type: misc

label: url

en: 目に見えない光が切り拓く『光の世紀』

ja: 目に見えない光が切り拓く『光の世紀』

en: Journal of the Japan Society for Precision Engineering

ja: 精密工学会誌


en: 南米出血熱ウイルスとその感染予防・治療法の最前線

ja: 南米出血熱ウイルスとその感染予防・治療法の最前線

en: Uirusu

ja: ウイルス


en: Inactivation of SARS-CoV-2 by deep ultraviolet light emitting diode: A review

en: Japanese Journal of Applied Physics

ja: Japanese Journal of Applied Physics


en: Withコロナ時代に向けた深紫外LEDの活用法 --- ∼深紫外LEDによるウイルス不活化の試み∼

en: クリーンテクノロジー

ja: クリーンテクノロジー


en: 深紫外LEDによる新型コロナウイルス不活化への試み

ja: 深紫外LEDによる新型コロナウイルス不活化への試み

en: OPTRONICS

ja: 月刊 オプトロニクス


en: 深紫外LEDを用いた新型コロナウイルスの不活化

ja: 深紫外LEDを用いた新型コロナウイルスの不活化

en: O plus E

ja: O plus E


en: Toward Understanding Molecular Bases for Biological Diversification of Human Coronaviruses: Present Status and Future Perspectives.

en: 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.

en: Frontiers in Microbiology

ja: Frontiers in Microbiology


en: HIV-1 mutates to adapt in fluxing environments.

en: 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.

en: Microbes and Infection

ja: Microbes and Infection


en: Review of Mammarenavirus Biology and Replication.

en: contain viruses responsible for causing human hemorrhagic fever diseases including New World viruses Junin, Machupo, Guanarito, Sabia, and Chapare virus and Old World viruses Lassa, and Lujo virus. These two groups of arenaviruses share the same genome organization composed of two ambisense RNA segments. These segments contain four open reading frames that encode for four proteins: the nucleoprotein, glycoprotein precursor, L protein, and Z. Despite their genome similarities, these groups exhibit marked differences in their replication life cycles. This includes differences in attachment, entry, and immune evasion. By understanding the intricacy of replication in each of these viral species we can work to develop counter measures against human diseases. This includes the development of vaccines and antivirals for these emerging viral threats. Currently only the vaccine against Junin virus, Candid#1, is in use as well as Ribavirin for treatment of Lassa Fever. In addition, small molecule inhibitors can be developed to target various aspects of the virus life cycle. In these ways an understanding of the arenavirus replication cycle can be used to alleviate the mortality and morbidity of these infections worldwide.


en: Innate immune response to arenaviral infection: a focus on the highly pathogenic New World hemorrhagic arenaviruses.

en: Arenaviruses are enveloped, negative-stranded RNA viruses that belong to the family Arenaviridae. This diverse family can be further classified into OW (Old World) and NW (New World) arenaviruses based on their antigenicity, phylogeny, and geographical distribution. Many of the NW arenaviruses are highly pathogenic viruses that cause systemic human infections characterized by hemorrhagic fever and/or neurological manifestations, constituting public health problems in their endemic regions. NW arenavirus infection induces a variety of host innate immune responses, which could contribute to the viral pathogenesis and/or influence the final outcome of virus infection in vitro and in vivo. On the other hand, NW arenaviruses have also developed several strategies to counteract the host innate immune response. We will review current knowledge regarding the interplay between the host innate immune response and NW arenavirus infection in vitro and in vivo, with emphasis on viral-encoded proteins and their effect on the type I interferon response.

en: Journal of Molecular Biology

ja: Journal of Molecular Biology