Not at all. <snip> Nicely put, thanks. You've studied it? Shit, I'd better shut up then... -- _______ ..'_/_|_\_'. Ace (brucedotrogers a.t rochedotcom) \`\ | /`/ GSX-R1000K3 (slightly broken, currently missing) `\\ | //' BOTAFOT#3, SbS#2, UKRMMA#13, DFV#8, SKA#2, IBB#10 `\|/` `
I really doubt that I'm any better now than I was then, and I really *really* hated my degree. -- Catman MIB#14 SKoGA#6 TEAR#4 BOTAFOF#38 Apostle#21 COSOC#3 Tyger, Tyger Burning Bright (Remove rust to reply) Alfa 116 Giulietta 3.0l (Really) Sprint 1.7 75 TS 156 TS S2 Triumph Speed Triple: Black with extra black bits www.cuore-sportivo.co.uk
Erm. OK, but development of immunity has nothing to do with the process of evolution per se. Evolution by definition is a product of random mutation and breeding across generation. An immune response isn't Actually, having said that, and bearing in mind that I'm rather pissed, I suspect you are downright wrong. ISTR it is possible to show an immune response to an antigen to which you have *never* been exposed. Ergo, development of immunity *can* be totally separate from the existence / exposure to any given pathogen. Not sure what the first sentence actually means. The selection isn't random, you are correct, but unless there is specific selective pressure, then no selection occurs IYSWIM Again, bearing in mind that I'm pissed, that's bollocks. Operative word *too* much harm. Over simplification. One of the most important factors is *not* lethality, it is speed of lethality. It matters not if a virus is 100% lethal if it takes long enough to kill to allow an infected host to breed. Of course. My money is on airborne filovirus or similar. I think not, but as ever ISTBC. Not trying to be offensive here, but most of the arguments you've just put forward are the ones that we had to be taught were wrong even before they tried to teach us what was right. The concepts are so persuasive simply because they are intuitive. Sadly just in-accurate. -- Catman MIB#14 SKoGA#6 TEAR#4 BOTAFOF#38 Apostle#21 COSOC#3 Tyger, Tyger Burning Bright (Remove rust to reply) Alfa 116 Giulietta 3.0l (Really) Sprint 1.7 75 TS 156 TS S2 Triumph Speed Triple: Black with extra black bits www.cuore-sportivo.co.uk
Verdigris wrote: But *each* step will have to confer some advantage. Because the resistance is always present in the population, but seldom confers an advantage. -- Catman MIB#14 SKoGA#6 TEAR#4 BOTAFOF#38 Apostle#21 COSOC#3 Tyger, Tyger Burning Bright (Remove rust to reply) Alfa 116 Giulietta 3.0l (Really) Sprint 1.7 75 TS 156 TS S2 Triumph Speed Triple: Black with extra black bits www.cuore-sportivo.co.uk
HIV is not very contagious, with a probability of infection of one in a hundred for a woman having unprotected vaginal sex with a HIV positive man. With this in mind, if HIV were to be rapidly damaging to the health of the host this would lead to very low levels of infection. Now, to say that "it's not in the interests of the virus to kill off it's host too quickly", well, I can see what you're getting at. Leaving aside the use of language for the moment. If HIV becomes more rapidly harmful, whilst retaining it's low transmission rate, this would lead to a fall in infection rates - possibly in the virus dying out. If it becomes less damaging to the host, whilst retaining it's low infection rate, or becoming more infectious, this would lead to a higher prevalence of the disease. If you follow Darwin's view on selfish genes this is the more likely case. The immune system is a product of evolution. The immune system does evolve, by the same process as everything else. Viral evolution is influenced by the environment, that environment is the host. If, through random mutation, a virus is formed that is able to spread to more individuals, either because it is less harmful to the host (giving it longer to spread) or it is more infectious, then this will become the predominant strain. If the immune system of the host is able to combat the virus then it will be killed off, if during the replication of one of these viral particles a strain arises that the immune system cannot cope with, then it will spread and become the predominant strain. So whilst it's quite true to say that an immune response isn't evolution, it is the result of evolution and it's an evolutionary environment. Yes it is, innate immunity. Through the arrangement of MHC, HLA, etc. there are a number of antigens to which you are conferred innate immunity. However, think about how this happened. Yep, evolution again. So we've considered the evolution of the virus, let's think about the evolution of the immune system. Viruses that are likely to kill before the host reproduces, or to leave the host less able to compete for a mate are going to have an effect on evolution. If amongst a population one member has a mutation that means they are less susceptible to the effects of one such virus, they are at a selective advantage. If this mutation is passed on to their offspring, then they too are at a selective advantage. This is perpetuated. The majority of the population will eventually have this mutation, conferring a level of herd immunity to the rest. There is always selective pressure, there are mutations which are not favourable, these may or may not spread, or ones that deleterious, these are selected against. Any mutation which benefits the propagation of the viral DNA is selected for, a mutation resulting in a less harmful course (meaning more opportunity to spread) would be selected for. This has already happened. HIV 1-B, the subtype which is believed to have spread from Thailand, and is associated with spread via drug users, is less harmful to the host and was becoming more prevalent - however, it appears to have recombined with HIV 1-D, resulting in HIV 1-E. The new 1-E strain retains the virulence of both, meaning it is more infective than either of the two parent strains, but retained the the host damage levels of 1-D. Such a change is likely to happen again, over time less harmful strains will become prevalent. It is and it isn't. The human genome, as I'm sure you know, is made up lots of DNA that is never transcribed. There is strong evidence to show that quite a lot of this is due to viral DNA having been incorporated into the host genome. Look at mitochondria, it's not a new way of making sure DNA spreads. To say that we get infected by lots of viruses which happily reproduce in our systems without bothering us isn't quite right, although it's true that we do acquire a number of viruses without noticing. And there is certainly a lot of truth to the last sentence of Verdi's paragraph. Retroviruses are rife in the the rest of the animal kingdom, but do little harm. They simply introduce their DNA in the genome of the host and that's about it. There is a retrovirus that affects talapoin monkeys, it's harmless to them, but in a zoo this virus spread to macaques - they all died rapidly. Spot on. There are two possible paths for a virus to take, one is to spread quickly and damn the damage to the host; the other is to spread more slowly, necessitating that the host is not damaged too quickly. Now, given that the easiest way for a virus to spread it's genes it to get something else to do it for them, as HIV does, it's likely that HIV will take the second path. Other viruses are different, of course.
Of course, that should be Dawkins, not Darwin. Verdi take a look here, http://www.royalsoc.ac.uk/page.asp?id=1110 I think you'll find it interesting. I've not looked at them myself yet, so can't comment on the content.
Verdigris wrote: Ah *ha*. Definitely some confusion. Yes, inherited resistance *may* be as a result of exposure to a pathogen, but it may not be, Not really, sorry Wonder what my Immunology lecturers would make of it being a straw man? Bloody hell, this is UKRM, on a Saturday night! OK, start again I think you'll find that's wrong. Some virulent viral diseases originated in other hosts, but I very much doubt that 'more of the most' or indeed 'most' did. Of course, I have no evidence to support this other than the fact that through my entire degree cross species pathogenesis was only mentioned in reference to very specific cases. Also there is another problem there. Take an example like tobacco mosaic virus (if memory serves) Completely harmless to a tobacco plant, lethal (AIUI) to tomatoes. Which one is it's host population? I'm fairly sure that those diseases are relatively ITYF that *never* happens I think, on balance, maybe all of them. Having said that, the disclaimer still applies. Even if I am right, I'm not really sure I can explain it face to face, let alone over Usenet -- Catman MIB#14 SKoGA#6 TEAR#4 BOTAFOF#38 Apostle#21 COSOC#3 Tyger, Tyger Burning Bright (Remove rust to reply) Alfa 116 Giulietta 3.0l (Really) Sprint 1.7 75 TS 156 TS S2 Triumph Speed Triple: Black with extra black bits www.cuore-sportivo.co.uk
Bacteria *possibly* -- Catman MIB#14 SKoGA#6 TEAR#4 BOTAFOF#38 Apostle#21 COSOC#3 Tyger, Tyger Burning Bright (Remove rust to reply) Alfa 116 Giulietta 3.0l (Really) Sprint 1.7 75 TS 156 TS S2 Triumph Speed Triple: Black with extra black bits www.cuore-sportivo.co.uk
MattG wrote: *Everything* is a product of immunity. OK, so I phrased it badly (no surprise there) but given your obvious understanding of the subject, I think my meaning would be pretty clear. Check these may or may not spread, or ones that deleterious, With you so far In this case, indeed. Nicely put. Yes, I am aware that it does happen. I'm more at odds with the 'numbers' implied. You seem to know rather more than I remember, so I shall stand to allow you to educate the pair of us Cheers -- Catman MIB#14 SKoGA#6 TEAR#4 BOTAFOF#38 Apostle#21 COSOC#3 Tyger, Tyger Burning Bright (Remove rust to reply) Alfa 116 Giulietta 3.0l (Really) Sprint 1.7 75 TS 156 TS S2 Triumph Speed Triple: Black with extra black bits www.cuore-sportivo.co.uk
Verdigris wrote: For which I am grateful. No malice was intended Don't feel you have to. I really doubt I can make coherent argument in the flesh, let alone on Usenet, and I'll probably be technically wrong as well -- Catman MIB#14 SKoGA#6 TEAR#4 BOTAFOF#38 Apostle#21 COSOC#3 Tyger, Tyger Burning Bright (Remove rust to reply) Alfa 116 Giulietta 3.0l (Really) Sprint 1.7 75 TS 156 TS S2 Triumph Speed Triple: Black with extra black bits www.cuore-sportivo.co.uk
I've noticed this phenomona up my way too. All the serving wenches in my work are Polish. I now drink far too much coffee.
Would it be true to suggest that the most aggressive viri, ie. the ones that really **** up tthe host, would die out quickly because there would be less time to spread on account of topping off the host too quickly?
Quite so. As I said. Because unless the non-resistant forms are in some way at a disadvantage, there's no "evolutionary pressure" for the resistant ones to become dominant. So the species doesn't evolve from the resistant to the non-resistant form unless, as has been stated several times now, each tiny change confers such an advantage that the new form becomes the dominant one, or finds a new niche in which this is the case. -- _______ ..'_/_|_\_'. Ace (brucedotrogers a.t rochedotcom) \`\ | /`/ GSX-R1000K3 (slightly broken, currently missing) `\\ | //' BOTAFOT#3, SbS#2, UKRMMA#13, DFV#8, SKA#2, IBB#10 `\|/` `
Not really as a generalisation, no. It's a bit more complex than that. Not least that the population of any virus will have individuals (and probably colonies) that are more or less lethal than the 'typical'. To get the situation that you describe you'd have to have a population of virus that a) All were lethal beyond some specific level b) Were lethal at such a speed as to prevent their host(s) from reproducing as fast as the virus is killing it c) Were infectious enough to kill their entire host population d) Expressed the level of lethality in *all* examples of their host e) Were incapable of finding another host population before extermination of their 'normal' host I suppose there may be / have been viruses that meet those requirements, but we may never know High levels of virulence can help contain outbreaks, though. Something like Zaire which is ~80% lethal in man, for example, tends to produce outbreaks that rapidly die out as the local host population die. There are often some that are innately immune, some that survive and so on. No sign of the virus dying out though, although that may be evidence that the reservoir is actually in a different species, probably some monkey. -- Catman MIB#14 SKoGA#6 TEAR#4 BOTAFOF#38 Apostle#21 COSOC#3 Tyger, Tyger Burning Bright (Remove rust to reply) Alfa 116 Giulietta 3.0l (Really) Sprint 1.7 75 TS 156 TS S2 Triumph Speed Triple: Black with extra black bits www.cuore-sportivo.co.uk
Better not wade through my post, then. -- Catman MIB#14 SKoGA#6 TEAR#4 BOTAFOF#38 Apostle#21 COSOC#3 Tyger, Tyger Burning Bright (Remove rust to reply) Alfa 116 Giulietta 3.0l (Really) Sprint 1.7 75 TS 156 TS S2 Triumph Speed Triple: Black with extra black bits www.cuore-sportivo.co.uk
Presuming you meant a product of evolution, yeah. Your meaning was fairly clear, but I wanted to state it thus as I wasn't entirely sure of what you were saying. Well, I've not got any statistics to hand, and the numbers are highly variable, depending upon which study you read. Heh, well it's an area of interest, covered broadly on my undergrad syllabus, which I've looked at a little further.
Wot? ah - I missed an 'i', I made up for it by an extra 't' somewhere else. Pikey keyboard and bad eyesight.
Fair enough I kind of thought they might be. Some of the things you mentioned sparked things I was taught IYSWIM. -- Catman MIB#14 SKoGA#6 TEAR#4 BOTAFOF#38 Apostle#21 COSOC#3 Tyger, Tyger Burning Bright (Remove rust to reply) Alfa 116 Giulietta 3.0l (Really) Sprint 1.7 75 TS 156 TS S2 Triumph Speed Triple: Black with extra black bits www.cuore-sportivo.co.uk
