Guest guest Posted July 30, 2005 Report Share Posted July 30, 2005 Those gene cassettes can make an infinite number of protein sequences. However, some (most) sections of most genes need to be preserved rather than varied, because it is their sequence that gives them their structure and hence their functionality. (If you have a porin and you start swapping out amino acid residues, bang its not a porin anymore, just a piece of crap!) It would be good for immune evasion for an organism to just not have any surface proteins at all, but it has to have them because proteins get stuff done. The thing is, there may be a way in which the variable proteins are able to physically screen over many or I guess maybe all of the invariant proteins on the organisms surface. (Or every exposed portion of protein could be a hypervariable chain, but that is probably alot more difficult to pull off.) Theoretically I guess this could be arranged so that almost nothing is accessable to antibody except the cut-and-paste cassette genes which are able to constantly change. This would make the antibody response pretty useless. This paper is very informative basic reading on Bb architecture: http://www.pubmedcentral.gov/picrender.fcgi?artid=38859 & blobtype=pdf Here Radolf showed Osps A B and C to be mostly inaccessible to antibody in living Bb. When he washed the bastards in methanol to nuke their outer membranes, the antibody then fixed very well. Perhaps the failure of antibody to fix on the living organisms could be due to cloaking by variable cut-and-paste proteins. A fairly recent experiment by A Barbour suggests one of the Osps (not a hypervariable one) serves to cover over another. Or perhaps there simply isnt much exposed protein at all, as Radolf concludes. The spirochetal OM is very fragile and it may get removed by most microscopy prep techniques. I am looking into this. The bowen assay is done on (essentially) unadulterated blood/humor but they do centrifuge, and that may remove the OM. (Heres their patent.) That would explain why they apparantly get robust antibody fixation. http://tinyurl.com/6ufoe So like, whatd you learn man? <jenbooks13@h...> wrote: > I spoke with one of the primary researchers yesterday, not for > publication, for me to understand the organism. Now I understand what > all the Osps do and when and what VLSE's do etc. > > This organism has so many tricks it has no worries about one > antibody. It just downregulates the one targetted at it and > upregulates others and makes lots of decoys. It has the capacity to > make millions of antigenic shifts through vlse mechanism alone. > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted July 30, 2005 Report Share Posted July 30, 2005 well what i learned is that it is too clever for words. so, ospA up in tickgut down in human ospC up in human, we make antibodies, kill 'em off, but some just cleverly downregulate ospC...so...we're still infected osp E essentially binds human complement ospB changes in diff tissues and vsle they're like the legs of the centipede, tons of vsle. ever changing and ever confusing. we ain't got nuthin to bind to that we know of y et. good point you made about studying it adn degrading its outer membrane. the researcher said something beautiful i'm paraphrasing but it was something like, you're witnessing millions of years of evolution, millions of mistakes perfected, summarized in one moment (ie in this bug) > > I spoke with one of the primary researchers yesterday, not for > > publication, for me to understand the organism. Now I understand what > > all the Osps do and when and what VLSE's do etc. > > > > This organism has so many tricks it has no worries about one > > antibody. It just downregulates the one targetted at it and > > upregulates others and makes lots of decoys. It has the capacity to > > make millions of antigenic shifts through vlse mechanism alone. > > Quote Link to comment Share on other sites More sharing options...
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