Oseltamivir-Resistant Influenza Virus A (H1N1), Europe, 2007–08 Season

Meijer, Adam; Lackenby, Angie; Hungnes, Olav; Lina, Bruno; Werf, Sylvie van der; Schweiger, Brunhilde; Opp, Matthias; Paget, John; Kassteele, Jan van de; Hay, Alan J.; Zambon, Maria

doi:10.3201/eid1504.081280

Cited by 270 publications

(254 citation statements)

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“…The NAI susceptibility of influenza virus was expressed as the concentration of NAI needed to inhibit the NA enzyme activity by 50% (IC 50 ), as described previously (19). ORV was defined as influenza virus with an IC 50 of Ͼ100 nmol/liter for oseltamivir (14). From a subset of viruses, the phenotypic oseltamivir susceptibility data were supplemented by NA sequence analysis.…”

Section: Methodsmentioning

confidence: 99%

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Adamantane- and Oseltamivir-Resistant Seasonal A (H1N1) and Pandemic A (H1N1) 2009 Influenza Viruses in Guangdong, China, during 2008 and 2009

et al. 2011

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Section: Methodsmentioning

confidence: 99%

“…During the 2007-2008 influenza season, the emergence of oseltamivir-resistant seasonal A (H1N1) viruses (ORVs) in Europe was a point of considerable concern (12,14). In the subsequent influenza season, ORVs spread worldwide.…”

mentioning

confidence: 99%

Adamantane- and Oseltamivir-Resistant Seasonal A (H1N1) and Pandemic A (H1N1) 2009 Influenza Viruses in Guangdong, China, during 2008 and 2009

et al. 2011

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“…Neuraminidase inhibitors (NAIs), such as oseltamivir (Tamiflu) and zanamivir (Relenza) are two FDA-approved drugs for the treatment of type A and type B influenza infections [7] . However, oseltamivir-resistant mutant (H1N1) viruses were detected and found to be quickly transmitted in several countries during the 2007 and 2008 influenza seasons, which has brought attention to the unpredictable consequences of mutational resistance to anti-viral compounds in the prevention and control of flu pandemics [8][9][10][11] .…”

Section: Introductionmentioning

confidence: 99%

Amelioration of influenza virus-induced reactive oxygen species formation by epigallocatechin gallate derived from green tea

Ling

Wei

et al. 2012

Acta Pharmacol Sin

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Aim: To study whether epigallocatechin gallate (EGCG), a green tea-derived polyphenol, exerted anti-influenza A virus activity in vitro and in vivo. Methods: Madin-Darby canine kidney (MDCK) cells were tested. The antiviral activity of EGCG in the cells was determined using hemagglutination assay and qPCR. Time of addition assay was performed to determine the kinetics of inhibition of influenza A by EGCG. The level of reactive oxygen species (ROS) were determined with confocal microscopy and flow cytometry. BALB/c mice were treated with EGCG (10, 20 or 40 mg·kg -1 ·d -1 , po) for 5 d. On the 3rd d of the treatment, the mice were infected with influenza A virus. Histopathological changes, lung index and virus titers in the lungs were determined. Results: Treatment of influenza A-infected MDCK cells with EGCG (1.25-100 nmol/L) inhibited influenza A replication in a concentration-dependent manner (the ED 50 value was 8.71±1.11 nmol/L). Treatment with EGCG (20 nmol/L) significantly suppressed the increased ROS level in MDCK cells following influenza A infection. In BALB/c mice infected with influenza virus, oral administration of EGCG (40 mg·kg -1 ·d -1 ) dramatically improved the survival rate, decreased the mean virus yields and mitigated viral pneumonia in the lungs, which was equivalent to oral administration of oseltamivir (40 mg·kg -1 ·d -1 ), a positive control drug. Conclusion:The results provide a molecular basis for development of EGCG as a novel and safe chemopreventive agent for influenza A infection.

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“…All current seasonal H1N1 (not H1N1 pdm) strains are genotypically (H275Y) and phenotypically resistant to oseltamivir [40,41].…”

Section: Antiviral Resistancementioning

confidence: 99%

Risk Factors Associated with Severe Clinical Outcomes of Pandemic H1N1 Infection

Fullen¹

2014

JHVRV

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The clinical outcome of pandemic H1N1 influenza infection is dependent on the interplay of virus and host factors. Influenza virus infections can range from relatively mild infections of the upper respiratory tract to fatal disease of the lower respiratory tract. A range of host factors play a role in the severity of clinical disease in pdm(H1N1)09 infection. With the exception of neonates age was directly proportional to the severity of clinical outcome; obesity, COPD and pregnancy play a key role in clinical outcome of infection. An important determinant in the pathogenesis of influenza infection is the tissue tropism of the influenza virus. The D222G and D222N mutations of pdm(H1N1)09 influenza appear to have an increased tropism for the tissues of the lower respiratory tract and are disproportionally associated with severe clinical disease. These α2-3 salicylic acid tropic mutations, which have been associated with fatal cases of influenza infection, have also been preferentially selected for during sequential passage in embryonated eggs and viruses of avian origin. KeywordsInfluenza; Pandemic; H1N1; pdm(H1N1)09; Oseltamivir IntroductionThe current H1N1 influenza vaccine strain A/ California/7/2009 has a surprisingly high no detectable antibody (NDA) rate of approximately 52% in a population of 200 subjects screened (unpublished data). Studies have shown that the A/California/7/2009 strain of pandemic H1N1 influenza causes alveolar haemorrhage in the ferret model [1,2]; similar "swine flu" viruses A/Mexico/4482/2009 and A/ Netherlands/602/2009 also presented severe pathology in the ferret model [3,4]. As a consequence it is clear that infection with this group of viruses represents a significant risk of a severe clinical outcome. Furthermore, the severe symptoms that are associated with a subset of A/California/7/2009 infections are atypical for previous seasonal influenza infections. Co-morbidities and their impact on clinical outcome of infectionThe clinical outcomes of infection by pdm(H1N1)09 are considerably affected by one or more host factors and comorbidities. Here we discuss these co-morbidities and the impact that they have on clinical consequences to infection. Case fatality ratiosBy July 2009 63,479 cases of influenza like illness were reported in Mexico; of these cases 11% (6,945) were confirmed as H1N1 influenza; 92% of confirmed positive cases (6,407) were treated as outpatients, 7% (475) were admitted to hospital and survived and <1% died (63) [5]. During the early phase of the pandemic the case fatality ratio (CFR) was calculated to be approximately 0.4-0.6% [6]. In the UK an estimated 540,000 people had symptomatic H1N1 infection during a study period with a CFR of (0.026%) 26 deaths per 100,000 [7]. There is little published information for the CFRs of seasonal H1N1 or H3N2 influenza. However using data from the Health Protection Agency (HPA) we were able to determine the CFR for influenza infections admitted to intensive care units (ICU). 2/7 SymptomsA meta-analysis of H1N1...

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Oseltamivir-Resistant Influenza Virus A (H1N1), Europe, 2007–08 Season

Cited by 270 publications

References 31 publications

Adamantane- and Oseltamivir-Resistant Seasonal A (H1N1) and Pandemic A (H1N1) 2009 Influenza Viruses in Guangdong, China, during 2008 and 2009

Adamantane- and Oseltamivir-Resistant Seasonal A (H1N1) and Pandemic A (H1N1) 2009 Influenza Viruses in Guangdong, China, during 2008 and 2009

Amelioration of influenza virus-induced reactive oxygen species formation by epigallocatechin gallate derived from green tea

Risk Factors Associated with Severe Clinical Outcomes of Pandemic H1N1 Infection

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