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BMC Biology: Q&A On What’s New With H1N1

 

 

 

# 4988

 


After wading through a number of pseudo-scientific and  often misleading media reports over the weekend it is refreshing to find an overview of the (former) pandemic H1N1 virus that is devoid of unbridled hyperbole and supposition.

 

It appears in the open access journal BMC Journal  Biology, and quite capably (and mostly in layman’s language) brings us up to date on what we know about last year’s pandemic virus.

 

The article is comprised of 12 questions and answers.  Among the items covered you’ll find:

 

The World Health Organization has announced the end of the (H1N1) influenza A (H1N1) pandemic - what does this mean?
Does this mean that the pandemic H1N1 influenza virus is no longer a threat?
Is there any sign of reassortment between different viruses?
What about antigenic drift?
Are there any new clues to why susceptibility was so high, especially among younger people, in the first place?

 

This report’s authors hail from such respected institutions as the Department of Microbiology and Immunology, The University of Melbourne – the Department of Immunology, St Jude Children's Research Hospital – and the WHO Collaborating Centre for Reference and Research on Influenza.

 

I’ve excerpted one section below (slightly reparagraphed to improve readability), so follow the link below to read this article in its entirety.

 

Personally, I’m saving this one to my desktop for future reference.

 

 

Q&A: H1N1 pandemic influenza - what's new?

Stephen J Turner , Peter C Doherty and Anne Kelso

Does this mean that the pandemic H1N1 influenza virus is no longer a threat?

Not necessarily, not altogether. Several features of this virus are a continued cause for concern; for example, most hospitalizations and deaths are still in those under 60 years old. This is probably because people in this age group are less likely to be immune.

 

Furthermore, of those people admitted to hospital in the USA with confirmed influenza (H1N1) 2009 pneumonia, almost two-thirds end up in intensive care. Recent clinical studies have identified risk factors for severe disease that include, but are not limited to, obesity, cardiovascular disease and pregnancy.

 

Importantly, however, about one-third of those who have died with (H1N1) 2009 lacked any known risk factors [1].

 

It is also of concern that the human influenza (H1N1) 2009 virus can be found in limited instances within pig populations, the species from which it emerged [2]. This increases the opportunity for the virus to reassort with other avian and swine viruses to produce new influenza strains of unpredictable transmissibility and virulence [3]. (Figure 1 illustrates schematically how new pandemic influenza viruses are thought to arise.)

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Figure 1. Mutation and reassortment giving rise to antigenic drift and antigenic shift in different hosts of influenza virus. The surface hemagglutinin and neuraminidase molecules (blue) of influenza viruses, which play an essential part in viral recognition of and entry into host cells, undergo frequent mutation (antigenic drift) in their human hosts, giving rise to new variants (red dots) that can elude antibodies made in many individuals against the parent virus.

 

Less frequently, entire segments of the eight-segment genome of an avian influenza virus and a human virus become reassorted into the same virion, usually through infection of swine by both viruses, and this can result in a virus that is still adapted to infect humans but expresses an avian hemagglutinin or neuraminidase (antigenic shift) to which there is no prior immunity in human populations. These give rise periodically to pandemics. Figure reproduced with permission from Figure 10-17 of: DeFranco AL, et al. 2007 [24].


 

Nicely done, and highly recommended.

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