Giuseppe
Emeritus
[Source: The Lancet Infectious Diseases, full text: (LINK). Extract.]
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The Lancet, Volume 381, Issue 9885, Pages 2230 - 2232, 29 June 2013
doi:10.1016/S0140-6736(13)61209-X
Copyright ? 2013 2013 Elsevier Ltd
Oseltamivir resistance during treatment of H7N9 infection
Original Text
Alan J Hay, Frederick G Hayden
Detection of an Arg292Lys mutation (N2 numbering) in the virus neuraminidase (NA) gene within 2 days of initiating oseltamivir treatment, in the first reported human infection by avian A(H7N9) influenza virus,1 raised concern about emergence of resistance during treatment with neuraminidase inhibitors. This is important because a Ser31Asn resistance mutation in the M2 protein of A(H7N9) viruses, also present in A(H1N1)pdm09 and seasonal A(H3N2) viruses, abrogates effectiveness of available M2 inhibitors (amantadine and rimantadine). In The Lancet, Yunwen Hu and colleagues2 report the emergence of oseltamivir-resistant virus with the Arg292Lys mutation in two patients among 14 adults infected with A(H7N9), treated initially with oseltamivir, starting at a median 5 days (range 2?10 days) following illness onset. Resistant virus emerged in two of the most severe cases, including one who was treated within 2 days of illness onset, and was associated with persistent or resurgent virus detection and poor outcomes. By contrast, no virus with this mutation was detected in a patient who died after 6 days of therapy, or in the remaining 11 patients infected with A(H7N9), four of whom required mechanical ventilation.
(?)
-doi:10.1016/S0140-6736(13)61209-X
Copyright ? 2013 2013 Elsevier Ltd
Oseltamivir resistance during treatment of H7N9 infection
Original Text
Alan J Hay, Frederick G Hayden
Detection of an Arg292Lys mutation (N2 numbering) in the virus neuraminidase (NA) gene within 2 days of initiating oseltamivir treatment, in the first reported human infection by avian A(H7N9) influenza virus,1 raised concern about emergence of resistance during treatment with neuraminidase inhibitors. This is important because a Ser31Asn resistance mutation in the M2 protein of A(H7N9) viruses, also present in A(H1N1)pdm09 and seasonal A(H3N2) viruses, abrogates effectiveness of available M2 inhibitors (amantadine and rimantadine). In The Lancet, Yunwen Hu and colleagues2 report the emergence of oseltamivir-resistant virus with the Arg292Lys mutation in two patients among 14 adults infected with A(H7N9), treated initially with oseltamivir, starting at a median 5 days (range 2?10 days) following illness onset. Resistant virus emerged in two of the most severe cases, including one who was treated within 2 days of illness onset, and was associated with persistent or resurgent virus detection and poor outcomes. By contrast, no virus with this mutation was detected in a patient who died after 6 days of therapy, or in the remaining 11 patients infected with A(H7N9), four of whom required mechanical ventilation.
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