Do we really need a new measles vaccine?

Measles, that deadly childhood infectious disease is almost a distant memory to most people nowadays, that is except for a few isolated outbreaks across the US and Europe. This is all because of a really amazing preventative therapy: the vaccine.

Vaccines are great. They are by far the most effective means that we have to control - and hopefully eradicate - infectious diseases from a range of species. Measles is one of these diseases that, over the last half a decade or so, we have backed into a corner across the world. Before the introduction of global immunisation the measles virus caused around 2.6 million deaths, most of which were children. To show just how great the vaccine is: 2008 saw only 164,000 deaths (see the WHO data here). A big number still but a 97% decrease in associated fatalities is pretty impressive, so why then - in an editorial piece in the esteemed journal Vaccine, are they calling for researchers to develop a new vaccine?

Certain strains put a strain on virus research

This is something I would like your input on: 

How important is strain choice in virus/microbiology research? 

Does it differ with certain aspects of research, like pathogenesis versus structural studies?

How far do we discount studies done on less 'wild-type' viruses?

How come people are happy working with these viruses?

We microbiologists uncover the secrets of how microbes interact with their hosts in order to better understand the infection process. We can use this knowledge to allow us to develop antiviral treatments, preventative vaccines and important applications for these molecular parasites, such as anti-cancer therapies.

All of this requires that we are studying what is real and what is actually going on in the world around us. This is all the more important when peoples lives depend on our work and when we are dependent on tax payers money to fund the research. Generally, this seems very obvious but you would be surprised about how much work is done on by far less-than-perfect viruses. This is because there a number of hurdles in the path of us understanding what is real-life.

Why you should be at this Spring's Society for General Microbiology conference in Dublin

From the 26th to the 29th of March this year, Dublin - the capital of the Republic of Ireland - will host the Spring conference of the Society for General Microbiology, the UK's (make that Europe's) major group for all things microbial. Most importantly, according to wikipedia it was founded in 1945 by none other than Alexander Fleming, plus the city is now becoming pretty cheap to live and stay in and has the best Guinness in the world - what more do you want from a science meeting?

Dublin at night -http://www.runawayjane.com/wp-content/uploads/2011/03/DublinRiverLiffey.jpg

Notes on a year in blogging

First, a little history about this blog - there's some comments from annual review below:

I was first exposed to world of blogging during my final year at university when a lecturer in a human genetics module suggested we took a look at one particular post regarding the sequencing of a genome belonging to an ancient human. This piece of writing was informative, entertaining and extremely relevant to what we were studying. This was a post on Ed Yong's, Not Exactly Rocket Science blog and it probably first set me off on wanting to write about science.

HIV restriction factor blocks respiratory viruses - but not how we thought

Measles virus - is it targeted by an HIV restriction factor?

Cellular organisms have evolved multiple defences to keep viruses and other genetic parasites at bay. One such shield is the development of an advanced adaptive immune system seen in vertebrates while another is the more evolutionary widespread 'innate' system made up of various expressed proteins and small RNAs. These molecules prevent particular stages of the viral replication cycle like entry, replication or exit. 

Another mechanism is to mutate the virus out of existence, i.e. change nucleotides throughout the viral genome so much so as to effectively knock-out that protein's function during infection and slow down replication so much so to allow your bodies' other defences to clear it. Since 2002 we have had tantalising clues that this is functioning during a viral infection, particular HIV and other retroviruses:

Isolation of a human gene that inhibits HIV-1 infection and is suppressed by the viral Vif protein.