Informatie h1n1 virus

From there it may finally have been introduced to the human population shortly before Regardless which of these interpretations is correct, the data imply that the pig is not only necessary for the creation of reassortants between avian and human influenza viruses, but also for the adaptation of avian influenza viruses to humans.

This indicates that the precursor of the pandemic virus of might have been a swine virus, which remained longer in the pig population than anticipated Rabadan et al.

This splitting-off must have occurred a very long time ago, since the RSCU signature of the PB1 gene is very different from that of the avian viruses, and it seems to have remained stable over a long time only a few changes over a period of 70 years.

These viruses seem to shift quite easily from pigs to birds. The domestic poultries e. According to the phylogenetic trees, the PB1 genes of the clade 2 viruses have undergone reassortment into the background of other avian viruses presumably from a precursor of the clade 1 viruses a long time ago, and have kept the corresponding RSCU signature almost unchanged. Our interpretation would imply that the human H1N1 virus lineage started shortly before by crossing the species barrier from pigs to humans, again with an avian virus as an ultimate precursor.

The evolutionary mechanisms that may have led to the creation of the specific pattern observed and the reason why this can only be detected so clearly in the PB1 gene remain unknown.

Given these patterns, there is a clear difference in the secondary RNA structure while the amino acid sequence is more or less preserved. Since the codon usage of Homo sapiens and Gallus gallus is very similar, there was apparently no need for adaptation to a different tRNA content when influenza viruses crossed the avian-human species barrier. Furthermore, the codon usage in the various genes of the same virus is quite different, e.

Altered codons may also result in the presence or absence of motifs for RNA methylation. Furthermore, a different secondary structure of mRNA caused by alternate codons results in a different local speed of protein synthesis and thereby causing altered protein folding Oresic and Shalloway, ; Komar et al. Assuming that the structural constrains of the PB1 gene are very tight, only a certain codon might be allowed at the respective position of avian versus human strains.

This may also explain the high evolutionary stability of this genetic pattern. Furthermore, selection of RNA segments for virus maturation might also depend on a specific secondary structure of the vRNA Noda et al. All in all, the issue of codon usage seems to be much more important at least for influenza viruses than previously thought.

In summary, our data supports the idea that the Spanish flu influenza virus was derived from a swine virus that itself might be a descendent of a distinct avian H1N1 virus.

What we can say for sure is that the H1N1 virus is not related to one of the known avian influenza strains, except the clade 1 viruses. A comprehensive list of all the sequences used is freely available upon request. All accession numbers Acc. No of the sequences of PB1 gene used in the RSCU analysis and of all eight gene segment sequences in the phylogenetic analyses were listed in the Supplemental Material Supplemental Table 2.

These most heterogeneous sequences were selected from different clades of avian isolates, e. Two methods were applied to estimate codon bias in influenza coding sequences: relative synonymous codon usage Sharp et al. RSCU is a simple method to calculate deviation from the expected random codon distribution that minimizes the bias from the amino acid composition. An RSCU value for a given codon is the observed frequency of that codon divided by the frequency expected under assumption of equal usage of the synonymous codons for a given amino acid and is calculated as follows:.

ENC was proposed by Wright and can be interpreted as the average homozygosity of codons used to code the same amino acid. However, the original Wright's has a major limitation, namely it assumes equal background nucleotide composition.

Since influenza genomes have biased nucleotide contribution, we calculated ENC values using Novembre's method. ENC values were calculated as follows:. The F value represents the average homozygosity for the k -fold degenerate codon group and is calculated according to the following formula:.

Please note that the ENC values range from 20 in only one codon is used for each amino acid to 61, when all codons are used equally. In-house software was developed in Java to calculate and graphically present codon usage bias.

Each of the eight genomic segments was anayzed separately. The aligned sequences were subjected to phylogenetic analysis using both distance and maximum likelihood methods. For the distance method, the neighbor-joining algorithm Saitou and Nei ; Tamura et al. The Tamura-Nei substitution model and maximum composite likelihood method were used to estimate evolutionary distances between sequences and the statistical significance of inferred branches was evaluated by bootstrap using replicas.

We would like to thank Dr. Webster, and J. Franks from the Division of Virology, St. Jude Children's Research Hospital, Memphis, TN, for the helpful discussions and suggestions, and for selecting some of the sequences of the various influenza virus strains. Furthermore, we would like to thank D. Demirov, M. Schmolke IMV , and G. Article published online ahead of print. National Center for Biotechnology Information , U.

Journal List RNA v. Christoph Scholtissek 3 St. Generally speaking, influenza viruses generate mutations by passing from one animal to another animal for several years and through virus replication in the animal host. These mutations are represented by changes in the nucleotides and amino acids found within influenza viruses. These small changes occur at a relatively stable rate in all influenza viruses. As a result, scientists can compare the number of mutations found within a new influenza virus with older, related influenza viruses to estimate the amount of time that it may have taken for one strain to evolve into a new strain of influenza virus.

Researchers at CDC used this molecular evolution method to determine that the H1N1 influenza virus likely evolved in nature — perhaps through circulation in an unknown animal host — for a number of years before being detected. Research so far suggests that the H1N1 influenza virus is changing at a normal rate as compared to other influenza viruses.

The H1N1 influenza virus does not have the adaptations that are typical of influenza viruses grown or created in laboratories. For example, the standard method of growing influenza virus in laboratories involves injecting the virus into fertilized chicken eggs. The H1N1 influenza virus lacks the properties associated with growth in eggs. Prior to the discovery of the H1N1 influenza virus, this particular combination of gene segments from North American and Eurasian swine had never been detected before in a single influenza virus and this new virus is different from the influenza viruses that normally circulate in North American and Eurasian pigs.

It is not known when reassortment occurred to create the H1N1 influenza virus. Testing of the virus suggests that this reassortment event may have occurred years prior to the first reports of H1N1 influenza infection in people.

Pigs can be infected by influenza viruses found in birds and other animals as well as people. They use a variety of different technologies, including:.

These include the vaccines produced by:. The H1N1 pandemic was caused by an influenza virus. Influenza viruses are part of the viral family Orthomyxoviridae.

Their genetic material consists of eight separate strands of RNA. How does this happen? Pigs can get several different types of influenza virus.

When this happens, the RNA strands from the different viruses can mix together through a process called reassortment. This can create a unique influenza virus, such as the H1N1 virus. Its genetic material consists of a single strand of RNA. In a study , researchers estimated that about , deaths occurred worldwide in the first 12 months of the H1N1 influenza pandemic.

COVID has caused significantly more deaths worldwide. Over , deaths have occurred in the United States. Pasien tersebut mengalami gagal napas lantaran infeksi paru-paru bagian bawah yang diakibatkan virus H1N1 pdm Dilansir dari cdc. Dapatkan informasi, inspirasi dan insight di email kamu. Daftarkan email. Virus ini terdeteksi pertama kali di Amerika Serikat dan menyebar dengan cepat ke seluruh dunia. Virus H1N1 mengandung kombinasi unik dari gen influenza yang sebelumnya tidak diidentifikasi pada hewan atau manusia.

Medio 12 April hingga 10 April , diperkirakan terdapat 60,8 juta kasus positif terpapar virus, CDC memperkirakan, Secara global, 80 persen dari kematian akibat virus H1N1 pdm09 diperkirakan terjadi pada orang berusia kurang dari 65 tahun. Hal ini sangat berbeda dari epidemi influenza musiman, di mana sekitar persen kematian diperkirakan terjadi pada orang berusia 65 tahun ke atas.

Pemberitaan November , menyebutkan, pandemi terjadi ketika virus influenza A muncul dapat menginfeksi orang dengan mudah dan menyebar dari orang ke orang dengan cara yang efisien dan berkelanjutan.

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