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Masato Tashiro

Bio: Masato Tashiro is an academic researcher from Nagasaki University. The author has contributed to research in topics: Virus & Influenza A virus. The author has an hindex of 51, co-authored 229 publications receiving 9511 citations. Previous affiliations of Masato Tashiro include National Institutes of Health & World Health Organization.


Papers
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Journal ArticleDOI
TL;DR: F influenza-associated encephalitis/encephalopathy progressed rapidly and was associated with poor outcomes, and thrombocytopenia and severely elevated transaminase levels were factors associated with a poor prognosis.
Abstract: During the winter of 1998-1999, there was an outbreak of encephalitis/encephalopathy in Japan that appeared to be associated with influenza. We conducted a national survey of the prevalence and clinical features of disease and the associated outcomes and prognostic factors related to this outbreak. A total of 202 cases were analyzed, of which 148 were diagnosed as influenza-associated encephalitis/encephalopathy on the basis of virologic analysis. Of the 148 cases studied, 130 (87.8%) were type A influenza and 17 were type B. Encephalitis/ encephalopathy developed mainly in children age <5 years, either on the day that influenza signs appeared or on the next day. The major signs included altered consciousness or loss of consciousness, convulsions, cough, and vomiting. In many patients, multiple-organ failure developed, and rates of mortality (31.8%) and disability (27.7%) were high. Thrombocytopenia and severely elevated transaminase levels were factors associated with a poor prognosis. Thus, influenza-associated encephalitislencephalopathy progressed rapidly and was associated with poor outcomes.

472 citations

Journal ArticleDOI
09 Jul 2015-Nature
TL;DR: Detailed epidemic models support differences in age of infection, combined with the less frequent travel of children, as probable drivers of the differences in the patterns of global circulation, suggesting a complex interaction between virus evolution, epidemiology, and human behaviour.
Abstract: Understanding the spatiotemporal patterns of emergence and circulation of new human seasonal influenza virus variants is a key scientific and public health challenge. The global circulation patterns of influenza A/H3N2 viruses are well characterized, but the patterns of A/H1N1 and B viruses have remained largely unexplored. Here we show that the global circulation patterns of A/H1N1 (up to 2009), B/Victoria, and B/Yamagata viruses differ substantially from those of A/H3N2 viruses, on the basis of analyses of 9,604 haemagglutinin sequences of human seasonal influenza viruses from 2000 to 2012. Whereas genetic variants of A/H3N2 viruses did not persist locally between epidemics and were reseeded from East and Southeast Asia, genetic variants of A/H1N1 and B viruses persisted across several seasons and exhibited complex global dynamics with East and Southeast Asia playing a limited role in disseminating new variants. The less frequent global movement of influenza A/H1N1 and B viruses coincided with slower rates of antigenic evolution, lower ages of infection, and smaller, less frequent epidemics compared to A/H3N2 viruses. Detailed epidemic models support differences in age of infection, combined with the less frequent travel of children, as probable drivers of the differences in the patterns of global circulation, suggesting a complex interaction between virus evolution, epidemiology, and human behaviour.

433 citations

Journal ArticleDOI
Jean Thierry Aubin1, Saliha Azebi1, Amanda Balish1, Jill Banks1, Niranjan Bhat1, Rick A. Bright1, Ian Brown1, Philippe Buchy1, Ana Maria Burguiere1, Hua Ian Chen1, Peter K.C. Cheng1, Nancy J. Cox1, Alice Crosier1, Aaron Curns1, Frédérique Cuvelier1, Guohua Deng1, Julia Desheva1, Stéphanie Desvaux1, Nguyen Hong Diep1, Ruben O. Donis1, Ruben O. Donis2, A. R. Douglas1, Scott F. Dowell1, Nguyen Tien Dung1, Lindsay Edwards1, Keiji Fukuda1, Rebecca Garten1, Elena A. Govorkova1, Victoria Gregory1, Alan W. Hampson1, Nguyen Thi Hong Hanh1, Scott A. Harper1, A. Hay1, Erich Hoffmann1, Diane J. Hulse1, Masaki Imai1, Shigeyuki Itamura1, Samadhan Jadhao1, Patricia Jeannin1, Chun Kang1, Jackie Katz1, Jae Hong Kim1, Alexander Klimov1, Yong Kuk Kwon1, Chang-Won Lee1, Phuong Song Lien1, Yanbing Li1, Wilina Lim1, Yi Pu Lin1, Stephen Lindstom1, La Morris Loftin1, Jan Mabry1, Le Quynh Mai1, Taronna R. Maines1, Jean Claude Manuguerra1, Masaji Mase1, Yumi Matsuoka1, Margaret McCarron1, Marie-Jo Medina1, Doan Nguyen1, Ai Ninomiya1, Masatsugu Obuchi1, Takato Odagiri1, Malik Peiris1, Michael L. Perdue1, Jean Marc Reynes1, James Robertson1, Claudine Rousseaux1, Takehiko Saito1, Somchai Sangkitporn1, Michael W. Shaw1, James Mark Simmerman1, Marek J. Slomka1, Catherine K. Smith1, San Sorn1, Erica Spackman1, Klaus Stöhr1, David L. Suarez1, Haan Woo Sung1, David E. Swayne1, Maryse Tardy-Panit1, Masato Tashiro1, Pranee Thawatsupha1, Terrence M. Tumpey1, Timothy M. Uyeki1, Phan Van Tu1, Sylvie van der Werf1, Sirenda Vong1, Richard J. Webby1, Robert G. Webster1, John Wood1, Xiyan Xu1, Guan Yi1, Wenging Zhang1 
TL;DR: Human infections were from a virus clade undergoing antigenic drift that showed resistance to adamantanes but sensitivity to neuraminidase inhibitors.
Abstract: Human infections were from a virus clade undergoing antigenic drift that showed resistance to adamantanes but sensitivity to neuraminidase inhibitors.

384 citations

Journal ArticleDOI
26 Sep 2013-Nature
TL;DR: The robust replicative ability in mice, ferrets and nonhuman primates and the limited transmissibility in ferrets of Anhui/1 suggest that A(H7N9) viruses have pandemic potential.
Abstract: Avian influenza A viruses rarely infect humans; however, when human infection and subsequent human-to-human transmission occurs, worldwide outbreaks (pandemics) can result. The recent sporadic infections of humans in China with a previously unrecognized avian influenza A virus of the H7N9 subtype (A(H7N9)) have caused concern owing to the appreciable case fatality rate associated with these infections (more than 25%), potential instances of human-to-human transmission, and the lack of pre-existing immunity among humans to viruses of this subtype. Here we characterize two early human A(H7N9) isolates, A/Anhui/1/2013 (H7N9) and A/Shanghai/1/2013 (H7N9); hereafter referred to as Anhui/1 and Shanghai/1, respectively. In mice, Anhui/1 and Shanghai/1 were more pathogenic than a control avian H7N9 virus (A/duck/Gunma/466/2011 (H7N9); Dk/GM466) and a representative pandemic 2009 H1N1 virus (A/California/4/2009 (H1N1pdm09); CA04). Anhui/1, Shanghai/1 and Dk/GM466 replicated well in the nasal turbinates of ferrets. In nonhuman primates, Anhui/1 and Dk/GM466 replicated efficiently in the upper and lower respiratory tracts, whereas the replicative ability of conventional human influenza viruses is typically restricted to the upper respiratory tract of infected primates. By contrast, Anhui/1 did not replicate well in miniature pigs after intranasal inoculation. Critically, Anhui/1 transmitted through respiratory droplets in one of three pairs of ferrets. Glycan arrays showed that Anhui/1, Shanghai/1 and A/Hangzhou/1/2013 (H7N9) (a third human A(H7N9) virus tested in this assay) bind to human virus-type receptors, a property that may be critical for virus transmissibility in ferrets. Anhui/1 was found to be less sensitive in mice to neuraminidase inhibitors than a pandemic H1N1 2009 virus, although both viruses were equally susceptible to an experimental antiviral polymerase inhibitor. The robust replicative ability in mice, ferrets and nonhuman primates and the limited transmissibility in ferrets of Anhui/1 suggest that A(H7N9) viruses have pandemic potential.

368 citations

Journal ArticleDOI
TL;DR: It is suggested that pegylated IFN-α protects type 1 pneumocytes from SCV infection, and should be considered a candidate drug for SARS therapy.
Abstract: The primary cause of severe acute respiratory syndrome (SARS) is a newly discovered coronavirus1,2,3,4,5,6,7. Replication of this SARS coronavirus (SCV) occurs mainly in the lower respiratory tract, and causes diffuse alveolar damage2,7,8. Lack of understanding of the pathogenesis of SARS has prevented the rational development of a therapy against this disease. Here we show extensive SCV antigen expression in type 1 pneumocytes of experimentally infected cynomolgus macaques (Macaca fascicularis) at 4 d postinfection (d.p.i.), indicating that this cell type is the primary target for SCV infection early in the disease, and explaining the subsequent pulmonary damage. We also show that prophylactic treatment of SCV-infected macaques with the antiviral agent pegylated interferon-α (IFN-α) significantly reduces viral replication and excretion, viral antigen expression by type 1 pneumocytes and pulmonary damage, compared with untreated macaques. Postexposure treatment with pegylated IFN-α yielded intermediate results. We therefore suggest that pegylated IFN-α protects type 1 pneumocytes from SCV infection, and should be considered a candidate drug for SARS therapy

368 citations


Cited by
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Journal Article
Fumio Tajima1
30 Oct 1989-Genomics
TL;DR: It is suggested that the natural selection against large insertion/deletion is so weak that a large amount of variation is maintained in a population.

11,521 citations

Journal Article
TL;DR: This report updates the 2000 recommendations by the Advisory Committee on Immunization Practices on the use of influenza vaccine and antiviral agents with new or updated information regarding the cost-effectiveness of influenza vaccination and the 2001-2002 trivalent vaccine virus strains.
Abstract: This report updates the 2002 recommendations by the Advisory Committee on Immunization Practices (ACIP) on the use of influenza vaccine and antiviral agents (CDC. Prevention and Control of Influenza: Recommendations of the Advisory Committee on Immunization Practices [ACIP]. MMWR 2002;51 [No. RR-3]:1-31). The 2003 recommendations include new or updated information regarding 1) the timing of influenza vaccination by age and risk group; 2) influenza vaccine for children aged 6-23 months; 3) the 2003-2004 trivalent inactivated vaccine virus strains: A/Moscow/10/99 (H3N2)-like, A/New Caledonia/20/99 (H1N1)-like, and B/Hong Kong/330/2001-like antigens (for the A/Moscow/10/99 [H3N2]-like antigen, manufacturers will use the antigenically equivalent A/Panama/2007/99 [H3N2] virus, and for the B/Hong Kong/330/2001-like antigen, manufacturers will use either B/Hong Kong/330/2001 or the antigenically equivalent B/Hong Kong/1434/2002); 4) availability of certain influenza vaccine doses with reduced thimerosal content, including single 0.25 mL-dose syringes; and 5) manufacturers of influenza vaccine for the U.S. market. Although the optimal time to vaccinate against influenza is October and November, vaccination in December and later continues to be strongly recommended A link to this report and other information regarding influenza can be accessed at http://www.cdc.gov/ncidod/diseases/flu/fluvirus.htm.

5,334 citations

Journal ArticleDOI
04 May 2006-Nature
TL;DR: It is found that RIG-I is essential for the production of interferons in response to RNA viruses including paramyxoviruses, influenza virus and Japanese encephalitis virus, whereas MDA5 is critical for picornavirus detection.
Abstract: The innate immune system senses viral infection by recognizing a variety of viral components (including double-stranded (ds)RNA) and triggers antiviral responses. The cytoplasmic helicase proteins RIG-I (retinoic-acid-inducible protein I, also known as Ddx58) and MDA5 (melanoma-differentiation-associated gene 5, also known as Ifih1 or Helicard) have been implicated in viral dsRNA recognition. In vitro studies suggest that both RIG-I and MDA5 detect RNA viruses and polyinosine-polycytidylic acid (poly(I:C)), a synthetic dsRNA analogue. Although a critical role for RIG-I in the recognition of several RNA viruses has been clarified, the functional role of MDA5 and the relationship between these dsRNA detectors in vivo are yet to be determined. Here we use mice deficient in MDA5 (MDA5-/-) to show that MDA5 and RIG-I recognize different types of dsRNAs: MDA5 recognizes poly(I:C), and RIG-I detects in vitro transcribed dsRNAs. RNA viruses are also differentially recognized by RIG-I and MDA5. We find that RIG-I is essential for the production of interferons in response to RNA viruses including paramyxoviruses, influenza virus and Japanese encephalitis virus, whereas MDA5 is critical for picornavirus detection. Furthermore, RIG-I-/- and MDA5-/- mice are highly susceptible to infection with these respective RNA viruses compared to control mice. Together, our data show that RIG-I and MDA5 distinguish different RNA viruses and are critical for host antiviral responses.

3,508 citations

Journal ArticleDOI
TL;DR: The approaches for developing effective vaccines and therapeutic combinations to cope with this viral outbreak are discussed and the emergence and pathogenicity of COVID-19 infection and previous human coronaviruses severe acute respiratory syndrome coronavirus (SARS-CoV) and middle east respiratory virus (MERS- coV) is analyzed.

2,643 citations