Here is a related story...
Scientists in Maryland have sequenced the genomes of 209 strains of influenza from the NYC area. Haven't heard whether they have as of yet attempted to calculate the overall diversity of this little (8 RNA chromosomes) virus, but no doubt someone will -- given that the data is now available. This would also seem to be of some relevance.
Here is an article regarding their achievement meant for the general public. (I will let someone else find the relevant technical article(s).)
October 05, 2005
Scientists at the Institute for Genomic Research in Maryland report
completing the first large-scale project to sequence the influenza
virus.
http://www.physorg.com/news7003.html
The "technical" article was published last week in Nature, here: http://www.nature.com/nature/
jou...ature04239.html
Again, this (the flu work) was done by TIGR--they're involved in a majority of the large-scale sequencing projects being carried out, and have all kinds of cool toys on their website (http://www.tigr.org). They can't really calculate the overall diversity in influenza viruses from that sample, though, since they purposely picked H3N2 viruses (and 2 H1N2 viruses) going back over the last 5 influenza seasons, so it's a very narrow sample. (In contrast, the GBS samples were specifically chosen to represent all known serotypes of the bacterium, and to represent different evolutionary lineages). The flu article is good, though, for showing how quickly mutations can happen and spread through the population, which has huge implications for vaccine development.
Agreed, that sample is too small, but it does suggest a fairly large "pan-genome", perhaps as much as doubling the core genome with strain-specific stuff. A somewhat disturbing development, indeed, but the real problem is that even this pool isn't really isolated, it can presumably pick up new genes through the usual inter-species methods.
Agreed, that sample is too small, but it does suggest a fairly large "pan-genome", perhaps as much as doubling the core genome with strain-specific stuff. A somewhat disturbing development, indeed, but the real problem is that even this pool isn't really isolated, it can presumably pick up new genes through the usual inter-species methods.
Absolutely. In humans, in addition to causing disease, these are commensal flora carried in the rectum and vagina (and occasionally in the throat). I mentioned in the article the diversity of bacteria in the GI and oral cavities; the vagina also has its own diverse flora. Just in those niches alone, within just one person, the potential for genetic exchange is enormous. Now multiply it by every human that carries it, and add in non-human strains (it was originally identified as a cause of mastitis in cows, and has been found in guinea pigs, dogs, cats, heck, even elephants), and their conclusions make a lot of sense. Imagine the pan-genome for something that's even more easily transformed and ubiquitious, such as E. coli...
Hi Tara,
I assume that Sag is your favorite organism? As a streptococcal biologist myself, I've always had a bit of a side interest in the group-Bs. A few thoughts about your discussion from that diversity paper (which I haven't read yet by the way): 1) Did they prove first that the strains they sequenced were all actually Sag? I assume they did a full analysis of the rRNA? I only ask this after spending >15 years with the viridans strep that to this day are still a systematics nightmare. 2)The normal ecological niche of Sag is the bovine teat. Is human vaginal colonization a recent occurance? Has anyone compared the human and bovine strains? How different are they? 3) Are any of the Sag strains naturally competent for transformation? If so, no big surprise on the diversity issue, just check out S. pneumoniae.
Hi GATC,
My current research focuses on group B strep, so you could probably say it's my favorite organism. My PhD was in virulence factor regulation in Strep pyogenes, and I'm putting together a few projects on Strep suis, so that genus is definitely my bread and butter. As far as your questions,
1) Did they prove first that the strains they sequenced were all actually Sag? I assume they did a full analysis of the rRNA? I only ask this after spending >15 years with the viridans strep that to this day are still a systematics nightmare.
They don't mention that in the paper, but all the isolates they used had already been extensively characterized and serotyped, so that's not an issue. And GBS isn't such a pain to identify, luckily.
2)The normal ecological niche of Sag is the bovine teat. Is human vaginal colonization a recent occurance?
Nope. It's actually commonly carried in the human vagina and rectum; about ~25% of the population is asymptomatically colonized. It's also caused infections of dogs, cats, hamsters, elephants...probably more species carry it than we realize. And it's been infecting us for awhile. If you look back at case reports, it was found back in the 1940s and 50s as a case of neonatal meningitis; the dogma that it was just a bovine pathogen didn't really break until there was a surge of neonatal cases in the 70's.
Has anyone compared the human and bovine strains? How different are they?
Yep, that's been looked at. Consensus is that they're largely 2 different populations, but interestingly, a lineage of serotype III GBS that causes a lot of invasive disease in neonates is closely related to a bovine lineage. (See Bisharat et al., JCM 2004 for more info on that one).
3) Are any of the Sag strains naturally competent for transformation? If so, no big surprise on the diversity issue, just check out S. pneumoniae.
Nope, they're not. They're actually quite a pain to get DNA into--much more similar to S. pyogenes than S. pneumo. That's one reason why the results are so surprising to some people. (Luckily, they jibe very nicely with a manuscript I have in progress
).
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