hello
I work on the genetic and antigenic variability of influenza virus in swine. Is the observed variability be due to PCR or are they all real? Why do my MDCK cells and eggs are mainly used to isolate virus?
Can anyone explain the variability? Thanks
Influenza A is a Orthomyxovirus having 8 segments of RNA, from which 18 different types encoding for Hemagglutinines and 11 different neuraminidases are known for the moment (H and N external expressed antigens). Each strain only expresses one single type of H or N antigens. More than 20 combinations of both antigens are known for the moment. It seems that there are a certain specificity of antigens for particular hosts (human, horses, dogs), but the virus is extremely mutant and may easily make RNA recombination and making shifts and drifts in its genome, adapting to new hots. Pigs are considered “mixing vassels” (and Human too), because in circumstances when they are hosting two different strains of the virus, they generally recombine.
You may find very easily basic information on http://en.wikipedia.org/wiki/Influenza
Since Influenza A ("InA" for short) is a single stranded RNA virus (as Bernado said single copies of multiple viral SS chromosomes in each virion) its replication is a bit unique from what you likely know if cellular replication involving the typical DNA polymerases.
InA, because of its ssRNA genome, relies on an "RNA dependent RNA polymerase" to replicate the viral genome segments. In other words, the template for this RNA polymerase is ssRNA, the viral genome segments. Like most DNA polymerases you are likely familiar with, this RNA polymerase is error prone, incorporating mis-matches as it copies. Unlike most DNA polymerases you are likely familiar with, the InA version of this RNA polymerase has little or no "proof-reading function". This leads to spontaneous and somewhat random point mutations potentially being incorporated into each genome uniquely as the segment is being copied.
Because of this, each time a cell is infected a single point mutation may lead to a slightly different variant of one of the hemagglutinin or neuraminidase gene products presented on the surface.
If that point mutation leads to an amino acid change on a portion of the protein which had served as an epitope for antibody binding previously, that set of antibodies specific to that epitope may no longer be able to bind and neutralize the novel virions.
In this way, our immune system essentially selects for mutant variants which can no longer be recognized and neutralized by the current pool of antibodies being produced in the individual. Of course, a healthy immune system will hopefully respond and begin, within 7 to 10 days, producing a new set of antibodies to this novel antigenic epitope which has arisen.
........ and the same process repeats and continues.... as the virus 'adapts' to its ever adapting hosts.... thus Antigenic Drift occurs.
Antigenic Shift, which InA is also capable of, is an somewhat different process and if you want to know more about that, ask specifically and someone will likely respond.
I hope this helps. GDF
1 / I get to have the results of whole genome sequencing of different viral strains and I need to know the positions of the mutations and their kind, so is there a bioinformatics software to do this step and how I can the analyzed
2 / I am trying to construct phylogenetic trees for every gene of influenza virus, so my question is: is that the variability observed on the trees are all real or may be due to the PCR reaction (enzyme)
3 / I want to understand response and antibody epitope knowing that I will soon start a IHA test
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