Saturday, May 18, 2013

CDC: Genetic Evolution Of The H7N9 Virus

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Credit NIAID

 

 

# 7289

 

Prior to the industrial revolution, everything built by man was pretty much made in a custom, one-off fashion. You hired an artisan or tradesman who worked (often alone) on a project until it was completed.  

 

It wasn’t until the idea came along of creating interchangeable parts – identical sub-components that can be used to to construct larger items – that the efficiencies of assembly line manufacturing were realized.

 

While a relatively new invention of humans, this is variation of something that influenza A viruses have been doing quite successfully for a very long time.

 

Influenza A viruses have 8 gene segments (PB2, PB1, PA, HA, NP, NA, M1, M2, NS1, NS2) that are largely interchangeable. Meaning that – under the `right conditions’ - any two strains can potentially produce 256 different combinations (2^8).

 

And within each of these combinations can be countless minor variants.

 

The operative phrase here is `under the right conditions’. Most of these potential combinations are unlikely to ever evolve, much less thrive, in the wild.

 

 

For swapping of gene segments to occur (known as Reassortment or Shift), two different influenza A strains must infect the same host at the same time.

 

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Although a rare occurrence, with hundreds of millions of influenza infections every year, it happens often enough in human and non-human hosts to allow for occasional hybrids to emerge (see An Influenza Double Whammy  & EID Journal: Co-Infection By Influenza Strains).

 

We know reassortments like this can happen, but it obviously doesn’t happen often, or all that readily, else we’d be hip deep in reassorted flu viruses all the time.

 

Luckily, most of these reassortant viruses turn out to be evolutionary dead ends; less able to replicate, spread, and compete than were their parental contributors.

 

Most hybrids die out unnoticed within the host in which they were generated, smothered by millions of more `biologically fit’ viruses.  

 

Only rarely does a successful reassortment appear. But when one does, it can be a game changer.

 

For a good, short, video presentation on how reassortment works you may wish to revisit NIAID Video: How Influenza Pandemics Occur.

 

Yesterday the CDC posted the following graphic that shows the evolutionary (reassortant) steps they believe led to the creation of the new H7N9 virus in China.

 

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The eight genes of the H7N9 virus are closely related to avian influenza viruses found in domestic ducks, wild birds and domestic poultry in Asia. The virus likely emerged from “reassortment,” a process in which two or more influenza viruses co-infect a single host and exchange genes.

 

This can result in the creation of a new influenza virus. Experts think multiple reassortment events led to the creation of the H7N9 virus. These events may have occurred in habitats shared by wild and domestic birds and/or in live bird/poultry markets, where different species of birds are bought and sold for food.

 

As the above diagram shows, the H7N9 virus likely obtained its HA (hemagglutinin) gene from domestic ducks, its NA (neuraminidase) gene from wild birds, and its six remaining genes from multiple related H9N2 influenza viruses in domestic poultry.

 

While this may help us understand where the H7N9 virus came from, the big mystery remains; in what host species is this virus circulating, and occasionally jumping to humans? 

 

While poultry are often mentioned, only a small handful of of the tens of thousands of samples taken from market and farm birds, and their environment, have tested positive for the virus.

 

For more on the topic of influenza reassortment, you may wish to revisit:

 

Because, Sometimes Shift Happens

EID Journal: Predicting Hotspots for Influenza Virus Reassortment

Professor Peter Doherty On Bird Flu

PNAS: Reassortment Potential Of Avian H9N2