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Measles virus (MeV), the causative agent of measles, can persist in the brain and cause a fatal neurodegenerative disease, subacute sclerosing panencephalitis (SSPE). Because wild-type MeV is not neurotropic, the virus is thought to evolve and acquire neuropathogenicity to cause SSPE. Our recent studies have shown that MeV acquires hyperfusogenic mutations in the fusion (F) gene that confer the ability to use cell adhesion molecule 1 (CADM1) and CADM2 as cis-acting receptor mimicking molecules and allow MeV to spread in neurons. Furthermore, under these conditions, multiple MeV genomes, rather than a single one, are likely to be transmitted transsynaptically between neurons through cell-cell fusion. Therefore, F proteins encoded by different genomes are co-expressed in infected cells, and positive and negative functional interactions between them can occur. These interactions determine the ability of the virus to spread in neurons as a population. In this article, we describe our studies to understand the mechanism by which MeV acquires neuropathogenicity in SSPE.

Rotavirus is a major cause of gastroenteritis in infants and is widely prevalent throughout the world regardless of the hygienic environment. However, it is not easy to understand the overall picture of rotavirus epidemic because of the great variety of genotypes and the large inter-seasonal and regional differences in the prevalent strains. Fortunately, the rotavirus vaccines now widely used around the world are highly effective and safe. The number of rotavirus gastroenteritis cases is declining dramatically, especially in high-income countries. In Japan, rotavirus vaccines have been included in the routine vaccination program since October 2020. Additionally, the impact of the SARS-CoV-2 pandemic control measures on the rotavirus epidemic was also very significant. These synergistic effects have resulted in few rotavirus outbreaks in recent years. Nevertheless, rotavirus is unlikely to be completely eradicated, and indeed a small number of sporadic cases continue to be reported. It will continue to be important to maintain high vaccination coverage and to continuously investigate prevalent strains. This review will provide an overview of the rotavirus epidemic situation in Japan and abroad. Annual changes in domestic epidemic strains that have been revealed by steady research to date will also be presented.

Viral hemorrhagic fevers such as Ebola virus disease, Marburg disease, Lassa fever, and Crimean-Congo hemorrhagic fever are infectious diseases that can cause severe, life-threatening illness. At present, there are only few licensed vaccines and antiviral drugs for these viral hemorrhagic fevers. The viruses which cause these viral hemorrhagic fevers are classified as BSL-4 pathogens and can be handled only in BSL-4 containment laboratories. Therefore, to develop the vaccines and treatments for these diseases, BSL-4 facility is essential. However, the BSL-4 facility available for the basic or applied research using infectious BSL-4 pathogens has not been established in Japan so far. In July 2021, the construction of BSL-4 facility was completed at the campus of Nagasaki University. After the preparation for the full operation, the facility will be approved by the Minister of Health, Labour and Welfare as a BSL-4 facility. Here, I introduce the BSL-4 facility project of Nagasaki University and state the contributions of the BSL-4 facility to research and development.

In a current life sciences research, we are in an era in which advanced technology emerging and utilize big data. Data-driven approaches such as machine learnings play an important role to analyze these datasets. However, limited clinical (time-course) datasets are available for infectious diseases, cancer, and other diseases. Especially in the case of emerging infectious disease outbreaks, clinical data obtained from a limited number of cases must be used to develop treatment strategies and public health policies. This means that many clinical data are not big data, which often makes the application of data-driven approaches difficult. In this paper, we mainly apply a mathematical model-based approach to the clinical data of COVID-19 and discuss how biologically important information can be extracted from the limited data and how they can benefit society.

South American Hemorrhagic Fever is caused by the Arenavirus, which belong to the Family Arenaviridae, genus mammarenavirus, infection at South America. South American Hemorrhagic Fever includes 1. Argentinian Hemorrhagic fever caused by Junin virus, 2. Brazilian hemorrhagic fever caused by Sabia virus, 3. Venezuelan Hemorrhagic fever caused by Guanarito virus, 4. Bolivian Hemorrhagic fever caused by Machupo virus, and 5. Unassigned hemorrhagic fever caused by Chapare virus. These viruses are classified in New World (NW) Arenavirus, which is different from Old World Arenavirus (ex. Lassa virus), based on phylogeny, serology, and geographic differences. In this review, the current knowledge of the biology and the development of the vaccines and antivirals of NW Arenaviruses which cause South American Hemorrhagic Fever will be described.

Zoonoses are caused by pathogens transmitted from animals. To prepare mitigating measures against emerging zoonoses, it is imperative to identify animal reservoirs that carry potential pathogens and also elucidate the transmission routes of these pathogens. Under the continuous collaboration with counterparts from Zambia and Indonesia, we have so far identified various viruses in wild animals. Some of the identified viruses were phylogenetically distinct from known virus species and this finding led to approved new virus species by the International Committee on Taxonomy of Viruses (ICTV). Our studies provided new insights into the divergence, natural hosts and lifecycle of viruses. Through the exploration and characterization of viruses in animals, we will endeavor to contribute to the existing knowledge on viral pathogens in wild animals. This is cardinal for evidence-based preemptive measures against future zoonoses.