No he encontrado ningún subforo en el que encaje mi artículo, por lo que lo dejo en la cafetería si a los admins no les importa

Aprovecho para comentar que estoy buscando a alguien que no le importe escribir unas líneas en mi blog, le estaría muy agradecido.
Gracias y un saludo.
An overview of source, mutations and vaccines of Pandemic H1N1/09 virus (by Caballero, A)
Spain was the first European country where a contagion case by the ‘Pandemic H1N1/09 virus’ occurred, on 26 April, 2009, and the second one with a confirmed case of decease, on 29 June. Despite the virus ‘only’ caused 271 deceases that year, it is important to stress that no vaccines existed previously and vaccination campaign did not begin until 16 November, moment that Spain was the second European country most affected by 88 deceases and more than a half of total contagions have already been produced. It is also necessary to mention that about 80% of deaths occurred for people less than 65 years old and median age was only around 44.5 years. With regard to the nearest source of H1N1 strain, coding genes for hemagglutinin, nucleoprotein, the two nonstructural and matrix proteins of ‘Classical swine H1N1’ lineage, both polymerase basic 1 and neuraminidase of ‘Human H3N2’, and polymerase basic 2 and acidic of an unknown avian recombined springing ‘Swine H3N2’. The reassortment between this last one and ‘Classical swine H1N1’ produced ‘Swine H1N2’ as a consequence, which finally joined to neuraminidase and the two matrix resultants of ‘Swine avian-like H1N1’ causing the concerning virus. In addition, asparagine amino acid conferred in position 31 of matrix 2 resistance to any antiviral of adamantane family.
According to a report from the Epidemiology National Centre dated on 28 December, the main mutation was D222E which aspartic acid amino acid of hemagglutinin turned to glutamic acid. Some studies point out that in this mutation, situated in the RBS within antigenic site Ca2, the extra carbon in the side chain of E222 makes the glutamate’s carboxyl group to move away from the RBS. Thus, E222 establish stable polar contacts through water-mediated hydrogen bonds with a close terminal mannose of glycosylations which came from site N87, being supported at the same time by van der Waals contacts with galactose from the receptor.[1] This rearrangement increases binding free energy of protein-ligand complexes and, from my point of view, the fact that the affinity of hemagglutinin to human cellular receptors is strengthened, produces consequently a raise of H1N1 infectivity which was the reason why, in this case, D222E was the most present in severe cases. To a lesser extent, the appearance of D222G mutation was confirmed where aspartic acid of hemagglutinin was replaced by glycine, therefore facilitating infection in the lower respiratory tract. In a more reduced group of cases, mutation H275Y occurred where histidine of neuraminidase was replaced by tyrosine, thereby producing resistance to Oseltamivir antiviral.
The European Commission authorized commercialization of Focetria and Pandemrix vaccines on 29 September, and Celvapan on 7 October. All of them are monovalent, composed of inactivated variants of 07/09 strain and elaborated through mock-up procedure from 1194/04 and 1203/04 H5N1 strains, respectively. Focetria is grown in embryonated eggs, it only includes X-181 superficial antigens and it is adjuvanted with MF59C.1 which is largely composed of squalene. Pandemrix is egg-based too, it is fractionated in X-179A superficial antigens as well as part of its nucleoprotein and matrix, and adjuvanted with AS03 which mainly consists of squalene and DL-α-tocoferol. Celvapan is propagated in vero cells culture, it posses the whole wild-type virus with superficial antigens and lipid or polysaccharide structures that facilitate its screening, and it lacks of adjuvant. The AEMPS licensed Panenza on 14 November, vaccine that has same features as Pandemrix but it has been developed from scratch, the amount of hemagglutinin is almost 5 times greater and it is not adjuvanted. Bearing in mind that recent studies indicate H1N1 mortality rates caused by respiratory pathologies could have been 10 times greater on average, I would argue that vaccination campaign of seasonal influenza should have started a couple of weeks before in order to advance H1N1 campaign to the beginning of November, especially for risk groups.
From the 40/13 week to the 20/14, H1N1 was the virus that produced the higher number of deceases, being a total of 175. History shows that rising of more pandemic viruses in future is unavoidable and, therefore, it seems to me that current research on cultivation of new H1N1 strains is on the right path, as long as biosafety level used is 4.
[1] Jiménez-Alberto A, Alvarado-Facundo E, Ribas-Aparicio RM, Castelán-Vega JA. ‘Analysis of Adaptation Mutants in the Hemagglutinin of the Influenza A(H1N1)pdm09 Virus’. PMC. 2013.
FUENTE: nsdsg.blogspot.com