Murakami Tomoyuki

Assistant Professor

BS, Saitama University, Japan
MS, University of Tokyo, Japan
PhD, University of Tokyo, Japan

Phone: 252-744-2699
Fax: 252-744-3104
Email: murakamit24@ecu.edu

Research

Human Immunodeficiency Virus Type 1 (HIV-1) is the causative agent of acquired immunodeficiency syndrome (AIDS). Although antiretroviral therapy (ART) helps reduce mortality and new infections, there is still no cure for HIV/AIDS. One of the main challenges in curing HIV/AIDS is the presence of latent viral reservoirs, which are resistant to ART. If ART is interrupted, these latent reservoirs can produce infectious virus particles, leading to the progression of AIDS. Therefore, to achieve a cure, these viral reservoirs must be eradicated.

Our research focuses on the role of the environment in secondary lymphoid organs during HIV-1 infection. Secondary lymphoid organs, including lymph nodes, play a central role in the spread of HIV-1 and contain latent viral reservoirs. Fibroblastic reticular cells (FRCs) are crucial components of these organs, regulating their environment. FRCs regulate the physiology of lymphocytes, including CD4+ T cells, which are primary targets of HIV-1.

Our research aims to fully understand the role of FRCs in HIV-1 spread, latency establishment, and maintenance of latent viral reservoirs, which is essential for comprehending HIV-1 pathogenesis and developing a cure. Currently, we are investigating how FRCs affect the permissiveness of CD4+ T cells to HIV-1 infection. CD4+ T cells in secondary lymphoid organs are more permissive to HIV-1 than those in peripheral blood. Since FRCs closely interact with CD4+ T cells in these organs, we hypothesize that FRCs enhance the permissiveness of CD4+ T cells to HIV-1 infection. To test this, we use co-culture systems containing both FRCs and CD4+ T cells.

Additionally, we previously reported that FRCs promote HIV-1 spread through a process called trans-infection. Trans-infection involves interactions between CD4+ T cells and uninfected cells that capture HIV-1 particles. FRCs can capture HIV-1, and these captured particles efficiently infect CD4+ T cells that come into contact with FRCs. To explore whether this mode of spread is conserved in HIV-related viruses, we use the simian immunodeficiency virus (SIV) and a rhesus macaque model in collaboration with Dr. Afam Okoye at Oregon Health & Science University.

 

Selected Publication

  1. Sato H, Murakami T, Matsuura R, Abe M, Matsuoka S, Yashiroda Y, Yoshida M, Akari H, Nagasawa Y, Takei M, Aida Y. A novel class of HIV-1 inhibitors targeting the Vpr induced G2-arrest in macrophages by new yeast- and cell-based high-throughput screening. Viruses.14(6)06/2022. PMID: 35746791.
  2. Murakami T*, Matsuura R*, Chutiwitoonchai N, Takei M, Aida Y. Huntingtin-Interacting Protein 1 promotes Vpr-induced G2 arrest and HIV-1 infection in macrophages. Viruses.13(11)11/2021. PMID: 34835114. *Co-First Authors.
  3. Murakami T**, Ono A. HIV-1 entry: Duels between Env and host antiviral transmembrane proteins on the surface of virus particles. Curr Opin Virol.50: 59-68, 10/2021. PMID: 34390925. **Corresponding Author.
  4. Murakami T**, Ono A. Roles of virion-incorporated CD162 (PSGL-1), CD43, and CD44 in HIV-1 infection of T cells. Viruses.13(10)09/2021. PMID: 34696365. **Corresponding Author.
  5. de Souza Cardoso R, Viana RM M, Vitti BC, Coelho AC L, de Jesus BL S, de Paula Souza J, Pontelli MC, Murakami T, Ventura AM, Ono A, Arruda E. Human respiratory syncytial virus infection in a human T cell line is hampered at multiple steps. Viruses.13(2)02/2021. PMID: 33540662
  6. Thornhill D, Murakami T, Ono A. Rendezvous at plasma membrane: cellular lipids and tRNA set up sites of HIV-1 particle assembly and incorporation of host transmembrane proteins. Viruses.12(8)07/2020. PMID: 32752131
  7. Murakami T, Carmona N, Ono A. Virion-incorporated PSGL-1 and CD43 inhibit both cell free infection and transinfection of HIV-1 by preventing virus-cell binding. Proc Natl Acad Sci U S A.117(14): 8055-8063, 04/2020. PMID: 32193343
  8. Murakami T, Kim J, Li Y, Green GE, Shikanov A, Ono A. Secondary lymphoid organ fibroblastic reticular cells mediate trans-infection of HIV-1 via CD44-hyaluronan interactions. Nature communications.9(1)01/2018. PMID: 29934525
  9. Miyatake H, Sanjoh A, Murakami T, Murakami H, Matsuda G, Hagiwara K, Yokoyama M, Sato H, Miyamoto Y, Dohmae N, Aida Y. Molecular mechanism of HIV-1 Vpr for binding to Importin-α. Journal of molecular biology.428(13)07/2016. PMID: 27181198
  10. Polat M, Takeshima S-N, Hosomichi K, Kim J, Miyasaka T, Yamada K, Arainga M, Murakami T, Matsumoto Y, de la Barra Diaz V, Panei CJ, Gonz.lez ET, Kanemaki M, Onuma M, Giovambattista G, Aida Y. A new genotype of bovine leukemia virus in South America identified by NGS-based whole genome sequencing and molecular evolutionary genetic analysis. Retrovirology.13: 4, 01/2016. PMID: 26754835
  11. Hagiwara K, Ishii H, Murakami T, Takeshima SN, Chutiwitoonchai N, Kodama EN, Kawaji K, Kondoh Y, Honda K, Osada H, Tsunetsugu-Yokota Y, Suzuki M, Aida Y. Synthesis of a Vpr-binding derivative for use as a novel HIV-1 inhibitor. PLoS One.10(12)12/2015. PMID: 26701275
  12. Zahoor MA, Xue G, Sato H, Murakami T, Takeshima SN, Aida Y. HIV-1 Vpr induces interferon-stimulated genes in human monocyte-derived macrophages. PLoS One.9(8)08/2014. PMID: 25170834
  13. Murakami T, Aida Y. Visualizing Vpr-induced G2 arrest and apoptosis. PLoS One.9(1)01/2014. PMID: 24466265
  14. Sasaki Y, Hagiwara K, Kakisaka M, Yamada K, Murakami T, Aida Y. Importin α3/Qip1 is involved in multiplication of mutant influenza virus with alanine mutation at amino acid 9 independently of nuclear transport function. PLoS One.8(1): e55765, 01/2013. PMID: 23383277
  15. Takeda E, Murakami T, Matsuda G, Murakami H, Zako T, Maeda M, Aida Y. Nuclear exportin receptor CAS regulates the NPI-1-mediated nuclear import of HIV-1 Vpr. PLoS One.6(11)11/2011. PMID: 22110766
  16. Hagiwara K, Murakami T, Xue G, Shimizu Y, Takeda E, Hashimoto Y, Honda K, Kondoh Y, Osada H, Tsunetsugu-Yokota Y, Aida Y. Identification of a novel Vpr-binding compound that inhibits HIV-1 multiplication in macrophages by chemical array. Biochemical and biophysical research communications.403(1)12/2010. PMID: 21036153

Staff

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