tsuneyama and Masako Nomaguchi : 3-Deazaguanosine exhibits anti-SARS-CoV-2 activity and blocks the development of COVID-19 pneumonis in hamsters., Supra FIBER International Summit for Nucleic Acids (S-FISNA) 2024, Mar. 2024.

Proceeding of Domestic Conference:

1.	Bao Quoc Le, Yokoyama Masaru, Naoya Doi, ICHINOMIYA Takumi, KOMODA Nanako, Tomoyuki Kondo, Akio Adachi, Kotani Osamu, Sato Hironori, Masako Nomaguchi and Takaaki Koma : The importance of a novel ITI triplet motif within Env V3 domain for R5-tropic HIV-1 replication, 第70回日本ウイルス学会学術集会, Sep. 2023.
2.	Takaaki Koma, RE Kuokku Bao, Naoya Doi, KOMODA Nanako, ICHINOMIYA Takumi, Tomoyuki Kondo, Akio Adachi and Masako Nomaguchi : Implications of Gag-NC and gRNA interactions in HIV-1 assembly, 第70回日本ウイルス学会学術集会, Sep. 2023.
3.	Tomoyuki Kondo, Takaaki Koma, Naoya Doi, RE Kuokku Bao, KOMODA Nanako, ICHINOMIYA Takumi, Akio Adachi and Masako Nomaguchi : Effect of naturally-occurring synonymous single-nucleotide mutations within the vpr-coding sequence on HIV-1 replication, 第70回日本ウイルス学会学術集会, Sep. 2023.
4.	Naoya Doi, Takaaki Koma, LE Quoc Bao, KOMODA Nanako, ICHINOMIYA Takumi, Tomoyuki Kondo, Akio Adachi and Masako Nomaguchi : PIM kinases suppress HIV virion production by inhibiting viral protein expression, 第70回日本ウイルス学会学術集会, Sep. 2023.
5.	Takaaki Koma, 小谷治, Naoya Doi, Tomoyuki Kondo, 横山勝, Akio Adachi, 佐藤裕徳 and Masako Nomaguchi : HIV-1 Gag MAのGag二量体化における役割の解明, 第36回日本エイズ学会, Nov. 2022.
6.	Tomoyuki Kondo, Takaaki Koma, Akio Adachi, Masako Nomaguchi and Naoya Doi : PIMキナーゼによるHIV型特異的な遺伝子発現調節の解析, 第36回日本エイズ学会学術集会・総会, Nov. 2022.
7.	Naoya Doi, Takaaki Koma, Chisato Gotohda, NAGASAKA Mari, Tomoyuki Kondo, Akio Adachi and Masako Nomaguchi : Importance of vpr-coding sequence in HIV-1 gene expression, 第69回日本ウイルス学会学術集会, Nov. 2022.
8.	Tomoyuki Kondo, Takaaki Koma, UDAGAWA Mei, OKUMURA Nozomi, Akio Adachi, Masako Nomaguchi and Naoya Doi : Analysis of HIV type-specific regulation of viral gene expression by PIM, 第69回日本ウイルス学会学術集会, Nov. 2022.
9.	Takaaki Koma, 小谷治, Naoya Doi, Tomoyuki Kondo, 横山勝, Akio Adachi, 佐藤裕徳 and Masako Nomaguchi : HIV-1 Gag-MAにおけるGag前駆体二量体化部位のウイルス学的解析, 第69回日本ウイルス学会, Nov. 2022.
10.	Tomoyuki Kondo, Takaaki Koma, Akio Adachi, Masako Nomaguchi and Naoya Doi : PIMキナーゼ及びPIM阻害剤によるHIV種特異的な遺伝子発現と複製への影響, 第265回徳島医学会学術集会, Jul. 2022.
11.	Takaaki Koma, Naoya Doi, Tomoyuki Kondo and Masako Nomaguchi : HIV-1 matrixタンパク質のウイルス粒子集合初期過程における役割解明, 第266回徳島医学学術集会, 2022.
12.	Takaaki Koma, Mitsuki Ishizue, Chizuko Tsukada, Chiaki Tokaji, Akio Adachi, Masako Nomaguchi and Naoya Doi : PIMキナーゼ阻害剤がHIV種特異的に複製に及ぼす影響の解析(若手優秀演題), 第35回日本エイズ学会学術集会・総会, Nov. 2021.
13.	Takaaki Koma, Naoya Doi, Chizuko Tsukada, Chiaki Tokaji, Mitsuki Ishizue, Akio Adachi and Masako Nomaguchi : HIV-1 vpr塩基配列の同義一塩基置換がウイルス複製に与える影響, 第68回日本ウイルス学会, Nov. 2021.
14.	横山勝, 小谷治, Naoya Doi, Takaaki Koma, Masako Nomaguchi and 佐藤裕徳 : Protein sector in HIV-1 envelope estimated by statistical analysis of amino acid sequences, 第42回日本分子生物学会年会, Dec. 2019.
15.	横山勝, 小谷治, Naoya Doi, Takaaki Koma, Masako Nomaguchi and 佐藤裕徳 : HIV-1 エンベロープにおける脆弱部位の推定, 第33回日本エイズ学会学術集会, Nov. 2019.
16.	小谷治, Takaaki Koma, 宮川敬, 梁明秀, 横山勝, Naoya Doi, Akio Adachi, Masako Nomaguchi and 佐藤裕徳 : HIV-1カプシド ''disorder'' 領域の構造機能解析, 第33回日本エイズ学会学術集会, Nov. 2019.
17.	Takaaki Koma, Naoya Doi, Akio Adachi and Masako Nomaguchi : HIV-1 Gag集合初期に関わる内在性集合促進因子の探索, 第33回日本エイズ学会学術集会, Nov. 2019.
18.	Takaaki Koma, Naoya Doi, Satoshi Nakashima, Akio Adachi and Masako Nomaguchi : Exploration for assembly-promoting factors involved in the early stage of HIV-1 Gag assembly, 第67回日本ウイルス学会学術集会, Oct. 2019.
19.	Masako Nomaguchi, Takaaki Koma, Naoya Doi, Hideki Yamamoto, Kyosuke Watanabe, Mai Takemoto and Akio Adachi : Molecular bases for determination of the Vif expression level by single-nucleotide mutations within SA1D2prox and by adaptive mutations in the HIV-1 genome, 第67回日本ウイルス学会学術集会, Oct. 2019.
20.	Naoya Doi, Takaaki Koma, Akio Adachi and Masako Nomaguchi : Analysis of molecular mechanism on species-specific growth enhancement by a single-amino acid mutation in V3 tip of CCR5-tropic HIV-1 Env, 第67回日本ウイルス学会学術集会, Oct. 2019.
21.	Takaaki Koma, 小谷治, Naoya Doi, 宮川敬, 梁明秀, 横山勝, 佐藤裕徳, Akio Adachi and Masako Nomaguchi : リンカードメインによるGag集合・ウイルス産生・感染性に関わるHIV-1カプシド構造のアロステリック制御, 第34回中国四国ウイルス研究会, Jun. 2019.
22.	Masako Nomaguchi, Naoya Doi, Takaaki Koma, 吉田和子 and Akio Adachi : SA1D2proxに関するHIV-1 Vif低発現変異体NL-gatは，Vif発現量適応変異あるいはenv変異の獲得により増殖能を向上させる, 第66回日本ウイルス学会学術集会, Oct. 2018.
23.	Akio Adachi, Naoya Doi, Takaaki Koma, Hayato Ohkubo, 吉田和子 and Masako Nomaguchi : SA1D2prox領域に関するHIV-1 Vif超低発現変異体 NL-tacのAPOBEC3G高発現下における適応過程の解析, 第66回日本ウイルス学会学術集会, Oct. 2018.
24.	Takaaki Koma, 小谷治, Naoya Doi, 宮川敬, 梁明秀, 横山勝, 佐藤裕徳, Akio Adachi and Masako Nomaguchi : HIV-1複製後期過程におけるGag-CAリンカードメインの役割, 第66回日本ウイルス学会学術集会, Oct. 2018.
25.	Naoya Doi, Takaaki Koma, Nina Nakanishi, Akio Adachi and Masako Nomaguchi : 馴化型R5-tropic HIV-1rmtで同定されたEnvによる増殖促進の解析, 第66回日本ウイルス学会学術集会, Oct. 2018.
26.	Shoko Nakanishi, Sakimi Watanabe, Naoya Doi, Takaaki Koma, Akio Adachi and Masako Nomaguchi : Single-amino acid mutations in V1 and C4 domains of HIV-1 Env cooperatively enhance viral replication ability by increasing CD4 affinity, 第65回日本ウイルス学会学術集会, Oct. 2017.
27.	Sakimi Watanabe, Shoko Nakanishi, Takaaki Koma, Naoya Doi, Akio Adachi and Masako Nomaguchi : Low vif type of HIV-1 SA1D2prox variants can adaptively mutate to enhance the Vif expression under the strong restrictive condition, 第65回日本ウイルス学会学術集会, Oct. 2017.
28.	Naoya Doi, Takaaki Koma, Shoko Nakanishi, Sakimi Watanabe, Masako Nomaguchi and Akio Adachi : Generation of R5-tropic HIV-1rmt clones with an enhanced replication ability by adaptive Env domain swapping, 第65回日本ウイルス学会学術集会, Oct. 2017.
29.	Akio Adachi, Naoya Doi, Takaaki Koma, Shoko Nakanishi, Sakimi Watanabe and Masako Nomaguchi : Linkage analysis of HIV-1 vif production level and SLSA1 structure/energy stability, 第65回日本ウイルス学会学術集会, Oct. 2017.
30.	Takaaki Koma, Naoya Doi, 宮川敬, 梁明秀, Akio Adachi and Masako Nomaguchi : Role for amino acid residues S149 and I150 of the Gag-CA linker domain in the late HIV-1 replication phase, 第65回日本ウイルス学会学術集会, Oct. 2017.

Grants-in-Aid for Scientific Research (KAKEN Grants Database @ NII.ac.jp)

PIM阻害剤によるHIVタイプ特異的な複製能調節機構の解明 (Project/Area Number: 21K08491 )
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Assistant Professor : Doi, Naoya

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Grants-in-Aid for Scientific Research (KAKEN Grants Database @ NII.ac.jp)