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.

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.

Viruses at the crossroads of infection

Last week I wrote about a recent paper showing that in some cases influenza viruses can escape from the lungs of an infected person; here, it makes it's way to the local lymph nodes by infecting your lung's sentinal immune cells, the dendritic cells. In this instance, this mechanism is probably being used by our own body's as a defence: by capturing influenza virus in the lung we can kick start our immune system by handing it directly to T and B cells within the lymph nodes. But it can also have deadly implication, especially considering that possibly every virus will have some run in with a dendritic cell during an infection.

**for a great discussion of what goes on inside lymph nodes during the induction of an immune response, see last weeks This Week in Virology**

Complicated diagram of the role of dendritic cells in the immune response. On the left, DC's grab antigen (for example a virus) and thus move into nearby lymph nodes. Here they present antigen to T cells ( or B cells). These cells leave the lymph nodes to hunt down their specific antigenic target (shown on the right here whether the T cells move into infected tissues. What DC's can also do is carry infectious viruses into the lymph nodes where they are free to replicate inside the dense population of T and B cells. http://www.biken.osaka-u.ac.jp/COE/eng/project/images/fig-hirata-jpg.jpg