Comments on: Virulence-transmission trade-offs and population divergence in virulence

Virulence-transmission trade-offs and population divergence in virulence

Blasdelb — Sun, 21 Oct 2012 04:35:01 -0800

"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.

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]

By: Kid Charlemagne

Kid Charlemagne — Sun, 21 Oct 2012 05:57:47 -0800

Isn't the problem with developing commensality, at some level, the same as the problem with developing sentience? I mean, sure, with the advent of gunpowder and internal combustion engine and atomic theory (and I'll be finishing the Oracle at Delphi in two turns) I'm feeling pretty smug and wondering why all the other animals haven't evolved sentience. But for a few hundred thousand years there my for-bearers spent a lot of time being eaten by leopards while everything else was feeling pretty smug for evolving the ability to run like hell. 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.

By: Malor

Malor — Sun, 21 Oct 2012 06:03:23 -0800

Kid Charlemagne, the thought occurs that intelligence may be a parasite that kills its host species.

By: Blasdelb

Blasdelb — Sun, 21 Oct 2012 06:24:16 -0800

"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.

By: leotrotsky

leotrotsky — Sun, 21 Oct 2012 07:39:25 -0800

Blasdelb, are you stalling on your thesis? This is the third mongo gigantic post in like a week.

By: The Whelk

The Whelk — Sun, 21 Oct 2012 07:44:00 -0800

Blasdelb can stall all they like, I'm LEARNING over here.

By: double block and bleed

double block and bleed — Sun, 21 Oct 2012 08:22:02 -0800

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."

By: zaelic

zaelic — Sun, 21 Oct 2012 08:24:20 -0800

"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.

By: BlueHorse

BlueHorse — Sun, 21 Oct 2012 09:53:23 -0800

Nature doesn't care about the individual*. Reproduction must occur. *But what about ME (and my parasites)? We are very special snowflakes!

By: msalt

msalt — Sun, 21 Oct 2012 10:19:11 -0800

Maybe this is an obvious point, but some harm to hosts (e.g. diarrhea) gives a big advantage in transmissibility, right?

By: Blasdelb

Blasdelb — Sun, 21 Oct 2012 12:02:30 -0800

"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.

By: Blasdelb

Blasdelb — Sun, 21 Oct 2012 12:24:39 -0800

"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

By: dephlogisticated

dephlogisticated — Sun, 21 Oct 2012 12:33:03 -0800

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.

By: Blasdelb

Blasdelb — Sun, 21 Oct 2012 12:47:12 -0800

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.

By: saber_taylor

saber_taylor — Sun, 21 Oct 2012 13:13:49 -0800

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.

By: maryr

maryr — Sun, 21 Oct 2012 14:57:46 -0800

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.

By: Joe in Australia

Joe in Australia — Sun, 21 Oct 2012 17:49:56 -0800

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.

By: vasi

vasi — Sun, 21 Oct 2012 19:55:04 -0800

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.)

By: Blasdelb

Blasdelb — Sun, 21 Oct 2012 23:49:49 -0800

"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.

By: Joe in Australia

Joe in Australia — Mon, 22 Oct 2012 03:07:01 -0800

What if it infected an embryo?

By: Blasdelb

Blasdelb — Mon, 22 Oct 2012 03:46:54 -0800

"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.

By: Blasdelb

Blasdelb — Mon, 22 Oct 2012 05:41:45 -0800

"Kid Charlemagne, the thought occurs that intelligence may be a parasite that kills its host species." LOL

By: msalt

msalt — Mon, 22 Oct 2012 08:44:30 -0800

It seems to compel its host to spread it to others, before it kills them off. So pretty much, yeah.

By: Kid Charlemagne

Kid Charlemagne — Mon, 22 Oct 2012 08:50:30 -0800

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.