Well my ‘Weekend Nanotech’ post from last week was a little delayed this week, primarily due to this little guy here:
A Rhinovirus. Most commonly known as the causative virus of the ‘common cold’, rhinoviruses are found pretty much everywhere  decent hosts are. And yes, unfortunately that included me! That said, despite their small size these little ‘critters’ (pardon the affectionate language – I certainly don’t mean to diminish the havoc and pain these can cause!) are absolutely AMAZING. Lets take a step back for a moment and look at what these guys have to achieve in order to infect you. Firstly they have no host ‘reservior’ other than humans so in order to become infected you must be in direct contact with another infected individual or recently contaminated surface. Then, several hundred of their little, individual ‘virions’ must be transferred to your upper-respiratory tract, as this is the only place that these guys can infect (they have an upper reproductive temperature limit of 32 degrees Celsius whereas most lower respiratory tract pathogens have an upper limit of 37 degrees C). Once there however they immediately (within 15 mins!) begin to proliferate. First, they bind to one of the receptors that cells use to communicate (specifically ICAM-1), and then inject their RNA into the host cell, hijacking its replicative machinery and producing hundreds of copies of itself. These build up inside the cell until essentially no more can fit, at which point the cell ruptures, spewing its viral contents all over adjacent cells and repeating the cycle anew. Or at least that’s what would have happened if my body wasn’t just a little bit nanotechnologically awesome as well!
Conveniently for me, the human body is equipped with a host of immune responses, and the ones which fixed me up within a couple of days of infection were those pictured above: cells of the innate immune system. These cells provide a quick general response to infection – for viruses this involves the production of heaps of interferon, natural killer cells and consequently, a wicked fever. The interferon causes cells to temporarily limit RNA and DNA replication, slowing the proliferation of the virus. The natural killer cells act do exactly what their names suggest and kill any cells they detect are infected with a virus, and sweep up the remains into nice little ‘cellular rubbish bags’ to prevent the debris from infecting other cells. The fever increased my average body temperature further away from the temperature at which the virus was able to proliferate, halting replication and in some cases destroying the viral RNA. That’s not the complete story though, as this requires immune system cells to ‘recognise’ infected cells – no mean feat when you consider just how jam-packed cells are with ‘stuff’ and how small the viral RNA is!
The image above shows a single human cell, filled to the brim with organelles, cytoplasm, DNA, proteins and all manner of other stuff – and somehow in the midst of all this mess the human immune system has to detect a tiny signal for a viral RNA infection. Hence we have another whole branch of the immune system, the adaptive immune system, which is slower (for novel infections anyway) but far, FAR more powerful. It looks for small RNA segments or proteins that are only found in the specific virus that is currently infecting you (by a system of presentation) and uses these markers to determine which cells are infected or not, long before the cells begin producing new copies of the virus. The details of this are beautifully complex and effective, but the end result is my immune system killing of any cells with this rhinovirus in them and preventing any future infection by the same virus.
But that’s not the full story either! As rhinoviruses are constantly evolving (their replication is not perfect for this exact reason), each year the ‘common cold’ that flies around during winter is an ever-so-slightly different version of the rhinovirus, different enough so that my adaptive immune system can’t recognise it as the same virus that infected me during previous years (well it’s not really! It has changed quite a bit) and so the whole process repeats on an almost perfectly yearly cycle (for me anyway!). This is a big part of why viruses are so incredible to me, they evolve at an incredibly rate and are hugely successful at what they do! This rapid change is why we don’t have a vaccine for rhinoviruses yet (although there are several in development) because they just change to quickly for any vaccine to keep up with!
And one last point. This is one species, of one type of virus. There are about 300 billion individual virus particles in a single glass of seawater. If we stacked all the viruses in our oceans end-to-end, they would extend to our nearest neighbouring galaxies . So next time you’re i’ll, spare a though for precious little critters infecting you! They’re pretty awesome, and also terrifying for some of the smallest organisms on our planet 🙂
3) C. Suttle “Viruses in the Sea” Nature 437, 356-361(2005) http://www.nature.com/nature/journal/v437/n7057/abs/nature04160.html,