# How does virus mutation work?

**URL:** <https://boards.straightdope.com/t/how-does-virus-mutation-work/595234>\
**Category:** Factual Questions\
**Created:** [September 5, 2011, 4:39am UTC](https://boards.straightdope.com/t/how-does-virus-mutation-work/595234 "2011-09-05T04:39:38Z")\
**Posts on this page:** 9\
**Page:** 1

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**Author:** ![elfkin477](https://avatars.discourse-cdn.com/v4/letter/e/a9a28c/32.png) [@elfkin477](https://boards.straightdope.com/u/elfkin477)\
**Post date:** [September 5, 2011, 4:39am UTC](https://boards.straightdope.com/t/how-does-virus-mutation-work/595234/1 "2011-09-05T04:39:38Z")

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So…I finally got around to watching\*\* I Am Legend\*\* tonight (very like [The Last Man on Earth](http://en.wikipedia.org/wiki/The_Last_Man_on_Earth_(1964_film)) unsurprisingly since they share a source), and now I’m curious about how viruses mutate, sort of. More to the point, I want to know how a mutation becomes dominant.

Viruses occupy the gray area between living and non-living, so I’m not sure how their mutations work (or why. I haven’t quite wrapped my mind around why something that’s not alive is able to reproduce at all or what the point of them is). Does a virus after a mutation become the dominant strain of a virus because it somehow out-competes the original strain by replicating faster? Or do virus mutations spread by the mutated strain infecting the original and changing each…um, what’s the term for a single germ? and making all the originals like itself?

And is there any way we can force a mutation to spread? It seems like if it were possible, it’d be very beneficial to spread a “fixed” version a virus altered in a lab to make it benign or even helpful. You know, until it mutates again and causes us to become zombies or vampires.

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**Author:** ![Triskadecamus](https://avatars.discourse-cdn.com/v4/letter/t/b19c9b/32.png) [@Triskadecamus](https://boards.straightdope.com/u/Triskadecamus)\
**Post date:** [September 5, 2011, 4:58am UTC](https://boards.straightdope.com/t/how-does-virus-mutation-work/595234/2 "2011-09-05T04:58:38Z")

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Keep in mind that most viruses never replicate at all. They just sit around until they become food for something else. One in a large number, let’s just pick a billion, happens to have a chemical characteristic that lets it hook onto a live cell, and inject itself into the reproductive machinery of that cell. Now the cell starts making viral particles.

The thing is, it kinda sucks at it. So, most of what it makes is pretty much like the original successful virus, but a lot of it is mutants. Most of both fail to infect another cell. But, the original chemical plan was successful, and so most of the good, and nearly good viral particles have a better chance of being successful. However, it’s all pretty much a variable. So, the number of “strains” of the original virus increases.

Sometimes the new generations are more successful than the parent. Not often, and even then, not usually enough different to be considered a new disease. But, every now and then a new variant is significantly more virulent, or more toxic than its parent. Even worse, sometimes the variant is able to infect some species other than the one in which it was formed. That variant will be much more likely to increase its population because it has more “territory” in which to expand.

Over and over, you need to remind yourself that most of the time the result is . . . nothing at all. But, the successful virus replicates itself many thousands of times, so even a 99 percent failure rate ends up being a highly successful virus.

Combinations of these types of events include a virus which is mildly successful, and almost entirely nontoxic to its host. The population will increase much more than say, Ebola, because dead hosts travel a lot less. But this innocuous strain of virus is only innocuous right now. Since it replicates so unreliably, its chemical nature could become highly toxic to its usual host, or to a newly available host and it suddenly becomes a pandemic disease vector. That lasts until it infects all the available susceptible hosts, or fails to replicate well enough to do so.

Tris

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**Author:** ![Smeghead](https://avatars.discourse-cdn.com/v4/letter/s/f1d935/32.png) [@Smeghead](https://boards.straightdope.com/u/Smeghead)\
**Post date:** [September 5, 2011, 12:12pm UTC](https://boards.straightdope.com/t/how-does-virus-mutation-work/595234/3 "2011-09-05T12:12:20Z")

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It’s basic natural selection. If a new variant of a virus arises that is more easily spread, or more successful at getting into cells, or can reproduce faster, or reach a wider range of hosts, it’s going to spread and outcompete the old versions. Viruses don’t have the capability of “reprogramming” old viruses\*. By the same token, we can’t really make this process go artificially. The things that make a virus successful also tend to make it nasty for us. Vaccination could sort of be seen as an artificial version of it, I suppose. We do the spreading for the virus by injecting each other, and the new “successful” variant is one that gives us immunity without making us sick.

\*As in all of biology, it’s difficult to ever make a blanket statement without counter-examples coming to mind. Some viruses, with multiple genetic strands (sort of like different chromosomes), are able to mix and match strands between different strains if they coinfect the same host. This is where new flu strains often come from.

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**Author:** ![Vlad\_Igor](https://avatars.discourse-cdn.com/v4/letter/v/7feea3/32.png) [@Vlad\_Igor](https://boards.straightdope.com/u/Vlad_Igor)\
**Post date:** [September 5, 2011, 1:12pm UTC](https://boards.straightdope.com/t/how-does-virus-mutation-work/595234/4 "2011-09-05T13:12:43Z")

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I would question the definition of a successful virus. I have been taught that a successful virus is one that minimally impacts the host, thus making it more likely to be spread. An unsuccessful one kills the host before the host has a chance to make and spread the virus. Influenza would be an example of a successful virus, even though it causes morbidity and sometime mortality. Ebola virus would be an example of an unsuccessful virus, as it causes rapid (and gruesome) death before the human host can make many viral copies and spread them.

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**Author:** ![Arkcon](https://avatars.discourse-cdn.com/v4/letter/a/96bed5/32.png) [@Arkcon](https://boards.straightdope.com/u/Arkcon)\
**Post date:** [September 5, 2011, 5:28pm UTC](https://boards.straightdope.com/t/how-does-virus-mutation-work/595234/5 "2011-09-05T17:28:36Z")

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> [@elfkin477](#):
>
> Viruses occupy the gray area between living and non-living, so I’m not sure how their mutations work (or why. I haven’t quite wrapped my mind around why something that’s not alive is able to reproduce at all or what the point of them is). Does a virus after a mutation become the dominant strain of a virus

Let me just snip this bit here for you. It is valid to say that, for some definitions of the word, viruses aren’t “alive”, in that they don’t metabolize like cells do. However, once they’ve infected a host cell, their genetic material behaves the same that genetic material in a living things would. So you could say, they’re “alive” at that point, and undergo mutations, some advantageous, just like other living things.

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**Author:** ![ZenBeam](https://avatars.discourse-cdn.com/v4/letter/z/3ab097/32.png) [@ZenBeam](https://boards.straightdope.com/u/ZenBeam)\
**Post date:** [September 5, 2011, 6:38pm UTC](https://boards.straightdope.com/t/how-does-virus-mutation-work/595234/6 "2011-09-05T18:38:29Z")

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> [@elfkin477](#):
>
> And is there any way we can force a mutation to spread? It seems like if it were possible, it’d be very beneficial to spread a “fixed” version a virus altered in a lab to make it benign or even helpful. You know, until it mutates again and causes us to become zombies or vampires.

Well, you can weaken the virus so it’s benign, like you suggest, then get it to spread by injecting it into people, and call it a [vaccine](http://en.wikipedia.org/wiki/Vaccine#Types).

I think there’d be a danger in a live vaccine that you made beneficial and still allowed to spread naturally, that it could mutate again, as you mention, or cross with another variety.

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**Author:** ![WarmNPrickly](https://avatars.discourse-cdn.com/v4/letter/w/d78d45/32.png) [@WarmNPrickly](https://boards.straightdope.com/u/WarmNPrickly)\
**Post date:** [September 5, 2011, 7:41pm UTC](https://boards.straightdope.com/t/how-does-virus-mutation-work/595234/7 "2011-09-05T19:41:24Z")

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> [@Triskadecamus](#):
>
> Keep in mind that most viruses never replicate at all. They just sit around until they become food for something else. One in a large number, let’s just pick a billion, happens to have a chemical characteristic that lets it hook onto a live cell, and inject itself into the reproductive machinery of that cell. Now the cell starts making viral particles.

I’ve never heard this. Can you give me a cite? I’m not doubting you, I just don’t like to take the word of random strangers on the Internet for things that I find fascinating. I’d always assumed most viruses were considerably more successful than you are making out. The norwalk virus is supposedly infectious with doses as small as ten virus particles. That could easily be a major exception though.

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**Author:** ![DSeid](https://sea3.discourse-cdn.com/straightdope/user_avatar/boards.straightdope.com/dseid/32/20194_2.png) [@DSeid](https://boards.straightdope.com/u/DSeid)\
**Post date:** [September 5, 2011, 10:48pm UTC](https://boards.straightdope.com/t/how-does-virus-mutation-work/595234/8 "2011-09-05T22:48:51Z")

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From an evolutionary perspective an entity is “successful” if it can spread the most copies of its genetic material.

A virus is successful if it can reproduce many copies within the organism, get those copies to where they can spread to other organisms (such as upper airway, nasal secretions, stool, sexual secretions, etc.), while keeping the organism alive and about long enough to do that job well, and be able to evade the defenses of its current and its potential new hosts, which often means changing itself along the way. Those different needs sometimes conflict. Evading defenses and getting to where it can spread sometimes kills, or at least completely disables, a host … fine for the virus as long as it reproduced in the host enough, and spread to other hosts enough first.

As far as your concept goes, yes, some vaccines did that to some small degree. The oral polio vaccine was a live weakened virus which was capable of very limited transmission to others, hence when it was used it benefited not only the vaccinated individual but also some number of people around them. OTOH the potential to [mutate back](http://www.immunizationinfo.org/es/issues/vaccine-safety/post-polio-syndrome-vaccine-associated-paralytic-polio-and-poliomyelitis-elimi) into a neurovirulent form is very real and presents a need to switch to an killed (injectable) form for a period of time after wild polio appears to be eliminated.

> [@](#):
>
> Most people vaccinated against polio have no adverse reactions. But the oral vaccine containing live viruses that are weakened can cause vaccine-associated paralytic polio (VAPP) in a very small percentage of those immunized or their close contacts since vaccinated persons can spread the vaccine virus to others. Immunocompromised people can shed vaccine virus in their feces for many years, with the virus becoming neurovirulent (capable of causing paralysis). Oral vaccine polioviruses can also spread from person to person in communities with low immunization levels. … There are two types of polio vaccine, OPV, oral polio vaccine, and IPV, inactivated polio vaccine. Initially, OPV was preferred because by spreading in the community it helped to increase community immunity to polio. The rapid reduction of cases of polio worldwide has largely resulted from using OPV, because it is easy to use in mass campaigns, provides long-term immunity, and rapidly reduces the spread of the polioviruses when many in the community are immunized.2
> 
> However, about 1 out of 2.4 million doses of OPV distributed in the US, caused vaccine-associated paralytic polio (VAPP).3 This is because OPV contains live-attenuated viruses that sometimes become neurovirulent—cause paralysis—again.4 Immune-compromised people are at increased risk for VAPP and may shed neurovirulent viruses for years. Continuous circulation of OPV-derived viruses in populations with poor hygiene and low immunity levels can lead to rare outbreaks of polio.2
> 
> In the United States, a new polio vaccine schedule was recommended in 1997 using both IPV and OPV3. Then, in 2000, an all-IPV schedule was recommended.5 OPV is no longer recommended and is not available for routine use in the US, although it is widely used elsewhere.
> 
> OPV continues to be used in countries where polio infections still occur and may be used if there were to be an outbreak in the United States—as OPV is felt by many to be the preferred vaccine to contain an outbreak. The World Health Organization estimates between 250 and 500 cases of VAPP occur each year worldwide.6
> 
> Rarely, as vaccine virus has spread in some populations it has mutated to become more like wild polio viruses by being able to damage nerve tissue (this is called ‘circulating vaccine derived polio viruses’ (cVDPV)). Mass vaccination with OPV has eliminated cVDPV.
> 
> Recently an unimmunized child was reported from Minnesota with poliovirus infection. So far, three other unimmunized children in the same community have also been identified as being infected.7 The virus isolates have been determined to have been derived from an OPV strain, probably acquired from a traveler to a region where the OPV is still being used in an effort to eliminate poliomyelitis worldwide. Because the community where these infections were detected is under immunized, it remains to be determined how widespread the current outbreak is. Although none of these children have had paralytic illness, prior experience would suggest that these types of viruses have the potential for spread in the community and to cause paralytic illness.

(The mechanics of how different viruses change is a whole separate discussion … one that I suspect will come up as flu season comes along, but a different discussion I think.)

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**Author:** ![Triskadecamus](https://avatars.discourse-cdn.com/v4/letter/t/b19c9b/32.png) [@Triskadecamus](https://boards.straightdope.com/u/Triskadecamus)\
**Post date:** [September 6, 2011, 3:46am UTC](https://boards.straightdope.com/t/how-does-virus-mutation-work/595234/9 "2011-09-06T03:46:20Z")

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> [@WarmNPrickly](#):
>
> I’ve never heard this. Can you give me a cite? I’m not doubting you, I just don’t like to take the word of random strangers on the Internet for things that I find fascinating. I’d always assumed most viruses were considerably more successful than you are making out. The norwalk virus is supposedly infectious with doses as small as ten virus particles. That could easily be a major exception though.

I can’t remember a particular cite, but, keep in mind that the ten Norwalk virus particles that infect someone are the ones that were emitted by a prior host, transferred through air, or fluids, or surfaces, and then somehow incorporated into another organism, avoided the immune system of that organism, and successfully injected themselves into a cell. Now go back and consider, all the particles that never got emitted, got irradiated or oxidized while in the air, evaporated while in fluids, buried or otherwise destroyed on surfaces, were destroyed by the immune system of the potential host, or were bound chemically to a cell without the necessary receptor sites to allow entrance to the nucleus, and you can see even in the very virulent case where ten particles will produce the disease, a whole lot of particles did no such thing.

Tris
