Shioda Lab/Division of Infectious Disease  Department of Viral Infections

Viruses are simple organisms composed of proteins, nucleic acids, and, in some cases, lipids. Nevertheless, they interact with several host factors and ultimately cause disease in humans. Our laboratory focuses on the molecular mechanisms underlying viral diseases, including human immunodeficiency virus (HIV).

Antiviral host factors and their application to a cure for HIV infection

HIV does not establish a productive infection in any monkey other than the chimpanzee. Also, the sensitivity of HIV infection and rate of disease progression vary from individual to individual. To date, several anti-HIV host restriction factors, responsible for these phenomena. Currently, we are trying to elucidate the molecular mechanism(s) underlying the anti-HIV activity of these factors. We also aim to cure HIV infection by establishing novel reproductive medicine-based strategies, including iPS cells from HIV patients.

Analysis of HIV-1 genome RNA dimerization

The genome of retroviruses such as HIV-1 always exists as a dimer; genome dimerization plays an important role at various stages of the viral life cycle, including genome packaging and reverse transcription as well as the genome recombination processes involved in viral diversification. Therefore, genome dimerization is a novel target for anti-HIV therapies. We are currently analyzing computer-assisted structural models of HIV-1 Dimer Initiation Sequences, which are the most important factors involved in genome dimerization, to get a more complete picture of HIV genome dimerization. We are also analyzing genome recombination in HIV-1
by constructing a novel system to measure recombination efficiency.

Human genome analysis of HIV-associated neurocognitive disorders

Despite successful antiretroviral therapy, nearly a quarter of HIV patients develop mild-to-severe neurocognitive disorders (HAND). We aim to undertake genome analysis of HAND patients to elucidate the underlying molecular mechanisms, thereby developing therapeutic strategies to treat/prevent this

  • Fig. 1.Host factors involoving in early replication steps of HIV

  • Fig. 2.Newly identified structure of DIS.
    A. Comparison of the current model (brown) with the previously proposed model (yellow). B. Structure in a dimeric form. The newly identified model shows more extended DIS structure possibly allowing stronger molecular interaction.


  • Prof.: Tatsuo Shioda
  • Assoc. Prof.: Emi E. Nakayama
  • Asst. Prof.: Tadahiro Sasaki



  • (1) Naturally Occurring Mutations in HIV-1 CRF01_AE Capsid Affect Viral Sensitivity to Restriction Factors. Nakayama E.E., et al., AIDS Res Hum Retroviruses. (2018) doi:10.1089/AID.2017.0212.
    (2) SL1 revisited: functional analysis of the structure and conformation of HIV-1 genome RNA. Sakuragi S., Retrovirology. 2016 Nov 11;13(1):79.
    (3) Genome-wide association study of HIV-related lipoatrophy in Thai patients: Association of a DLGAP1 polymorphism with fat loss. Uttayamakul S., et al. AIDS Res Hum Retroviruses. (2015) Aug;31(8):792-6.
    (4) Impact of TRIM5α in vivo. Nakayama E.E., et al. AIDS. (2015) Sep 10;29(14):1733-43.
    (5) A Single-Nucleotide Polymorphism in ABCC4 Is Associated with Tenofovir-Related Beta2-Microglobulinuria in Thai Patients with HIV-1 Infection. Likanonsakul S., et al. PLoS One (2016) Jan 25;11(1):e0147724.
    (6)Novel mutant human immunodeficiency virus type 1 strains with high degree of resistance to cynomolgus macaque TRIMCyp generated by random mutagenesis. Sultana T., et al. J Gen Virol. (2016) Apr;97(4):963-76. a