A Mathematical Model of Avian Influenza for Poultry Farm and its Stability Analysis

This paper aims to estimate the basic reproduction number for Avian Influenza outbreak in local and global poultry industries. In this concern, we apply the SEIAVR compartmental model which is developed based on the well-known SEIR model. The SEIAVR model provides the mathematical formulations of the basic reproduction number, final size relationship and a relationship between these two phenomena. The developed model Equations are solved numerically with the help of Range-Kutta method and the values of initial parameters are taken from the several literatures and reports. The calculated result of basic reproduction number shows that it is locally and globally stable if it is less than and greater than one at disease free equilibrium and at endemic equilibrium, respectively. Furthermore, we have compared among the calculated susceptive, expose, infective, removal, virus and asymptotic compartments where infection rate and expose period are observed very sensitive compared to other parameters. In addition, the model result of infective is compared with the field data and other’s model where the present model shows good performance against the field data

Investigating alternative AUG codon usage in avian influenza A virus segment 2

Influenza A viruses (IAVs) have a segmented, negative sense RNA genome. PB1-F2 is an IAV accessory protein encoded by segment 2, in the +1 reading frame. Avian IAVs predominantly encode full length PB1-F2s, whereas human IAVs often have stop codons resulting in C-terminus truncations or ablation of PB1-F2 expression. One reported function of PB1-F2 is innate immune antagonism, which requires C-terminal motifs. Full length PB1-F2 is translated from AUG 4 of segment two, however there are often one or more in frame downstream AUGs (AUGs 7, 8, or 9). Although there have been previous reports of expression from AUGs 7-9, no one has matched a protein product to a specific AUG codon. There have also been reports of an increase in N-terminal truncations of PB1-F2 in recent years. The aim of this PhD was to assess AUG 7-9 usage and possible phenotypes of the products, and assess whether the increase in N-terminal truncations allowed continued expression of possibly functional C-terminal fragments. Bioinformatic analysis of avian IAV segment 2 sequences indicates conservation of open reading frames encoding the PB1-F2 C-terminus, particularly in domestic birds, despite some subtypes acquiring N-terminal stop codons that persist through several years. Conservation of the C-terminus from AUGs 7 and 9 leads to the hypothesis that these serve as independent initiation codons for the C-terminus. C-terminal fragment expression from specific AUG codons has been shown in 293T cells using tagged proteins. Persistence of N-terminal truncations suggests that only producing C-terminal fragments has no detrimental effects on the virus. This could be a method of host-specific adaptation of the virus. Segment 2 mutants were generated in an avian H5N1 IAV background, which differed in the presence or absence of the AUG start codons or stop codon positions in PB1-F2. Significant differences in viral polymerase activity, measured using mini-replicon assays in avian cells, were observed for some stop codons, but none of the AUG mutants. It was also found that any C-terminal expression of PB1-F2 is sufficient to antagonise the poly(I:C) induced IFN response in avian cells, raising questions on the true minimal requirements for PB1-F2 function. Annotation of segment 2 sequences may need to be adapted to account for continued expression of C-terminal fragments from sequences with an N-terminal truncation