All The (Incredibly) Small Things

Last week felt oddly empty. Maybe it was because I wasn't in the lab, or that I wasn't constantly thinking of (hopefully) funny things to put into my blog. (Or maybe, I actually missed blogging in general. What a weird concept to think about.) Either way, my break was relaxing. Mentally, at least. It was pretty physically challenging with soccer games, so I suppose these balance each other out.

On a separate - but not any less important - topic, the decisions are coming, the decisions are coming! I'd like to thank all the "reach" schools I applied to for waiting until the last moment to release their decisions (some will be released as late as March 31st in the evening). I guess this is all a lesson in patience. 

Since not much new has happened, I've decided to go back to the basics for this blog post and describe how the influenza virus works. I don't claim to be an expert in this subject, so bear with me.

Sadly, I didn't draw this. (Surprising, right?)
 Credit to: http://www.nature.com/nbt/journal/v28/n3/fig_tab/nbt0310-239_F1.html

In replication, the virus first binds to a sialic acid-contating receptor on the host cell, which triggers the endocytosis of the virus. On a side note, do you recall that the types of the flu are labeled as HXNY, where X and Y are numbers? (If you didn't, now you do.) The "H" part of this - the hemagglutinin (HA) part - is responsible for the binding of the virus onto the host cell. There are around 18 known variations of the HA, although only a few, such as H 1, 2, and 3, are common in humans.

Once the virus is engulfed, it's inside an endosome that has a pH of about 5 or 6. Because of this low pH, the M2 channels in the virus allow protons to enter the virus, which then changes the virus's conformation, essentially activating it. This is the step that my lab is trying to prevent. Block the M2 channels, block the proton uptake - and therefore block viral replication. (In theory, anyways.)

The pH also allows the virus to release its eight single-stranded "negative-sense" RNA into the cytoplasm and, eventually, nucleus. In this stage, new HAs can be formed when two different strands of the influenza virus, such as a human and avian strand, infect the same host. The RNAs are mixed, and the viruses that are produced contain RNA from both sources. The "negative-sense" means that the RNA cannot be directly made into proteins; first, it must be translated into "positive-sense" RNA. (At least this naming makes sense.)

The host cell makes more "negative-sense" viral RNA. The virus even prevents the host cell from making its regular mRNA, so the host cell is basically converted into a virus-producing factory for the rest of its short lifespan. After enough viruses are produced, the cell breaks down. Poor cell.

Viruses are produced when they "bud" off of the host cell. In doing so, the RNA is enclosed in the host cell's membrane, along with the HAs and neuraminidases (NAs) - the "N" part of HXNY - that the host cell also produced. (You totally remembered these too, right?) After the "budding," the virus is still attached to the cell through the sialic acid. The NA cleaves the sialic acid, releasing the virus, which can then go on to infect more cells. (More viruses. Yay.)

And that's the process. Simple enough, right? If not, I'm always open for questions. In the meantime, good luck to anyone who's waiting for more college decisions!

Until next time!

- Lauren