We’d better start evolving our vaccination practices too…

A January post on one of my favourite science blogs raised an interesting question about vaccination as selective pressure. As part of her highly recommended “Viruses are Cool” series, Mad Hatter discussed a potential universal flu vaccine that should be effective against multiple strains of the virus, removing the need for annual shots against the strain that is most likely to cause problems in a given year.
The downside is that immunising everyone with the universal strain might put pressure on the targeted viral protein to evolve into a form that can evade the host’s vaccine-stimulated antibodies.

I left a comment on the post saying the following:
“I don’t know much about immunisation – would pre-existing immunity against the virus be as strong a selective pressure as, say, an antibiotic would be against bacteria? I’m thinking that if the infection can’t even get started then there might not be enough rounds of viral replication for new mutations to appear very often, whereas antibiotics are usually introduced once the infection is already established and replication is in full swing.”
Mad Hatter replied:
“I’m no expert on immunization either, but viruses might be able to replicate for a few cycles in some immunized individuals. It’s entirely possible people who have had the flu shot still get infected at a cellular level, but the infection is subclinical or asymptomatic. And for the small RNA viruses, one round of replication may be enough to produce a huge viral mutant repertoire.”
(Sorry for the bulk copy and pasting, it’s all relevant, honest!).
Well, a paper just came out in Virology Journal, entitled Avian influenza: genetic evolution under vaccination pressure. As you might expect from the title, the paper demonstrates that the avian flu virus does indeed evolve in vaccinated populations, and will provide a basis for the kind of studies that might answer the questions that Mad Hatter and I discussed.
Magdalena Escorcia and colleagues from around Mexico and the US isolated flu virus from chickens that had been vaccinated under the the Mexican government’s 14-year old avian influenza vaccination programme, but that were nonetheless displaying some signs of infection. The vaccine strain was derived from the most common variant infecting chickens in 1994, and the same viral strain has been used to vaccinate birds ever since.
The authors found considerable variation in the sequences of the isolated virus – namely between 0.4 and 13.2% nucleotide difference from the vaccine strain. Strains isolated in the same year tended to cluster together, as expected if the virus constantly evolves.
So I guess Mad Hatter was right – viruses must be able to replicate, and therefore accumulate mutations, to some limited extent in immunised individuals. This has important consequences for vaccination programmes and probably explains the apparent increase in flu symptoms observed in the Mexican poultry industry. Perhaps a new vaccine will be required soon.
I hope the people who are coordinating our protection against avian flu are paying attention…

About Cath@VWXYNot?

"one of the sillier science bloggers [...] I thought I should give a warning to the more staid members of the community." - Bob O'Hara, December 2010
This entry was posted in Uncategorized. Bookmark the permalink.

7 Responses to We’d better start evolving our vaccination practices too…

  1. Mad Hatter says:

    Thanks for the link and free publicity–I’m very flattered! For all the sophistication of the immune system, viruses are simply more nimble and adaptable than we are. Of course, that’s part of why they’re so interesting. Looking forward to reading more of your posts.

  2. Cath Ennis says:

    Thanks mate!

  3. NORMAN SMITH says:

    Niacin stimulates PPAR lipid metabolism to increase HDL. Over-expressing PPAR will shift catbolism to increase apolipoprotein release. Dendrite cell and macrophage cells will release more apoE into the enviroment. Infected non-reactive TC will overcome the suppressive viral activities to increase its apoE level. Apolipoprotein-E binds exogenous lipid complex and present the complex within endocytic compartment to CD1d molecules. The CD1d-lipid antigen complex interact with NKT-TC to trigger a systemic immune response. Any chronic immune response can be converted to an active adaptive immune response by increase the level of apolipoprotein E. This approach using niacin to promote apo-E should be benefitical for AD to restore appropiate distribution of apolipoprotein E,A.

  4. Cath Ennis says:

    Erm… OK then.

  5. Åsa Karlström says:

    Cath> In general influenza, and other viruses too, mutate easily since you have many possibilities since the cells replicate so many copies. There has been studies regarding the amount of mutations you get from infections of one type of influenza strain into cells… I’ll see if I can dig up the reference.
    Regarding what you said here> I’m thinking that if the infection can’t even get started then there might not be enough rounds of viral replication for new mutations to appear very often, whereas antibiotics are usually introduced once the infection is already established and replication is in full swing
    I’m not sure if you are advocating the if we used antibiotics in “preventive” medicine, that we wouldn’t get sick? I wouldn’t place my bets on that since bacteria would most likely pick u[ the resistance gene faster then something… Not to mention you would have a bad stomach in no time. And maybe fungi infections – in the world of “you’ll have something on the surface whereyou have good bacteria today”.
    The idea of preventing the virus from infecting and replicate is used when one talks about taking antivirals^, when you think you might have been exposed to say bird flu.
    ^ amantadine/ rimantadine hinders access to cells, uptake.
    ^^ zanamivir/ oseltamivir are two other antiviral drugs – Tamiflu – that hinders the release of virus particles from the cells…

  6. Åsa Karlström says:

    Interesting blog post and discussion though. Should’ve said so 😉 Good post about science.
    I’ll think a bit about that immunity/vaccination….

  7. Cath Ennis says:

    There’s life in this old thread yet!
    Don’t worry, I was definitely not advocating prophylactic antibiotic use! I was just pondering (On Mad Hatter’s original post) on the differences between antibiotic use and vaccination, and on how the way we use these tools might affect their potency as selective pressures. Then reading the paper I linked to here helped to clarify those thoughts in my mind. It was nice to spot this paper so soon after having the original discussion about the same topic! Science really is awesome sometimes.

Comments are closed.