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89 swine flu deaths in India this week
The 30 Aug. 2010 at 21:13Last newsComments (0)Add a comment
New Delhi, Aug 30, PTI:
Swine flu continued its grip on India with 89 deaths reported from across the country in the week ending August 29.
Maharashtra reported the maximum number of 50 deaths, followed by 14 from Orissa and six each from Gujarat and Delhi. ive deaths were reported from Madhya Pradesh while four were reported from Andhra Pradesh.
A total of 1,247 cases reported during the week. All are indigenous cases. Till date, samples from 1,67,846 people have been tested for swine flu in government laboratories and a few private laboratories across the country and 39,977 (23.8 per cent) of them have been found positive. The World Health Organisation has officially declared that the swine flu pandemic was over.
Oseltamivir-resistant variants of the 2009 pandemic H1N1 influenza A virus are not attenuated in the guinea pig and ferret transmission models
The 26 Aug. 2010 at 22:06Last newsComments (0)Add a comment
Christopher W. Seibert, Michael Kaminski, Jennifer Philipp, Dennis Rubbenstroth, Randy A. Albrecht, Folker Schwalm, Silke Stertz, Rafael A. Medina, Georg Kochs, Adolfo García-Sastre, Peter Staeheli*, and Peter Palese*
Dept. of Microbiology, Institute of Global Health and Emerging Pathogens, Dept. of Medicine, Mount Sinai School of Medicine, New York, New York, USA; Dept. of Virology, University of Freiburg, Freiburg, Germany; Dept. of Virology, University of Marburg, Marburg, Germany
Abstract
Oseltamivir is routinely used worldwide for the treatment of severe influenza A virus infection, and should drug-resistant pandemic 2009 H1N1 viruses become widespread, this potent defence strategy might fail. Oseltamivir-resistant variants of the pandemic 2009 H1N1 influenza A virus have been detected in a substantial number of patients, but to date, the mutant viruses have not moved into circulation in the general population. It is not known whether the resistance mutations in the viral neuraminidase reduce viral fitness. We addressed this question by studying transmission of oseltamivir-resistant mutants derived from two different isolates of the pandemic H1N1 virus in both the guinea pig and ferret transmission models. In vitro, the virus readily acquired a single histidine to tyrosine mutation at position 275 (H275Y) in the viral neuraminidase when serially passaged in cell culture with increasing concentrations of oseltamivir. This mutation conferred a high degree of resistance to oseltamivir but not zanamivir. Unexpectedly, in guinea pigs and ferrets, the fitness of viruses with the H275Y point mutation were not impaired detectably and both wild-type and mutant viruses were transmitted equally well from animals that were initially inoculated with 1:1 virus mixtures to naïve contacts. In contrast, a reassortant virus containing an oseltamivir resistant seasonal NA in the pandemic H1N1 background showed decreased transmission efficiency and fitness in the guinea pig model. Our data suggest that the currently circulating pandemic 2009 H1N1 virus has a high potential to acquire drug-resistance without losing fitness.
Kansas H1N1 Is Tamiflu and Relenza Sensitive
The 26 Aug. 2010 at 19:41Last newsComments (0)Add a comment
Recombinomics Commentary 16:26
August 26, 2010
In vivo antiviral resistance
Adamantanes: Unknown
Oseltamivir: Sensitive
Zanamivir: Sensitive
Peramivir: Unknown
Other: Unknown
The GISAID antiviral characterization sheet for A/Kansas/05/2010 has been corrected as indicated above.
The initial sheet (posted yesterday) indicated (see list here) the isolate was resistant to Oseltamivir (Tamiflu) and Zanamivir (Relenza).
This morning the CDC contacted Recombinomics to indicate the entry was in error and likely linked to the recent GISAID upgrade of the site (which now allows BLAST analysis of the database).
The other NA sequence released with the Kansas sequence, A/Connecticut/23/2009, has not been tested for antiviral resisitance.H1N1 Tamiflu and Relenza Resistance in Kansas Case NOT
The 26 Aug. 2010 at 19:38Last newsComments (0)Add a comment
Recombinomics Commentary 23:40
August 25, 2010On August 26 the CDC notified Recombinomics that the GISAID entry on antiviral resistance is in ERROR. A/Kansas/05/2010 is SENSITIVE to oseltamivir and Zanamivir.
The US CDC released an NA sequence, A/Kansas/05/2010, today (at GISAID), which had in vivo Tamiflu (oseltamivir) and Relenza (zanamivir) resistance. The sample was collected March 17, 2010 and had two non-synonymous changes, S363N and I 466M (S364N and I467M in N1 numbering).
A second sequence, A/Connecticut/23/2009, was also released by the CDC today, and it also had I466M, which was also on an earlier sequence from Poland, A/Poland/37/2009. None of the above sequences had H274Y.
Resistance to the two first line neuramindase inhibitors (and it is likely that the M2 sequence also has S31N, conferring resistance to adamantines) in the same sequence is cause for concern.
Information on the resistance in the patients from Connecticut and Poland would be useful.Emergence of Extensive Drug Resistant XDR-pH1N1 NOT
The 26 Aug. 2010 at 19:37Last newsComments (0)Add a comment
Recombinomics Commentary 13:44
August 26, 2010On August 26 the CDC notified Recombinomics that the GISAID entry on antiviral resistance is in ERROR. A/Kansas/05/2010 is SENSITIVE to oseltamivir and Zanamivir.
Yesterday the US CDC released two pandemic H1N1 sequences. Both were partial NA sequences (1386 BP) from original samples. One of the sequences, A/Kansas/05/2010, was tested for antiviral activity for oseltamivir (Tamiflu) and zamanivir (Relenza) and was resistant to both, representing the first pandemic influenza sequence reported to show resistance to Relenza, and the first sequence resistant to both FDA approved neuraminidase inhibitors. The NA sequence did not have H274Y, but did have two rare polymorphisms, S363N and I466M. The other sequence, A/Connecticut/23/2009, also had I466M, but antiviral resistance was not reported.
Relenza resistance has been previously reported in seasonal H1N1, but the responsible polymorphism, Q136K, was only detected in virus in culture. Sequencing of original samples failed to detect Q136K, suggesting it was either generated during viral isolation, or was at levels below detection in the original sample.
In contrast, I466M was in both original pandemic H1N1 samples and was also in an earlier isolate from Poland, A/Poland/37/2009, as well as a swine H1N1 isolate, A/swine/Germany-SN/siv-leipz6340/09. In addition to I466M, another change at the same position, I466V, has been reported in A/Guam/NHRC0023/2009 and A/Bayern/73/2009, as well as swine isolates, A/swine/Germany-NW/IDT2884/04 and A/swine/Greven/IDT2889/2004.
These changes at NA position 466 (467 in N1 numbering) raise concerns that XDR (eXtensive Drug Resistant) strains of H1N1 are emerging in human pandemic as well as swine sequences.
More information on the quantitative aspects of the resistance is useful, as well as the resistance results for A/Connecticut/23/2009.
Additional NA sequences from isolates represented in Genbank and GISAID databases, as well as HA and MP sequences from the above isolates from Kansas and Connecticut would also be useful.