Identification and characterization of a late AH1N2 human reassortant in France during the 2002–2003 influenza season

Faress, Shaker Al; Ferraris, Olivier; Moulés, Vincent; Valette, Martine; Hay, Alan J.; Lina, Bruno

doi:10.1016/j.virusres.2007.10.007

Cited by 10 publications

(10 citation statements)

References 36 publications

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“…The 1968 influenza virus A (H3N2) pandemic also continued to reassort after the pandemic year, resulting in viruses during 1969–1971 with a different N2 gene than those earlier in the pandemic ( 30 ). Reassortants of influenza virus A (H1N2) with the HA of seasonal influenza A (H1N1) and the NA of seasonal influenza A (H3N2) viruses have been isolated from humans during previous influenza seasons, thereby confirming that reassortant influenza viruses with such an HA/NA combination can emerge in humans ( 15 , 16 ). Moreover, influenza (H1N2) viruses frequently have been detected in pigs around the world ( 31 ).…”

Section: Discussionmentioning

confidence: 90%

“…Dual infections by seasonal influenza A (H1N1) and seasonal influenza A (H3N2) viruses have been reported ( 12 ), as well as mixed infections of pandemic (H1N1) 2009 and seasonal influenza A (H3N2) viruses ( 13 , 14 ), highlighting the potential for reassortment of currently circulating influenza viruses. Subtype H1N2 reassortant influenza viruses that contain the HA of seasonal influenza A (H1N1) and the NA of seasonal influenza A (H3N2) viruses have been isolated from humans during previous influenza seasons, confirming that such HA/NA combinations can emerge in humans ( 15 , 16 ). …”

mentioning

confidence: 92%

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Possible Increased Pathogenicity of Pandemic (H1N1) 2009 Influenza Virus upon Reassortment

Schrauwen

Herfst²,

Chutinimitkul³

et al. 2011

Emerg. Infect. Dis.

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Since emergence of the pandemic (H1N1) 2009 virus in April 2009, three influenza A viruses—seasonal (H3N2), seasonal (H1N1), and pandemic (H1N1) 2009—have circulated in humans. Genetic reassortment between these viruses could result in enhanced pathogenicity. We compared 4 reassortant viruses with favorable in vitro replication properties with the wild-type pandemic (H1N1) 2009 virus with respect to replication kinetics in vitro and pathogenicity and transmission in ferrets. Pandemic (H1N1) 2009 viruses containing basic polymerase 2 alone or in combination with acidic polymerase of seasonal (H1N1) virus were attenuated in ferrets. In contrast, pandemic (H1N1) 2009 with neuraminidase of seasonal (H3N2) virus resulted in increased virus replication and more severe pulmonary lesions. The data show that pandemic (H1N1) 2009 virus has the potential to reassort with seasonal influenza viruses, which may result in increased pathogenicity while it maintains the capacity of transmission through aerosols or respiratory droplets.

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Section: Discussionmentioning

confidence: 90%

mentioning

confidence: 92%

Possible Increased Pathogenicity of Pandemic (H1N1) 2009 Influenza Virus upon Reassortment

Schrauwen

Herfst²,

Chutinimitkul³

et al. 2011

Emerg. Infect. Dis.

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“…Reassortment events between seasonal influenza viruses have been reported previously, though they have appeared relatively infrequently in France in 2002–2003 (Al Faress et al, 2008), in Cambodia in 2005–2008 (Fourment et al, 2009), and in Thailand in 2006–2008 (Bai et al, 2009). Natural coinfections of influenza are also reported rarely (Eshaghi et al, 2009; Falchi et al, 2008; Takao et al, 2005; Toda et al, 2006).…”

Section: Discussionmentioning

confidence: 76%

Genotyping assay for the identification of 2009–2010 pandemic and seasonal H1N1 influenza virus reassortants

Ducatez

Sonnberg

Hall

et al. 2010

Journal of Virological Methods

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New Zealand identified its first pandemic H1N1 influenza cases in late April 2009, immediately prior to the historical start of the New Zealand influenza season. Both pandemic and oseltamivirresistant seasonal H1N1 viruses cocirculated in the population for a period of time. Thus, concerns were raised about the possibility of reassortment events between the two strains. An RT-PCRbased genotyping assay was developed so that H1N1 influenza coinfections and reassortants could be detected quickly. The assay differentiated effectively the seasonal and pandemic strains. It also confirmed the identification of the first reported coinfection of pandemic and seasonal H1N1 strains during the 2009 Southern Hemisphere influenza season in New Zealand.

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“…Influenza A virus infection is a common cause of respiratory illness in humans, and the epidemics occur almost annually in many countries with attack rates of over ten percent of the population, in spite of the wide availability of influenza vaccines [17], [18]. The persistent threat of currently circulating human influenza A viruses (H1N1, H1N2, and H3N2), and the recent outbreaks of avian influenza A virus (H5N1) and swine-origin influenza A virus (H1N1) have raised serious concerns about the potential of a new influenza pandemic [19]–[22].…”

Section: Introductionmentioning

confidence: 99%

Methamphetamine Reduces Human Influenza A Virus Replication

Chen

2012

PLoS ONE

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Methamphetamine (meth) is a highly addictive psychostimulant that is among the most widely abused illicit drugs, with an estimated over 35 million users in the world. Several lines of evidence suggest that chronic meth abuse is a major factor for increased risk of infections with human immunodeficiency virus and possibly other pathogens, due to its immunosuppressive property. Influenza A virus infections frequently cause epidemics and pandemics of respiratory diseases among human populations. However, little is known about whether meth has the ability to enhance influenza A virus replication, thus increasing severity of influenza illness in meth abusers. Herein, we investigated the effects of meth on influenza A virus replication in human lung epithelial A549 cells. The cells were exposed to meth and infected with human influenza A/WSN/33 (H1N1) virus. The viral progenies were titrated by plaque assays, and the expression of viral proteins and cellular proteins involved in interferon responses was examined by Western blotting and immunofluorescence staining. We report the first evidence that meth significantly reduces, rather than increases, virus propagation and the susceptibility to influenza infection in the human lung epithelial cell line, consistent with a decrease in viral protein synthesis. These effects were apparently not caused by meth’s effects on enhancing virus-induced interferon responses in the host cells, reducing viral biological activities, or reducing cell viability. Our results suggest that meth might not be a great risk factor for influenza A virus infection among meth abusers. Although the underlying mechanism responsible for the action of meth on attenuating virus replication requires further investigation, these findings prompt the study to examine whether other structurally similar compounds could be used as anti-influenza agents.

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Identification and characterization of a late AH1N2 human reassortant in France during the 2002–2003 influenza season

Cited by 10 publications

References 36 publications

Possible Increased Pathogenicity of Pandemic (H1N1) 2009 Influenza Virus upon Reassortment

Possible Increased Pathogenicity of Pandemic (H1N1) 2009 Influenza Virus upon Reassortment

Genotyping assay for the identification of 2009–2010 pandemic and seasonal H1N1 influenza virus reassortants

Methamphetamine Reduces Human Influenza A Virus Replication

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