MIT reveals the mechanism behind flu vaccine induced antigenic drift towards more infectious viruses

[Emily]

http://machineslikeus.com/news/stopping-influenza-evolution-it-starts

Stopping influenza evolution before it starts
Tuesday, 20 December 2011
by Anne Trafton
Story Source

An influenza strain. Image: Centers for Disease Control

Model of flu proteins suggests new way to design vaccines that slow mutations.

If you get vaccinated against the flu and then become infected with the virus, your body mounts an immune response that prevents you from getting sick. However, that pressure from the immune system can provoke the virus to mutate into a slightly different form ? one that could be more infectious....

 

[tetano]

Re: MIT reveals the mechanism behind flu vaccine induced antigenic drift towards more infectious viruses

Networks link antigenic and receptor-binding sites of influenza hemagglutinin: Mechanistic insight into fitter strain propagation


Venkataramanan Soundararajan,
Shu Zheng,
Neel Patel,
Ken Warnock,
Rahul Raman,
Ian A. Wilson,
S. Raguram,
V. Sasisekharan
& Ram Sasisekharan

Affiliations
Contributions
Corresponding author

Scientific Reports
1,
Article number:
200
doi:10.1038/srep00200

Received
26 July 2011
Accepted
09 November 2011
Published
19 December 2011


Influenza viral passaging through pre-vaccinated mice shows that emergent antigenic site mutations on the viral hemagglutinin (HA) impact host receptor-binding affinity and, therefore, the evolution of fitter influenza strains. To understand this phenomenon, we computed the Significant Interactions Network (SIN) for each residue and mapped the networks of antigenic site residues on a representative H1N1 HA. Specific antigenic site residues are ?linked? to receptor-binding site (RBS) residues via their SIN and mutations within ?RBS-linked? antigenic residues can significantly influence receptor-binding affinity by impacting the SIN of key RBS residues. In contrast, other antigenic site residues do not have such ?RBS-links? and do not impact receptor-binding affinity upon mutation. Thus, a potential mechanism emerges for how immunologic pressure on RBS-linked antigenic residues can contribute to evolution of fitter influenza strains by modulating the host receptor-binding affinity.

http://www.nature.com/srep/2011/111219/srep00200/full/srep00200.html