Viruses (Viri?) why so difficult?

Been wondering about this ol’ virus I been living with . . .

Science ain’t really my thang so I might have some of the facts mixed up.

Let’s start with my understanding of the topic so you folks can correct me if I’m starting out with bad info. I seem to remember from school that we don’t have any cures for any viral diseases/infection. Bacterial? We’ve got a lot of the bacterial problems taken care of, but viruses we just can’t seem to get around.

So, the question(s): First of all: Am I correct that there are no cures for any viral diseases/infections?

Why are viruses so much more difficult to figure out?

Once some genius figures out a cure for one virus, will all the other viruses fall like dominos?

Read all about it:


Viruses are more difficult than, say, bacteria to kill because whereas bacteria are complete living organisms with a metabolism and all sorts of balanced chemical reactions going on that can be interfered with, killing them… A virus is just a set of instructions on how to make more copies of itself(probably a bit of an oversimplification) - it has to hijack the internal machinery of a cell to reproduce; it isn’t really alive in every conventional sense of the word (or at least it isn’t until it inserts itself into one of your cells) and because it isn’t really alive that makes it particularly hard to kill.

Mangetout makes some good points: To put things bluntly, a virus is a bit of genetic material (DNA or RNA) wrapped in a protein shell. The protein can be relatively complex, but it’s nothing on the order of a living cell. It isn’t alive, which means it cannot metabolize food, react to stimuli, or self-repair. It also lacks a cellular structure and cannot reproduce without a host, but it can hijack a cell to reproduce copies of itself.

So, since it’s so simple, why can’t we develop drugs that simply rip the protien to shreds? Well, something that blunt would probably do a number on the host’s proteins. Reducing your patient to a slurry of simple carbon compounds isn’t a way to get repeat business. Why can’t we develop our own proteins that interfere with the virus’s reproductive mechanisms? Well, I think Interferon does just that. But it’s expensive, not completely effective, and we’re faced with a moving target: Viruses mutate at a rate only matched by similar vermin, such as spammers and computer crackers. To develop a drug that works against this year’s mix of flu viruses will do you next to no good against next year’s, and it will be powerless against the latest superstrain to come out of Asia.

That is why getting a flu shot every year is important: A flu shot isn’t a drug, but a mix of proteins culled from inactive (That which is dead cannot die.) viruses from that year’s mix of strains. Your immune system, effective machine it is (in most people), gets mug shots' of the proteins (in the form of T-cells) and puts out an APB’ for anything that looks like them (in the form of those T-cells glomming on to them and making them more visible to your white cells, which proceed to eat the whole package).

In this case, close enough can count: If your T-cells get 70% of the viruses in your body, you’ll feel much better for it (maybe you’ll get off with a slight runny nose and some minor fatigue). Which is why flu shots can frequently reduce the intensity and duration of the common cold: Apparently, the mix of flu viruses has something in common with the mix of cold virurses.

A magic bullet would be very nice and would make a lot of people very rich, but I just don’t see it coming out of current methods. The drug would have to be both highly specific and highly nonspecific, to both leave your own cells alone and to get all possible variations on the given virus. And curing one virus would not make it trivial to cure another, but it might be a crucial first dozen steps.

So, why are bacteria a solved problem? Well, they’re not. Certain strains of TB (tuberculosis), for example, have become all but immune to everything we have. Tetracycline, a very expensive and rarely-used drug, is the only weapon we have left against that scourge. Other infections have become superbugs, as they’re called, and are immune to 99% of all traditional antibiotics. So, how do antibiotics work and how do bugs become superbugs?

Basic antibiotics

Antibiotics hijack the cell’s reproductive machinery. They clog up the works so the cell can’t reproduce, and let the cell die on its own. It’s a miracle, in that it doesn’t affect us nearly as much (though stronger antibiotics can cause problems of their own) but ends infections in a rather clean way. Of course, their effectiveness is dependent upon how, exactly, the cells reproduce. Mutation can change that.

Bug and Superbug

To misquote Friedreich Nietzsche, Superbugs have “The Will to Mutate”: They’ve mutated into something most antibiotics aren’t effective against. Their reproductive machinery is so different from the average that the usual mainstays (penicillin, amoxicillin, etc.) won’t work. We need the heavy artillery to kill them, and we hope against hope that those drugs work. I’ve never heard of Tetracycline-resistant TB, but it’s certainly possible.

"Apres moi, le deluge"
–King Louis XIV, noted antibiotic. :wink:

So, how do superbugs get created? Misuse of antibiotics. Every time someone takes less than they should, or uses them as a remedy for something that isn’t bacterial, they kill the weak and leave the strong standing. The strong reproduce, and they are that much more resistant to that antibiotic in the future. If a member of a slightly resistant strain gets hit with a different drug that doesn’t wipe out its descendants, those offspring will have resistance to two forms of antibiotics. Don’t rinse, and repeat. Eventually, you end up with people home-growing their own bioweapons. There’s a lesson here: Use antibiotics wisely. Don’t take them as placebos, and don’t take them until you feel better.

Just to add: Yes, there are antiviral drugs out there. Herpes, HIV, influenza, and Hepatitis C are all targeted viruses for various drugs.

But as with antibiotics, we see side-effect, and the development of resistance.

Rabies can be cured post-infection with a vaccine, which is quite unusual. The reason being that normally, the virus stays in nerve cells, and doesn’t provoke an immune response. The vaccine “wakes up” the immune system, which can then clear the infection pretty easily.

Thanks, Smeghead! That was one of the things that made me wonder about this subject. Someone I know is currently taking the vaccine after being bitten by a bat carrying Rabies. Luckily, he thought quickly enough to kill the bat and take it for testing, so they could confirm and get him on it straight away.

Does that mean that companies are conducting research into similar cures for other nerve-cell-hiding viruses like cold sores and the nastier forms of herpes? I mention that particular virus as I’m guessing that one is fairly static unlike the mutating flu viruses mentioned by Derleth?

So why not start patients on the more powerful antibiotics to make sure to kill both the strong and the weak every time. (If the answer has to do with side effects, than start with the most powerful drug that still has mild side effects. I’ve personally never experienced any negative side effects from any antibiotic I’ve been on and I’m sure I’ve had some powerful ones in my life). Seems like simply using weaker ones will facillitate this Darwinistic nightmare. What if everyone took lots of really powerful antibiotics for some time, and we could somehow be sure that they all took the full amount? Couldn’t we wipe out a lot of harmful bateria? How naive exactly am I actually being?

There are already several anti-herpes drugs on the market that are quite effective, but they work on a different principle - they’re antiviral drugs, not vaccines. A vaccine, like the rabies vaccine, causes the body’s immune system to fight the infection, while an antiviral drug kills the virus directly.

Very, I’m afraid. The only reason for taking antibiotics is to stop an infection by pathogenic bacteria which are causing a significant problem. We’ve thousands of species of bacteria living in us doing us no harm, and many of them benefit us, and actually keep the pathogenic (harmful) ones in check just by occupying a niche the harmful ones would otherwise get into and cause illness.

Besides, the bad bacteria don’t reside just in the human body. They live in places like the dirt, hot tubs, plants, animals, etc etc. No way to knock them out.

And don’t think of antibiotics in terms of “strong” and “weak”. That’s not how they work. An antibiotic is either able to kill certain types of bacteria, or stop them from reproducing enough to halt and infection, or it isn’t. And bacteria are real good at evolving defense mechanisms to antibiotics, so the more we use them, the more the opportunity to develop resistance.

We need to use fewer antibiotics, not more.


Hey Moe,

One of the problems with this is that your body contains a whole host of symbiotic bacteria. One of the things these guys do is prevent the colonization of your body by pathogens. If you wiped all them out via antibiotics, your body would be a great target for pathogenic bacteria once you stopped taking the drugs.


Very naive. You probably haven’t had the real powerful ones because they require isolation and months of IV therapy. They also cost upwards of $125 per day (for instance 6 weeks of Vancomycin therapy in some cases of Methicillin Resistant Staph Aureus (MRSA)).

Vancomycin kills a lot of bacteria that are resistant to other antibiotics. But now there is a Vancomycin resistant enterococcus that doesn’t respond to much at all.

If everyone was taking the most powerful antibiotics, the most resistent strains would be selected for and the cheap antibiotics that work for most everyday infections wouldn’t work anymore.

If your doctor is up to date on susceptibilities and common pathogens then the antibiotics that he/she selects should be more than adequate to eradicate the offending organism. On the off chance you have a rare resistant organism, then the bug can be tested against several different medicines to see which ones it responds to and your treatment can be appropriately tailored.
On preview, I see that Qadqop and Apoptosis have also made valid points.

Mmm, intraveneous Vancomycin… diarrhea, bad taste in mouth, just can’t beat it for “Yep, I really WAS sick, boss.” Of course, the “Wake him up every couple hours to make sure he’s still alive.” regimen is a bit of an experience, too, and nothing completes that sent to the hospital with raging fever experience like the room-mate who decides to have a dementia episode at 3:00am.

(Small hospital, bed shortage…)

Anyway, to get onto topic, antiviral drugs generally work by hijacking the hijack. Acyclovir (anti-herpes agent), for example, is an analogue to a DNA base. It gets incorporated into the DNA and stops it from being further synthesized. The idea behind it is that viruses do a lot more DNA synthesis than our cells, so the intent is to trip the “runners” more than one trips the “walkers”.

Minor clarification, Derleth: the flu shot isn’t quite “that year’s mix of strains”.

It takes several months for the companies to manufacture the thousands of doses of flu shots needed each flu season, and only a few of the possible flu strains can be included in the shot.

So sometime last summer, the ‘flu experts’ got together and chose the half-dozen or so strains that they estimated were most likely to be the worst strains this coming flu season, and that’s what they put into this years’ flu shots. If they guess right, and get the worst ones, the flu shots are quite effective. But sometimes everyone is surprised, and a strain that was thought to be minor turns out the be the most widespead flu strain this year. In that case, the flu shots that year are ineffective, if you get exposed to that strain.

Luckily, the ‘flu experts’ are getting pretty good at predicting which strains will be worst each coming year. And the drug companies are getting faster at producing doses of flu shots, so the experts can watch a bit longer before choosing the strains to include in this years’ flu shots. Nowadays, it’s well worth getting the flu shot each year.

Thanks to all 3 who responded to my question, and sorry 'bout the hijack.

Of course, the problem with posting a long post is twofold: You risk shooting yourself in the foot, and you can never hit every possible interpretation of your text.

I posted a very long post, considering the forum and my level of knowledge, and I’m getting responses.

Of course, a select group of my compadres have fixed any of my errors. I’m sorry if I made a big mess (I don’t think I did).

I do have a question for Qadgop: If you cannot meaningfully classify antibiotics by strength, how do you account for the existence of certain antibiotics which both kill strains resistant to a variety of other antibiotics and cause fairly severe side effects in the user? I’m referring to the IV Vancomycin mentioned by USCDiver and Dogface, which seems to have side effects orders of magnitude more severe than anything I’ve used. So, are side effects truly unrelated to how effective the antibiotic is?

t-bonham: I knew they’d have to do some amount of prediction to generate the vaccines, but months in advance? You learn something every day. I hope the flu shot I plan to get tomorrow (the soonest I can bum one off my nurse friend ;)) will be a mix guided by a bit of effective ESP.

I think we’ll see a new generation of drugs to fight viruses in the near future because many virus structures are being solved via X-ray Crystallography (my field of study). I took a Computer-Based Drug Design class last year and it was amazing - basically we downloaded a structure (a coordinate file) for a protein from an online database, found the active site, marked several important groups (like H-bond donor, acceptor, hydrophobic pocket, pi-stacking interactions) and then scanned an online database of 90,000 drugs. The computer tried to fit every drug into the active site and the user could then browse the results. The drug could be tested and modified to fit more tightly into the pocket.

Here is a screenshot of the program Sybyl which we used in class. This is actually what I’d like to do one day, but I’m learning the Crystallography side first. I know there is at least one antiviral on the market which was completely designed on the computer (anti-influenza I think, starts with an R).

I’d like to say the days of viral infection is limited, but those suckers mutate at such a high rate that they can counter just about anything. Our only hope may be for the most virulent to just establish some sort of symbiosis with us, as seen with some viruses and bacteria already (cytomegalovirus, some herpes viruses like Kaposi’s Sarcoma, E.coli - lots of things that don’t usually attack us). It’s not usually to the virus’s advantage that it’s host die!

This doesn’t answer the question, but I wanted to add that I once heard an interview with a virologist and it was the most gripping thing I’d heard in ages. They’re such shifty little buggers! I mean, the viruses, not the folks who study them. Presumably.

Re: Vancomycin

I just wanna say … earlier this year, following major abdominal surgery, I had to have two five-day courses of IV Vancomycin, about two weeks apart, and the only side effect I suffered was extreme sleepiness. Apart from that I felt great, so it’s not always the horror story it’s made out to be. :slight_smile: