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I have yet to understand why so many viruses or bacteria haven't evolved to be harmless (specifically, I don't know of any harmless virus). I think it would be greatly beneficial for a virus to control his population and use natural transfer channels that dont cause discomfort(like feces), since it would be allowed to stay in an organism indefinitely and would have a lifetime channel for transmission, hopefully getting to be the most common strain.

So, why have viruses not evolved to be harmless to their hosts?

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    $\begingroup$ Many are harmless. Some are not. They occupy different niches. If there are 6 billion humans, why would a virus care to take down a few? Plus, many don't kill, only harm. If the host lives, why would a parasite care if its host gets sick? $\endgroup$ – AliceD Dec 18 '15 at 22:22
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    $\begingroup$ This is a good question. I know at least some models of pathogen spread have a parameter for lethality of the virus, and high lethality decreases pathogen spread. Part of the answer could be that high infecitivty (pathogen spread, would be selected for) is associated with high lethality/morbidity (not necessarily beneficial for the pathogen per se) $\endgroup$ – C_Z_ Dec 18 '15 at 22:31
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    $\begingroup$ @Christiaan The parasite should care about the host getting sick because if so the host would evolve antibodies. Both could continue the biological arms race, but the side-channel of harmlessness seems pretty effective to me. $\endgroup$ – chubakueno Dec 18 '15 at 22:33
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    $\begingroup$ Although I still don't have a full answer, the wikipedia page on Optimal Virulence seems to be relevant: en.wikipedia.org/wiki/Optimal_virulence $\endgroup$ – C_Z_ Dec 19 '15 at 0:39
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    $\begingroup$ The post "why-do-parasites-sometimes-kill-their-hosts?" is very much related. $\endgroup$ – Remi.b Dec 19 '15 at 9:54
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There are actually many examples of viruses that have integrated into the human genome and were rendered harmless, perhaps even helpful.

This New Scientist article referencing this Nature article describes endogenous retroviruses, which are ancient viruses which have integrated into the human genome.

About 9 per cent of our genome is thought to have come about this way. Until recently, these viral relics were largely dismissed as inactive “junk” that ceased to have any impact on their host many thousands of years ago. The discovery that HERVK, the most recent ERV to make itself at home in our DNA – probably around 200,000 years ago – is active in human embryos challenges that notion.

Joanna Wysocka and her colleagues at Stanford University in California made the unexpected find while they were analysing gene activity in 3-day-old human embryos, which are bundles of eight cells. Besides DNA from the parents, they found genetic material from HERVK. “The cells were full of viral protein products, some of which had assembled to form viral-like particles,” says Wysocka.

Further experiments revealed that the virus appears to produce a protein that prevents other viruses penetrating the embryo, suggesting it protects the embryo from dangerous circulating viruses, such as influenza. It also seems to play a crucial role in the genetic activity of the embryonic cells, helping to genetic instructions to the cellular protein factories.

Additionally, the endosymbiotic theory is also another possible example. It is thought that mitochondria and chloroplasts are previously free-living, possibly parasitic organisms that ended up integrating into the host cell and living as an organelle.

In short, parasites absolutely can and do evolve into harmless versions of themselves. There are already discovered examples, and as the human genome is better understood, doubtlessly more would be discovered.

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    $\begingroup$ Chloroplasts and mitochondria are unlikely to have been parasitic. They are rather tamed preys captured by unicellular predators. $\endgroup$ – WYSIWYG Dec 19 '15 at 5:49
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    $\begingroup$ Why do you think so, @WYSIWYG? $\endgroup$ – Rodrigo Dec 21 '15 at 13:04
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Pathogens don't evolve to be harmless to their hosts, because that doesn't benefit the pathogen.

For example, think about a pathogen, like cholera, that spreads by fecal/oral contamination. How could it enhance its transmission? One obvious way is by increasing the amount of fecal contamination, which means causing diarrhea, which means harming the host.

Or think about a pathogen, like myxomavirus, that spreads via sand fleas. The fleas bite one rabbit, jump to a new one, and infect it. How could the virus enhance its transmission? It turns out that sand fleas don't bite dead rabbits, so viruses that kill their hosts immediately lose out. But on the other hand, perfectly healthy rabbits groom away the fleas, and those viruses lose out. The viruses that transmitted best made their hosts very, very sick, too sick to groom, for a long time, to maximize transmission.

Or think about a pathogen that's transmitted through saliva, like rabies. Maximizing the number of new hosts that get bitten, by damaging the brain, would help there.

There are generally balances for maximizing transmission. Sexually-transmitted pathogens might not make the host sick for a longer time. Respiratory agents might do better with hosts that can mingle more with potential new hosts, while fecal contamination doesn't need such a healthy host. But in general, pathogens evolve toward maximizing transmission, not host health.

(You may wonder why pathogens don't change their mode of transmission - why don't fecal transmitters evolve the ability to spread by respiratory transmission? The answer is generally the same as any other "Why doesn't X evolve Y?" questions -- because the path toward a new complex ability means going through a phase where the pathogen is not as good at either ability, and gets out-competed by its more traditional relatives.)

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    $\begingroup$ It doesn't follow that if pathogens (like all evolved organisms) maximise fitness, they would necessarily harm their hosts. Symbiosis is not a zero-sum game. If a pathogen evolved into a mutualistic relationship, they could maximise fitness of themselves along with their host. $\endgroup$ – March Ho Dec 19 '15 at 3:41
  • $\begingroup$ @MarchHo symbiosis actually is much more complicated than parasitism and involves an intricate genetic interaction. Pathogens usually have a reduced genome and to evolve into a harmless species they have to gain a function (which is more difficult than losing one). $\endgroup$ – WYSIWYG Dec 19 '15 at 5:45
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    $\begingroup$ @WYSIWYG Did you mean mutualism? Parasitism is a kind of symbiosis. $\endgroup$ – March Ho Dec 19 '15 at 6:22
  • $\begingroup$ @MarchHo yes mutualism. AFAIK parasitism is not included in symbiosis (only mutualism and commensalism are considered symbiosis). $\endgroup$ – WYSIWYG Dec 19 '15 at 6:55
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    $\begingroup$ @WYSIWYG This paper suggests that parasitism is also a kind of symbiosis, and that this definition is widely accepted in biology textbooks. $\endgroup$ – March Ho Dec 19 '15 at 7:18
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I think the key to your answer is in the word "parasite": parasitic relationships always involve the parasite taking something from its host, causing it some (possibly slight) amount of harm. Once the parasite has evolved to cause an insignificant amount of harm to its host, we no longer call their relationship "parasitism" but "commensalism".

There are lots of commensal bacteria -- you have more in and on your body right now than you have cells in your body -- and many of them may have evolved from parasites.

All viruses need to hijack cellular machinery, particularly the protein generation machinary, in order to reproduce themselves. So it's hard to imagine a commensal virus that doesn't harm the cell it uses to reproduce itself. As @March Ho pointed out, however, they might eventually become incorporated into their hosts' genome, potentially giving that host additional capabilities that it might not have otherwise possessed.

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Great question! Christiaan's comment is the best way to start thinking about this; why should the virus care? In other words, what determines the selection pressure to increase or reduce virulence?

The most common definition of virulence in ecology is the reduction in host fitness resulting from infection by a pathogen. If reductions in host fitness also reduce the probability of successful transmission then there is selective pressure on the virus to become less virulent. Conversely, if reductions in host fitness make no difference (or actively increase the likelihood of transmission) then there is no selective pressure to reduce virulence.

Consequences of pathogen infection which increase the likelihood of transmission via certain routes often reduce host fitness (the trade-off hypothesis). For example, diarrhoea increases the potential for faeco-oral transmission of the pathogen but increases the host's risk of death from dehydration. Differences in optimal virulence reflect differences in the degree to which host and pathogen fitness are correlated. If transmission is typically rapid and/or unrelated to host fitness then there is no selective pressure to reduce virulence.

As another simple illustration, a mosquito-transmitted pathogen that makes the vertebrate host sick (and thus less likely to react to mosquito feeding) will probably be transmitted more effectively, while one which makes the mosquito sick (and reduces its host-seeking frequency) will be transmitted less often. Vertically-transmitted viruses often become less virulent because host reproductive success and virus transmission are linked. This paper explores this theory with reference to a natural system (Plasmodium infection) and considers some implications that might not be immediately obvious, such as the consequences of better control via drug treatment etc.

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  • $\begingroup$ I'm not convinced it strengthens my answer much (if anyone thinks it does I can edit it in) but I happened to come across this reference today which mentions that in WNV-infected bird species viraemia mostly correlates with mortality (although with some exceptions): ncbi.nlm.nih.gov/pmc/articles/PMC3939481 $\endgroup$ – arboviral Apr 22 '16 at 15:42
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There is generally a pressure for parasites to be harmless towards their hosts (apart from the drain in resources), especially if those two species have co evolved for a long time.

This sets them apart from parasitoids. Though those terms are sometimes used interchangeably, a parasite requires its host to live on while a parasitoid aims to ultimately kill the host.

By far the most harmful parasites are those that did not co-evolve with their current host or ended up there by accident or in the wrong stages of their life cycle (for instance, the fish tapeworm in humans).

The same principle applies not only to parasitic animals but diseases in general, where most of the infections with the highest mortality rates are, at least initially, zoonotic in nature.

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    $\begingroup$ Welcome to BiologySE... we always appreciate references accompanying answers as well as questions. This is so others can read about and better understand what you are asking/saying. $\endgroup$ – Vance L Albaugh Apr 19 '16 at 19:20

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