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The recent emergence of seasonal influenza A(H1N1) strains resistant to oseltamivir makes it necessary to monitoring carefully the susceptibility of human influenza viruses to neuraminidase inhibitors. We report the prevalence of the oseltamivir resistance among influenza A viruses circulating in south-western France over the past three years: seasonal influenza A(H1N1), seasonal influenza A(H3N2), and the influenza A(H1N1)v viruses associated with the ongoing 2009 pandemic. The main result of the study is the absence of oseltamivir resistance in the pandemic H1N1 strains studied so far (n=129).

Reports of human cases of infection with avian influenza A(H5N1) virus have received increased public attention because of the potential for the emergence of a pandemic strain. In the end of 2005 and the beginning of 2006, avian influenza A(H5N1) virus caused outbreaks among domestic poultry and was isolated from wild swans in many European countries, including Bulgaria. Between January and March 2006, samples were collected from 26 patients who had been in close contact with ill or dead birds and developed a subsequent respiratory illness. The testing took place at the National Laboratory of Influenza in Sofia. Specific ?(H5N1) assays were applied for screening (Sacace RT-PCR and real-time kit). Avian flu ?(H5N1) virus was not detected in any of the patients tested. In three patients, human subtype ?(H1N1) influenza virus, identifiable by RT-PCR was isolated and further characterized by hemagglutination inhibition test (HIT). The reliability of the molecular assays used in this investigation was demonstrated in an International Quality Control for Human and Avian ?(H5N1) Influenza performed later in 2006 by INSTAND (Society for Promotion of Quality Assurance in the Medical Laboratories), Germany.

The threat of an influenza pandemic has been heightened in the past two years by outbreaks of avian influenza concentrated in South East Asia which have resulted in human deaths. So far, the avian influenza virus seems difficult to transmit from human to human, but changes in the virus genome may well increase transmissibility

In the past eight years there have been three pandemic 'false alarms' caused by avian H5N1 viruses. The first of these in 1997 was a turning point in our understanding of the difficulties of vaccine development from a lethal avian virus.

During the 2003 outbreak of avian influenza caused by highly pathogenic avian influenza (HPAI) virus A/H7N7 in the Netherlands, human infection with this virus occurred in unexpectedly high numbers. The first signs of human infection were found in a veterinarian who visited several farms with infected poultry and subsequently developed acute conjunctivitis caused by the A/H7N7 virus. Human influenza virus (mostly A/H3N2) was circulating in the community simultaneously. In view of the potential risk of co infection and reassortment, active case finding among people exposed to infected poultry was implemented immediately.

At the beginning of March 2003 an outbreak of highly pathogenic avian influenza (A/H7N7) in several Dutch poultry farms was reported (1). On 11 March 2003, several workers, who had been exposed to A/H7N7 infected poultry, developed conjunctivitis. Some of them tested positive for influenza A/H7N7 (2). One week later, two close contacts of a worker with H7N7 infection developed similar eye symptoms. They had also been infected with the avian influenza virus, although they had had no exposure to infected poultry themselves, which strongly suggests human to human transmission of the virus (3).