Virulence-transmission trade-offs and population divergence in virulence
October 21, 2012 4:35 AM Subscribe
"Why do parasites harm their hosts? Conventional wisdom holds that because parasites depend on their hosts for survival and transmission, they should evolve to become benign, yet many parasites cause harm. Theory predicts that parasites could evolve virulence (i.e., parasite-induced reductions in host fitness) by balancing the transmission benefits of parasite replication with the costs of host death. This idea has led researchers to predict how human interventions—such as vaccines—may alter virulence evolution, yet empirical support is critically lacking." Two papers demonstrate empirical evidence for related models predicting the origin of virulence:
de Roode JC, Yates AJ, & Altizer S. 2007. Timing of transmission and the evolution of virulence of an insect virus. Proc. R. Soc. Lond. B 269(1496); 1161-1165.
de Roode JC, Yates AJ, & Altizer S. 2007. Timing of transmission and the evolution of virulence of an insect virus. Proc. R. Soc. Lond. B 269(1496); 1161-1165.
We used the nuclear polyhedrosis virus of the gypsy moth, Lymantria dispar, to investigate whether the timing of transmission influences the evolution of virulence. In theory, early transmission should favour rapid replication and increase virulence, while late transmission should favour slower replication and reduce virulence. We tested this prediction by subjecting one set of 10 virus lineages to early transmission (Early viruses) and another set to late transmission (Late viruses). Each lineage of virus underwent nine cycles of transmission. Virulence assays on these lineages indicated that viruses transmitted early were significantly more lethal than those transmitted late. Increased exploitation of the host appears to come at a cost, however. While Early viruses initially produced more progeny, Late viruses were ultimately more productive over the entire duration of the infection. These results illustrate fitness trade-offs associated with the evolution of virulence and indicate that milder viruses can obtain a numerical advantage when mild and harmful strains tend to infect separate hosts. [Full Text HTML] [Full Text PDF]Cooper VS, Reiskind MH, Miller JA, Shelton KA, Walther BA, Elkinton JS, & Ewald PW. 2002. Virulence-transmission trade-offs and population divergence in virulence in a naturally occurring butterfly parasite (PDF). PNAS 105(21); 7489-7494.
Why do parasites harm their hosts? Conventional wisdom holds that because parasites depend on their hosts for survival and transmission, they should evolve to become benign, yet many parasites cause harm. Theory predicts that parasites could evolve virulence (i.e., parasite-induced reductions in host fitness) by balancing the transmission benefits of parasite replication with the costs of host death. This idea has led researchers to predict how human interventions—such as vaccines—may alter virulence evolution, yet empirical support is critically lacking. We studied a protozoan parasite of monarch butterflies and found that higher levels of within-host replication resulted in both higher virulence and greater transmission, thus lending support to the idea that selection for parasite transmission can favor parasite genotypes that cause substantial harm. Parasite fitness was maximized at an intermediate level of parasite replication, beyond which the cost of increased host mortality outweighed the benefit of increased transmission. A separate experiment confirmed genetic relationships between parasite replication and virulence, and showed that parasite genotypes from two monarch populations caused different virulence. These results show that selection on parasite transmission can explain why parasites harm their hosts, and suggest that constraints imposed by host ecology can lead to population divergence in parasite virulence. [Abstract HTML] [Full Text PDF]
Kid Charlemagne, the thought occurs that intelligence may be a parasite that kills its host species.
posted by Malor at 6:03 AM on October 21, 2012 [10 favorites]
posted by Malor at 6:03 AM on October 21, 2012 [10 favorites]
"Isn't the problem with developing commensality, at some level, the same as the problem with developing sentience?"
I think this is really the take home message with these papers, that we can apply the same sort of thinking already used about the tradeoffs within r/K selection theory to these sorts of tradeoffs between commensalism and virulence. We can also then use this sort of model to make verifiable predictions. For example, before the advent of antibiotics, we lived with Staphylococcus aureus strains on our skin that existed in a complex mixture of commensal and virulent strategies, but antibiotics suddenly applied very strong selective pressure against any vaguely virulent strategy. Thus, following this model, the observed sudden decrease in both virulence and transmissibility of virulent strains makes a lot of sense. However, the sudden increase in both virulence and transmissibility of virulent strains that we've seen in multi-drug resistant (MRSA) strains also makes sense. Indeed, if you look back far enough in the literature all of the crazy new shit we are now seeing in MRSA strains all existed before the 30s.
For example, while the pyomyositis and necrotizing pneumonia we are now seeing is commonly associated with poverty, tropical climates and HIV, ie: things which didn't get much attention prior to 1935, it was described. (You'll need to wade your way past phrases like "Africans are not different from any other humans, however, ..." to page 1214) Until recently it would not be terribly remarkable, being easily addressed with a simple round of I.V. antibiotics.
I just found a reference in my Robbins Basic Pathology (8th ed.) which confirms that Staphylococcus aureus, as well as Klebsiella pneumoniae and Streptococcus pyogenes, has been implicated in causing necrotizing pneumonia since the turn of the century. Additionally, the PVL toxin which that first paper describes as now being found in pneumonia was initially discovered by Van deVelde in 1894 and was named after Sir Philip Noel Panton and Francis Valentine when they associated it with soft tissue infections in 1932. All of this makes logical sense anyhow, the mechanisms of antibiotic resistance are not associated with pathogenesis.
posted by Blasdelb at 6:24 AM on October 21, 2012 [2 favorites]
I think this is really the take home message with these papers, that we can apply the same sort of thinking already used about the tradeoffs within r/K selection theory to these sorts of tradeoffs between commensalism and virulence. We can also then use this sort of model to make verifiable predictions. For example, before the advent of antibiotics, we lived with Staphylococcus aureus strains on our skin that existed in a complex mixture of commensal and virulent strategies, but antibiotics suddenly applied very strong selective pressure against any vaguely virulent strategy. Thus, following this model, the observed sudden decrease in both virulence and transmissibility of virulent strains makes a lot of sense. However, the sudden increase in both virulence and transmissibility of virulent strains that we've seen in multi-drug resistant (MRSA) strains also makes sense. Indeed, if you look back far enough in the literature all of the crazy new shit we are now seeing in MRSA strains all existed before the 30s.
For example, while the pyomyositis and necrotizing pneumonia we are now seeing is commonly associated with poverty, tropical climates and HIV, ie: things which didn't get much attention prior to 1935, it was described. (You'll need to wade your way past phrases like "Africans are not different from any other humans, however, ..." to page 1214) Until recently it would not be terribly remarkable, being easily addressed with a simple round of I.V. antibiotics.
I just found a reference in my Robbins Basic Pathology (8th ed.) which confirms that Staphylococcus aureus, as well as Klebsiella pneumoniae and Streptococcus pyogenes, has been implicated in causing necrotizing pneumonia since the turn of the century. Additionally, the PVL toxin which that first paper describes as now being found in pneumonia was initially discovered by Van deVelde in 1894 and was named after Sir Philip Noel Panton and Francis Valentine when they associated it with soft tissue infections in 1932. All of this makes logical sense anyhow, the mechanisms of antibiotic resistance are not associated with pathogenesis.
posted by Blasdelb at 6:24 AM on October 21, 2012 [2 favorites]
Blasdelb, are you stalling on your thesis? This is the third mongo gigantic post in like a week.
posted by leotrotsky at 7:39 AM on October 21, 2012 [13 favorites]
posted by leotrotsky at 7:39 AM on October 21, 2012 [13 favorites]
Blasdelb can stall all they like, I'm LEARNING over here.
posted by The Whelk at 7:44 AM on October 21, 2012 [9 favorites]
posted by The Whelk at 7:44 AM on October 21, 2012 [9 favorites]
He or she isn't stalling. The thesis is titled "Measuring and predicting human vs. AI responses to exposure to new scientific findings using metafilter.com, reddit.com, 4chan.com/b/ and the IBM WATSON system."
posted by double block and bleed at 8:22 AM on October 21, 2012 [2 favorites]
posted by double block and bleed at 8:22 AM on October 21, 2012 [2 favorites]
"But once you learn the ways of these exotic parasites..
You'll see that independance is a bore..."
Dan Kahn and Painted Bird discuss toxiplasma and opther cunning parasites.
posted by zaelic at 8:24 AM on October 21, 2012 [1 favorite]
You'll see that independance is a bore..."
Dan Kahn and Painted Bird discuss toxiplasma and opther cunning parasites.
posted by zaelic at 8:24 AM on October 21, 2012 [1 favorite]
Nature doesn't care about the individual*. Reproduction must occur.
*But what about ME (and my parasites)? We are very special snowflakes!
posted by BlueHorse at 9:53 AM on October 21, 2012 [1 favorite]
*But what about ME (and my parasites)? We are very special snowflakes!
posted by BlueHorse at 9:53 AM on October 21, 2012 [1 favorite]
Maybe this is an obvious point, but some harm to hosts (e.g. diarrhea) gives a big advantage in transmissibility, right?
posted by msalt at 10:19 AM on October 21, 2012 [2 favorites]
posted by msalt at 10:19 AM on October 21, 2012 [2 favorites]
"Maybe this is an obvious point, but some harm to hosts (e.g. diarrhea) gives a big advantage in transmissibility, right?"
You've got it, this is exactly the point demonstrated empirically by these papers as a rule. That the harm caused to hosts, which is sub-optimal for the parasite, is a function of the parasite finding a new host. Such that, so long as the harm causes the parasite to spread effectively enough, it doesn't really matter how much harm is caused to the host - as the parasite will have already found new hosts. Similarly, commensal bacteria don't have nearly the same need to spread as parasitic ones, as they keep their hosts happy and alive. The spectrum can be seen as a tradeoff between two strategies, or of course a mix between the two. The symbiont can care little for its host and make as many infectious particles as possible at the host's expense, thus increasing virulence. In this strategy it doesn't matter so much that the host becomes quickly unsuitable because the parasite has already found replacement hosts sneezed on, or transmitted to, by the time that happens. Or it can do the opposite and try its best to reduce impact on the host, shed infectious particles slowly or even not at all, and thus not need to spread too quickly because it will last a while in each host. Commensal symbionts are at that end of the spectrum, and have become so adept at not fucking up their host as to actually benefit them in some way. On the other end are parasitoids. These are the parasites that not only fuck up their host in their race to infect as many more hosts as possible, but spend the majority of their life cycle doing so and ultimately sterilize or kill, and sometimes consume the host in the process. The Xenomorphs from the movie Alien are a beautiful example of a bunch of these sorts of parasitiod strategies, each inspired by real fucked up shit in nature.
Tomorrow's post will be a paper on a parasitoid creature that makes Xenomorphs seem like particularly trusting and cuddly hamsters, as well as the creatures they consume from the inside out, their parasites, and their parasites parasites.
posted by Blasdelb at 12:02 PM on October 21, 2012 [1 favorite]
You've got it, this is exactly the point demonstrated empirically by these papers as a rule. That the harm caused to hosts, which is sub-optimal for the parasite, is a function of the parasite finding a new host. Such that, so long as the harm causes the parasite to spread effectively enough, it doesn't really matter how much harm is caused to the host - as the parasite will have already found new hosts. Similarly, commensal bacteria don't have nearly the same need to spread as parasitic ones, as they keep their hosts happy and alive. The spectrum can be seen as a tradeoff between two strategies, or of course a mix between the two. The symbiont can care little for its host and make as many infectious particles as possible at the host's expense, thus increasing virulence. In this strategy it doesn't matter so much that the host becomes quickly unsuitable because the parasite has already found replacement hosts sneezed on, or transmitted to, by the time that happens. Or it can do the opposite and try its best to reduce impact on the host, shed infectious particles slowly or even not at all, and thus not need to spread too quickly because it will last a while in each host. Commensal symbionts are at that end of the spectrum, and have become so adept at not fucking up their host as to actually benefit them in some way. On the other end are parasitoids. These are the parasites that not only fuck up their host in their race to infect as many more hosts as possible, but spend the majority of their life cycle doing so and ultimately sterilize or kill, and sometimes consume the host in the process. The Xenomorphs from the movie Alien are a beautiful example of a bunch of these sorts of parasitiod strategies, each inspired by real fucked up shit in nature.
Tomorrow's post will be a paper on a parasitoid creature that makes Xenomorphs seem like particularly trusting and cuddly hamsters, as well as the creatures they consume from the inside out, their parasites, and their parasites parasites.
posted by Blasdelb at 12:02 PM on October 21, 2012 [1 favorite]
"Blasdelb, are you stalling on your thesis? This is the third mongo gigantic post in like a week."
No need to worry about my thesis, it's turned in, diploma acquired, and ACHIEVEMENT UNLOCKED. I've made five science posts along these lines in the last six days, you can follow them through a Tag I'm hoping to popularize: LinksToTheDamnPaper
posted by Blasdelb at 12:24 PM on October 21, 2012 [12 favorites]
No need to worry about my thesis, it's turned in, diploma acquired, and ACHIEVEMENT UNLOCKED. I've made five science posts along these lines in the last six days, you can follow them through a Tag I'm hoping to popularize: LinksToTheDamnPaper
posted by Blasdelb at 12:24 PM on October 21, 2012 [12 favorites]
The funny thing about MRSA (insofar as something so horrible can be funny) is that the virulence of some strains is due to genes acquired from bacteriophages. So the parasite of a parasite makes it a more harmful parasite—which is a humbling reminder that host-parasite interactions never operate in a vacuum. Selective pressures can come from many sources, and not all of them will be obvious or predictable.
posted by dephlogisticated at 12:33 PM on October 21, 2012
posted by dephlogisticated at 12:33 PM on October 21, 2012
To add clarity for the less sciencified,
Many strains of pathogenic S. aureus as well as the Jack in the Box E. coli O157:H7, Shigella, cholera, botulism, diphtheria, scarlet fever, and a whole bunch of described shrimp and insect diseases are associated with prophages. Essentially, all "live" phages can go through what is called a lytic life cycle when they infect a cell, shut down host metabolism and substitute their own, replicate their DNA, construct and pack viral particles, and then lyse the cell for the new particles to hunt for more cells. Some phages (known as temperate phages and somewhat analogous to retroviruses) can also go through a lysogenic life cycle where instead of shutting down the hosts metabolism, they insert their genomes into the host chromosome and wait. This creates what are call lysogens, sort of a phage/bacteria hybrid, where the phage hides and lets the host replicate it with its own chromosome when it divides. Now these temperate phages have an interest in their hosts doing well and sometimes have exotic genes, which get expressed independently of the host lethal ones, that often contribute to host success in weird situations, like pathogenesis. However, as the phages become more beneficial to their hosts the need for phage virulence decreases and they begin to lose the genes necessary to enact a lytic life cycle, and becoming what are often called cryptic prophages. These kinds of degraded helpful viruses are critical in evolution, more than 8% of the human genome is immediately recognizable as viral and undoubtedly most of it has at least distant viral origins.
posted by Blasdelb at 12:47 PM on October 21, 2012 [1 favorite]
Many strains of pathogenic S. aureus as well as the Jack in the Box E. coli O157:H7, Shigella, cholera, botulism, diphtheria, scarlet fever, and a whole bunch of described shrimp and insect diseases are associated with prophages. Essentially, all "live" phages can go through what is called a lytic life cycle when they infect a cell, shut down host metabolism and substitute their own, replicate their DNA, construct and pack viral particles, and then lyse the cell for the new particles to hunt for more cells. Some phages (known as temperate phages and somewhat analogous to retroviruses) can also go through a lysogenic life cycle where instead of shutting down the hosts metabolism, they insert their genomes into the host chromosome and wait. This creates what are call lysogens, sort of a phage/bacteria hybrid, where the phage hides and lets the host replicate it with its own chromosome when it divides. Now these temperate phages have an interest in their hosts doing well and sometimes have exotic genes, which get expressed independently of the host lethal ones, that often contribute to host success in weird situations, like pathogenesis. However, as the phages become more beneficial to their hosts the need for phage virulence decreases and they begin to lose the genes necessary to enact a lytic life cycle, and becoming what are often called cryptic prophages. These kinds of degraded helpful viruses are critical in evolution, more than 8% of the human genome is immediately recognizable as viral and undoubtedly most of it has at least distant viral origins.
posted by Blasdelb at 12:47 PM on October 21, 2012 [1 favorite]
I was thinking that the pressure of flu shots would select viruses that transmit before flu season, but it looks like they would have to evolve to being stable in hotter weather. Also the shots can protect over multiple years.
posted by saber_taylor at 1:13 PM on October 21, 2012
posted by saber_taylor at 1:13 PM on October 21, 2012
Man, bacterophage - lamdba are like perfect little infecting machines. They have the most brilliant DNA, you couldn't design it better (in my undereducated opinion. which reminds me, i should go read some textbooks for fun.)
Molecular biology. Fuck yeah.
posted by maryr at 2:57 PM on October 21, 2012
Molecular biology. Fuck yeah.
posted by maryr at 2:57 PM on October 21, 2012
Do viruses acquire genes from multicellular organisms? If so, I can't see any reason why these genes might not be inserted into other genomes, leading to what are effectively weird hybrids between species.
posted by Joe in Australia at 5:49 PM on October 21, 2012
posted by Joe in Australia at 5:49 PM on October 21, 2012
Joe in Australia: "Do viruses acquire genes from multicellular organisms? If so, I can't see any reason why these genes might not be inserted into other genomes, leading to what are effectively weird hybrids between species."
I'm not sure what the mechanism is, but there is evidence of horizontal gene transfer in multicellular organisms. Definitely in the case of bacteria, HGT is a confounding factor in phylogenetic analysis. (In English: it's harder to figure out how species are related, because there are random bits of genome that were transferred between otherwise unrelated individuals, not inherited.)
posted by vasi at 7:55 PM on October 21, 2012
I'm not sure what the mechanism is, but there is evidence of horizontal gene transfer in multicellular organisms. Definitely in the case of bacteria, HGT is a confounding factor in phylogenetic analysis. (In English: it's harder to figure out how species are related, because there are random bits of genome that were transferred between otherwise unrelated individuals, not inherited.)
posted by vasi at 7:55 PM on October 21, 2012
"Do viruses acquire genes from multicellular organisms? If so, I can't see any reason why these genes might not be inserted into other genomes, leading to what are effectively weird hybrids between species."
The rub with multicellular critters is that for the Horizontal Gene Transfer to last more than one generation, the virus would need to infect a germ-line cell, essentially a sperm or an egg, as the lineage of all of our other cells will die. As vasi mentions this has been seen, but it isn't a trivial effort.
posted by Blasdelb at 11:49 PM on October 21, 2012
The rub with multicellular critters is that for the Horizontal Gene Transfer to last more than one generation, the virus would need to infect a germ-line cell, essentially a sperm or an egg, as the lineage of all of our other cells will die. As vasi mentions this has been seen, but it isn't a trivial effort.
posted by Blasdelb at 11:49 PM on October 21, 2012
What if it infected an embryo?
posted by Joe in Australia at 3:07 AM on October 22, 2012
posted by Joe in Australia at 3:07 AM on October 22, 2012
"What if it infected an embryo?"
Depends, so long as stem cells that will grow up to be gametes are infected then the endogenous virus will be passed on to the gametes of the progeny, and those gametes' progeny. We have the remnants of this sort of thing happening all over our genome, they are called Endogenous Retroviruses (ERVs) and they are a facinating area of study.
posted by Blasdelb at 3:46 AM on October 22, 2012
Depends, so long as stem cells that will grow up to be gametes are infected then the endogenous virus will be passed on to the gametes of the progeny, and those gametes' progeny. We have the remnants of this sort of thing happening all over our genome, they are called Endogenous Retroviruses (ERVs) and they are a facinating area of study.
posted by Blasdelb at 3:46 AM on October 22, 2012
"Kid Charlemagne, the thought occurs that intelligence may be a parasite that kills its host species."
LOL
posted by Blasdelb at 5:41 AM on October 22, 2012
LOL
posted by Blasdelb at 5:41 AM on October 22, 2012
It seems to compel its host to spread it to others, before it kills them off. So pretty much, yeah.
posted by msalt at 8:44 AM on October 22, 2012
posted by msalt at 8:44 AM on October 22, 2012
I was thinking that the pressure of flu shots would select viruses that transmit before flu season...
The flu shot only targets a handful of viri, so it's only going to have that kind of selective pressure or the few that it targets. In the larger scheme of things it's going to mostly select for things that aren't the viri in this years formulation. The big issue with the flu vaccine is guessing right which are going to be the problem strains in the comming year. Sometimes they get it right, and sometimes not.
posted by Kid Charlemagne at 8:50 AM on October 22, 2012
The flu shot only targets a handful of viri, so it's only going to have that kind of selective pressure or the few that it targets. In the larger scheme of things it's going to mostly select for things that aren't the viri in this years formulation. The big issue with the flu vaccine is guessing right which are going to be the problem strains in the comming year. Sometimes they get it right, and sometimes not.
posted by Kid Charlemagne at 8:50 AM on October 22, 2012
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And we're just about as Kayee as K strategists get. If you're a parasite working on an r strategist I'd think there would be even less pressure to not kill your host.
posted by Kid Charlemagne at 5:57 AM on October 21, 2012 [6 favorites]