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Influenza viruses resistant to oseltamivir, news and updates
>There are different questions that need to be answered regarding the strange pattern of oseltamivir-resistant-H1N1 human influenza viruses.
Agreed.
>1) Why do European Union experience a such large variation between incidence in countries that share borders and million of citizens?
Obviously, there are factors unrelated to Tamiflu-use that influence the distribution of resistance polymorphism acquisition in human influenza viral strains, 2007-08.
>2) Is there a bias in samples' collection and testing methods?
Not likely, no (scale of effect is too large, and one would expect errors to be significant in certain countries that have less than stellar health care infrastructure, but that is not the case from the pattern reported)
CDC graph of European Tamiflu-resistant isolates, as of June 25 '08
>3) Seasonal human influenza vaccines: population coverage, type of strain selected to manufacturing process, demographic stratification of different area (ie: Paris region has more than 50% resistant isolates compared with lower rate detected in southern France).
Are you saying the vaccines used might have influenced the resultant distribution? Non. Nor have European nor US Disease Control Centers identified relevant factors that determine resistant influenza isolate distribution pattern.
>4) Movement of the population: why do countries like Italy experience low rate of resistant isolates detection but it shares important traffic route (terrestrial - road, turnpikes, railroads; aerial; by the sea) with France and no increasing of resistantance was observed?
These factors aren't relevant to the observed pattern in Europe.
>5) Direction of the spread of influenza epidemics: North to South, East to West or viceversa.
Irrelevant to the pattern detected.
>6) Migration patterns from Africa and Europe, Asia and Europe, Middle East to Europe.
Obviously relevant, but secondary to a larger set of determinants.
>I hope at least one of these questions could find an explanation.
Yes, an explanation would be useful, but first, the 'experts' must recognize that the polymorphisms in question are acquired from H5N1 from the previous years of geographic range expansion and is therefore determined by avian influenza clade expression of antiviral resistance. That acknowledgment would require the 'experts' to admit that wild bird migration is at the center of dissemination/acquisition of crucial drug resistance polymorphisms.
The 'experts' are still very uneasy with the notion that an avian influenza subtype can fluidly infect many mammal species, including humans. Influenza viruses are supposed to be species-specific, and yet, we see this as a common factor for many emerging infectious diseases of the last 50 years.
When one observes influenza infection in a species (felines, domestic and wild) that has never been reported historically and moreover appears to be transmitted within species relatively easily (in test conditions but also anecdotally reported in Indonesia by research veterinarians), it's yet another indicator of mounting risk for an influenza pandemic.
I was wondering if someone could confirm the following summary of the situation:
"?If those resistant strains begin to propagate, then that?s when we?re going to be in trouble, because we don?t have any antivirals active against them,? said Rommie Amaro, a postdoctoral fellow in chemistry at UC San Diego."
I was wondering if someone could confirm the following summary of the situation:
"“If those resistant strains begin to propagate, then that’s when we’re going to be in trouble, because we don’t have any antivirals active against them,” said Rommie Amaro, a postdoctoral fellow in chemistry at UC San Diego."
I was wondering if someone could confirm the following summary of the situation:
"?If those resistant strains begin to propagate, then that?s when we?re going to be in trouble, because we don?t have any antivirals active against them,? said Rommie Amaro, a postdoctoral fellow in chemistry at UC San Diego."
I was only able to find reports of Relenza resistance to one influenza virus: type B, which I believe hadn't shown antiviral resistance before this year. I hadn't heard about Relenza resistance.
I've wondered if substandard dosing is the culprit behind sudden rise of geographically distinct, but not distant (as in Paris and Southern France) resistance of H1N1 to tamiflu.
(the following is purely speculative babble)...
Maybe there is something in the food or regional favorite drink that either inhibits the esterase cleavage of precursor form of Tamiflu or enhances its drug metabolism, clearing it from the system before it has a chance to work properly. Provence and Parisian/Bordeaux cuisine are quite different.
Tamiflu is, after all, derived from natural product (unlike Relenza, which is purely synthetic and I believe active in its administered form, although it has poor uptake when administered orally).
The spice it is most like is burned as incense in Japan, and consumed elsewhere in Arabic and European cooking/appertifs.
do we have improved numbers for resistance in H3N2 and B
meanwhile ? If they are also increased we have another
pessimistic indication for its development due to drug use.
Just to emphasize another transparency problem is that we're not getting needed info on resistant patterns. This needs both sequence analysis to look for known genetic variations and live virus to use in tests with the actual antivirals to look for other patterns of resistance
A Meijer (a.meijer@nivel.nl)1 2, A Lackenby3 4, A Hay3 5, M Zambon3 4
European Influenza Surveillance Scheme (EISS) Co-ordination Centre, Nederlands Instituut voor Onderzoek van de Gezondheidszorg (Netherlands Institute for Health Services Research, NIVEL), Utrecht, the Netherlands
Laboratory for Infectious Diseases and Screening, Rijksinstituut voor Volksgezondheid en Milieu (National Institute of Public Health and the Environment, RIVM), Bilthoven, the Netherlands
European Surveillance Network for Vigilance against Viral Resistance (VIRGIL)
Respiratory Virus Unit, Centre for Infection, Health Protection Agency, London, United Kingdom
World Health Organization Collaborating Centre for Reference and Research on Influenza, National Institute for Medical Research, London, United Kingdom
Due to the influenza pandemic threat, many countries are stockpiling antivirals in the hope of limiting the impact of a future pandemic virus. Since resistance to antiviral drugs would probably significantly alter the effectiveness of antivirals, surveillance programmes to monitor the emergence of resistance are of considerable importance.
During the 2006/2007 influenza season, an inventory was conducted by the European Surveillance Network for Vigilance against Viral Resistance (VIRGIL) in collaboration with the European Influenza Surveillance Scheme (EISS) to evaluate antiviral susceptibility testing by the National Influenza Reference Laboratories (NIRL) in relation to the national antiviral stockpile in 30 European countries that are members of EISS.
All countries except Ukraine had a stockpile of the neuraminidase inhibitor (NAI) oseltamivir. Additionally, four countries had a stockpile of the NAI zanamivir and three of the M2 ion channel inhibitor rimantadine. Of 29 countries with a NAI stockpile, six countries' NIRLs could determine virus susceptibility by 50% inhibitory concentration (IC50) and in 13 countries it could be done by sequencing. Only in one of the three countries with a rimantadine stockpile could the NIRL determine virus susceptibility, by sequencing only. However, including the 18 countries that had plans to introduce or extend antiviral susceptibility testing, the NIRLs of 21 of the 29 countries with a stockpile would be capable of susceptibility testing appropriate to the stockpiled drug by the end of the 2007/2008 influenza season.
Although most European countries in this study have stockpiles of influenza antivirals, susceptibility surveillance capability by the NIRLs appropriate to the stockpiled antivirals is limited.
Since the widespread emergence of antiviral resistance would likely have a significant impact on clinical effectiveness of antiviral therapy and prophylaxis, it is important to track resistance through regional and national surveillance programmes. In addition, it is important that these surveillance programmes are appropriate to the antivirals being stockpiled. Therefore, VIRGIL and EISS, as the European public-funded consortia working on these subjects, carried out this study in order to evaluate the actual and future antiviral susceptibility testing activities by the NIRLs in relation to the national antiviral stockpile in the 30 European countries that are members of EISS.
All European countries (except Ukraine) that participated in this study indicated that antiviral stockpiles are available. This is an encouraging observation as it relates directly to national pandemic preparedness activities. However, the number of countries in which NIRLs performed influenza antiviral susceptibility testing appropriate to the stockpiled antivirals was limited.
The creation of antiviral stockpiles involves substantial allocation of resources, and in the event of a pandemic it will be important to use such resources efficiently. Emerging information about the potential for the development of resistance against influenza antiviral drugs suggests that information about susceptibility of circulating strains should be taken into consideration for decisions on recommending drug use,
Antiviral susceptibility testing should exist to support the stockpiling of antiviral drugs, to analyse the susceptibility of viruses to the stockpiled antivirals in the early stages of a pandemic and to assess possible treatment failure.
Most NIRLs test for NAI resistance by sequencing, indicating that this type of analysis is much more widespread, compared with phenotypic susceptibility testing that is dependent on working with virus isolates. However, phenotypic NAI susceptibility analysis is still necessary to fully evaluate NAI resistance, given the uncertainty of purely genotypic methods for assessment of resistance as only a few mutations conferring NAI resistance have been described so far, and several more are likely to emerge. Therefore, we recommend that if a surveillance programme for NAIs is developed, both genotypic and phenotypic methods are used and data combined from both methods.
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