Replication and pathogenesis of the pandemic (H1N1) 2009 influenza virus in mammalian models

Kwon, Donghyok; Shin, Kyeong‐Cheol; Kim, Seungtae; Ha, Yoon‐Cheol; Choi, Jang‐Hoon; Yang, Jeong Seon; Lee, Joo-Yeon; Chae, Chanhee; Oh, Hee-Bok; Kang, Chun

doi:10.1007/s12275-010-0120-z

Cited by 21 publications

(19 citation statements)

References 19 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In addition, the sustained fever may have affected the animal’s appetite because body weight recovery did not occur until the body temperature returned to baseline. Consistent with other H1N1 studies in ferrets [29], [30], we detected viral titers in lung from both the 2009 A/Beijing/501 H1N1- and the A/California/07 H1N1-infected groups at day 3 and 7 post-infection. Ferrets infected with A/Beijing/501 H1N1 virus strain exhibited mild clinical signs of infection.…”

Section: Discussionsupporting

confidence: 91%

Characterization of the 2009 Pandemic A/Beijing/501/2009 H1N1 Influenza Strain in Human Airway Epithelial Cells and Ferrets

Yang

Deng

et al. 2012

PLoS ONE

View full text Add to dashboard Cite

BackgroundA novel 2009 swine-origin influenza A H1N1 virus (S-OIV H1N1) has been transmitted among humans worldwide. However, the pathogenesis of this virus in human airway epithelial cells and mammals is not well understood.Methodology/Principal FindingIn this study, we showed that a 2009 A (H1N1) influenza virus strain, A/Beijing/501/2009, isolated from a human patient, caused typical influenza-like symptoms including weight loss, fluctuations in body temperature, and pulmonary pathological changes in ferrets. We demonstrated that the human lung adenocarcinoma epithelial cell line A549 was susceptible to infection and that the infected cells underwent apoptosis at 24 h post-infection. In contrast to the seasonal H1N1 influenza virus, the 2009 A (H1N1) influenza virus strain A/Beijing/501/2009 induced more cell death involving caspase-3-dependent apoptosis in A549 cells. Additionally, ferrets infected with the A/Beijing/501/2009 H1N1 virus strain exhibited increased body temperature, greater weight loss, and higher viral titers in the lungs. Therefore, the A/Beijing/501/2009 H1N1 isolate successfully infected the lungs of ferrets and caused more pathological lesions than the seasonal influenza virus. Our findings demonstrate that the difference in virulence of the 2009 pandemic H1N1 influenza virus and the seasonal H1N1 influenza virus in vitro and in vivo may have been mediated by different mechanisms.Conclusion/SignificanceOur understanding of the pathogenesis of the 2009 A (H1N1) influenza virus infection in both humans and animals is broadened by our findings that apoptotic cell death is involved in the cytopathic effect observed in vitro and that the pathological alterations in the lungs of S-OIV H1N1-infected ferrets are much more severe.

show abstract

Section: Discussionsupporting

confidence: 91%

Characterization of the 2009 Pandemic A/Beijing/501/2009 H1N1 Influenza Strain in Human Airway Epithelial Cells and Ferrets

Yang

Deng

et al. 2012

PLoS ONE

View full text Add to dashboard Cite

show abstract

“…Several aptamers against influenza virus have been described, mainly targeting hemagglutinin, 37,38,39 and an aptamer was capable of mediating a reduction in viral pathogenicity in mice models. 39 Other aptamers targeting NS1 40 or the PA polymerase subunit 41 have also been studied, although aptamers directed against cellular factors that establish essential interactions with influenza virus proteins have not yet been reported.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of Influenza Virus Replication by DNA Aptamers Targeting a Cellular Component of Translation Initiation

Rodriguez

Pérez-Morgado

González

et al. 2016

Molecular Therapy - Nucleic Acids

View full text Add to dashboard Cite

The genetic diversity of the influenza virus hinders the use of broad spectrum antiviral drugs and favors the appearance of resistant strains. Single-stranded DNA aptamers represent an innovative approach with potential application as antiviral compounds. The mRNAs of influenza virus possess a 5′cap structure and a 3′poly(A) tail that makes them structurally indistinguishable from cellular mRNAs. However, selective translation of viral mRNAs occurs in infected cells through a discriminatory mechanism, whereby viral polymerase and NS1 interact with components of the translation initiation complex, such as the eIF4GI and PABP1 proteins. We have studied the potential of two specific aptamers that recognize PABP1 (ApPABP7 and ApPABP11) to act as anti-influenza drugs. Both aptamers reduce viral genome expression and the production of infective influenza virus particles. The interaction of viral polymerase with the eIF4GI translation initiation factor is hindered by transfection of infected cells with both PABP1 aptamers, and ApPABP11 also inhibits the association of NS1 with PABP1 and eIF4GI. These results indicate that aptamers targeting the host factors that interact with viral proteins may potentially have a broad therapeutic spectrum, reducing the appearance of escape mutants and resistant subtypes.

show abstract

“…It can also be observed with human seasonal influenza virus isolates, although their neurovirulence may be strain- and dose-dependent (Zitzow et al, 2002; Kwon et al, 2010; van den Brand et al, 2012). In contrast, influenza-associated encephalitis or encephalopathy is rarely reported in human influenza, and evidence of virus replication in the human CNS is limited (Studahl, 2003; Gambotto et al, 2007; Fonseca and Lavoie, 2014).…”

Section: Animal Models Of Influenzamentioning

confidence: 99%

Animal models for influenza virus pathogenesis, transmission, and immunology

Thangavel

Bouvier

2014

Journal of Immunological Methods

167

153

View full text Add to dashboard Cite

In humans, infection with an influenza A or B virus manifests typically as an acute and self-limited upper respiratory tract illness characterized by fever, cough, sore throat, and malaise. However, influenza can present along a broad spectrum of disease, ranging from sub-clinical or even asymptomatic infection to a severe primary viral pneumonia requiring advanced medical supportive care. Disease severity depends upon the virulence of the influenza virus strain and the immune competence and previous influenza exposures of the patient. Animal models are used in influenza research not only to elucidate the viral and host factors that affect influenza disease outcomes in and spread among susceptible hosts, but also to evaluate interventions designed to prevent or reduce influenza morbidity and mortality in man. This review will focus on the three animal models currently used most frequently in influenza virus research -- mice, ferrets, and guinea pigs -- and discuss the advantages and disadvantages of each.

show abstract

Replication and pathogenesis of the pandemic (H1N1) 2009 influenza virus in mammalian models

Cited by 21 publications

References 19 publications

Characterization of the 2009 Pandemic A/Beijing/501/2009 H1N1 Influenza Strain in Human Airway Epithelial Cells and Ferrets

Characterization of the 2009 Pandemic A/Beijing/501/2009 H1N1 Influenza Strain in Human Airway Epithelial Cells and Ferrets

Inhibition of Influenza Virus Replication by DNA Aptamers Targeting a Cellular Component of Translation Initiation

Animal models for influenza virus pathogenesis, transmission, and immunology

Contact Info

Product

Resources

About