Takaji Wakita - Infectious Diseases

Author Information

Takaji Wakita is affiliated with the National Institute of Infectious Diseases in Tokyo, Japan. His research primarily focuses on virology and infectious diseases, with an emphasis on hepatitis viruses and SARS-CoV-2. His extensive work in these areas contributes significantly to the understanding of viral pathogenesis, immune responses, and potential therapeutic interventions.

Research Contributions

Takaji Wakita has made substantial contributions to the field of infectious diseases, particularly in understanding the mechanisms of hepatitis B and C viruses and SARS-CoV-2. In 2022, his research explored various mechanisms of viral entry, replication, and immune response modulation, such as the role of kinesin KIF4 in HBV/HDV entry and the impact of SARS-CoV-2 spike protein mutations. His work also delves into the development of vaccines and therapeutic strategies, as evidenced by his publications on DNA vaccines for hepatitis C and the antiviral action of interferon in HBV-infected cells. His efforts are pivotal in advancing both basic and applied research in virology.

Aliases

Takaji Wakita is known by several aliases including T Wakita, T. Wakita, and Taka Wakita. These variations are commonly found in academic publications and databases.

Publication and Citation Metrics

Metric	Value
Citation Count	28,531
H-index	83
Paper Count	594

Publications:

The kinesin KIF4 mediates HBV/HDV entry through the regulation of surface NTCP localization and can be targeted by RXR agonists in vitro

DOI: 10.1371/journal.ppat.1009983

Year: 2022

Induction of neutralizing antibodies against hepatitis C virus by a subviral particle-based DNA vaccine.

DOI: 10.1016/j.antiviral.2022.105266

Year: 2022

The function of SARS-CoV-2 spike protein is impaired by disulfide-bond disruption with mutation at cysteine-488 and by thiol-reactive N-acetyl-cysteine and glutathione

DOI: 10.1016/j.bbrc.2022.01.106

Year: 2022

Hepatitis C Virus-Induced ROS/JNK Signaling Pathway Activates the E3 Ubiquitin Ligase Itch to Promote the Release of HCV Particles via Polyubiquitylation of VPS4A

DOI: 10.1128/jvi.01811-21

Year: 2022

Galectin-9 restricts hepatitis B virus replication via p62/SQSTM1-mediated selective autophagy of viral core proteins

DOI: 10.1038/s41467-022-28171-5

Year: 2022

Identification of anti-severe acute respiratory syndrome-related coronavirus 2 (SARS-CoV-2) oxysterol derivatives in vitro

DOI: 10.1101/2021.01.31.429001

Year: 2021

Interferon signaling suppresses the unfolded protein response and induces cell death in hepatocytes accumulating hepatitis B surface antigen

DOI: 10.1371/journal.ppat.1009228

Year: 2021

Author response: Revisiting the guidelines for ending isolation for COVID-19 patients

DOI: 10.7554/elife.69340.sa2

Year: 2021

Epigenetic reprogramming promotes the antiviral action of IFNα in HBV-infected cells

DOI: 10.1038/s41420-021-00515-y

Year: 2021

Temporal maturation of neutralizing antibodies in COVID-19 convalescent individuals improves potency and breadth to circulating SARS-CoV-2 variants

DOI: 10.1016/j.immuni.2021.06.015

Year: 2021

How is HSV Diagnosed?

How is PCR Used in Epidemiological Studies?

How Can Infectious Diseases be Diagnosed During Pregnancy?

What is AIDS?

What Are the Symptoms of STIs?

Is There a Treatment?

Which Are the Common Bacterial Pathogens?

What Causes Muscle and Joint Pain in Infectious Diseases?

What are the Symptoms of Measles?

What are the Challenges in Treating Sporozoite-Related Infections?

Partnered Content Networks

Relevant Topics