Occasionally for my classwork I stumble across a project that contains information that I can share that people will care about. I mean, sure, I think making haploid fish is cool, but unless you're doing mutagenesis in zebrafish, the chance that you'll care about haploid fish is pretty slim. Flu though, I think everyone can relate to. I can relate to it, which was why I picked the topic, given that our theme for this quarter is host and pathogens interactions, which is so far from my area of interest (genetics / neuroscience) that it was hard to pick out something that won't lead to me banging my head against the desk over some aspect of immunology. (I'm terrible at immunology.)
So, the flu, also known as influenza, is a type of virus. I'll take another moment to broadcast the crusade that most of the people in the medical field have been engaged in for the past decade, which is "antibiotics don't work on cold / flu". Antibiotic is for bacterial infection. Cold and flu are caused by viruses. You need antivirals.
Given this is the case, you say, why aren't people just popping antivirals left and right every flu season? The answer to that is evolution, actually. A virus particle is mostly just a protein shell, which gets the virus in and out of cells, and protects the nucleic acid enclosed in that shell, which codes for the proteins. Influenza codes for 11 proteins. It's a small, simple system for a small simple organism, which means replication doesn't take that long. (We have gazillions of proteins and a cell cycle of around one replication per day, so starting from one cell it takes US a lot longer to procreate than a virus, which is much, much simpler than a cell, and much smaller (image: the small blob with the cheerios stuck on it is the virus, the ocean-covered mini-planet is your cell).
What does this mean? This means that a virus has no proof-reading mechanism or correction mechanism like we do, because it's so simple, which means each time it makes a copy of its genes to give to its progeny whatever mistake it made during copying is just going to get passed on. Take into account that a virus replicates extremely fast under optimal conditions (read: your cell), and that the location of the mistake is random, the chances that a random mistake will be a mistake that'll mutate the protein that our antiviral targets are pretty good.
While all this is happening, you have to wonder about our immune system. I mean it has to be pretty good, right? Because otherwise we wouldn't be here. We do have innate immunity that can recognize viral particles, namely the proteins exposed on the outside of a virus. If we develop antibodies against them, we won't get infected. If the virus somehow makes it past that stage (hey, innate immunity takes time to develop), we also have cell-mediated immunity, which can recognize proteins that will only be exposed once the virus has made its way into your cell (and shed the cheerios). If we develop antibodies against these, we can still get infected, but our symptoms will be less severe. Our cells will be able to clear the virus from themselves but they won't be able to prevent the initial infection.
(In case if you're curious, this is how flu shots work. There're two types of vaccines. One with killed viruses so your body gets a chance to be exposed to the viral proteins without being exposed to a live virus, so basically it'll have the time to come up with working antibodies without the risk of infection. However, the downside is, the virus is dead, which means when your body first sees it, it sees only the dead-virus-appearance and even though you won't get sick, you can still serve as a live incubator for virus. Or something. I'm a little shaky on the details on this one. The other type is the live virus vaccine, which means that yes your body gets to see a less virulent strain of the infective virus. It takes a bit longer for your body to cope with this one because it's a live virus and it does infect things a little, but it also means your body can go "ZMG VIRUS!" from the moment the real disease-causing-virus makes its way into your mucosal lining of your airway.)
And THEN you take into account that one of the antiviral targets we use is targeted against an exposed protein, neuroaminidase (needed for the baby viruses to bud from your cells so they can infect your other cells) (viruses like to share). Proteins exposed on the surface of a virus evolve extremely fast. That's why you have to get a flu shot every year. Both the immune system and the antivirals are essentially selecting for viruses with mistakes in their genes that allows them to not be killed by your immune system or your drugs. Which means that yes, we have viruses resistant to antivirals right now so we try to keep a lid on it by not using antivirals until we absolutely have to (decrease selection means that all viruses are created equal, and a smaller fraction of it will be antiviral resistant and so your immune system has a better chance to win against it) (as opposed to antiviral all the time which means all the non-resistant viruses will be killed off and the only viruses left will ALL be resistant). (By the way, this is another reason why med people get so pissed about people adding antibacterial drugs to practically everything; we're running out of working antibiotics, folks.)
Does that mean we're doomed? No. Our immune system is quite good if you consider humanity as a whole. Immune system of the host is constantly evolving to keep up with the pathogen; we have people who are naturally resistant to HIV. In addition, we are doing more research to find better targets for antivirals than just hemagglutinin and neuroaminidase (the two main protein exposed on the surface of viruses and the fastest evolving proteins) (random FYI: the names H5N1 and H1N1? Stands for Hemagglutinin class 5 Neuroaminidase class 1 -- their outer-shell is used as a way to classify viruses and does correlate with how infectious the virus is). I'll be doing a presentation the week after next week on a paper by Konig et. al, where they figured that since the virus proteins are changing so fast, why don't we target human cell machinery that the viruses steals to replicate with drugs instead? And they managed to find some targets that will not kill human cells (very important to check for, as I'm sure you'll understand) that if targeted, will reduce virus infectivity. Pretty cool, I think.
If anyone wants more information, PLoS (open-access to all) has a pretty decent review article here, called "Pandemic Influenza: the Inside Story". It's got relatively little tech-babble compared to the other stuff I've been reading.
And one last thing? After all this talk about no gold bullet for the flu, you know what's a tested and proven way of flu-prevention? Hygiene. Cover your mouth when you sneeze / cough, people! (And wash your hands...etc.) As someone who braves the public transit twice a day AND works in a biology lab, I'm at the point where I involuntarily flinch when someone sneezes on me. Vitamin C can also help a little by giving your immune system a little boost, but I've seen too many people randomly over-dose themselves on vitamins to feel comfortable endorsing it. It doesn't need endorsement.
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