March 11, 2010
Category: Virology
Weve all heard of that stupid book/diet that tries to tell you what to eat based on your blood type. Of course thats stupid and just a gimmic to get you to buy hundreds of dollars of crap 'supplements' for your blood-type (oh for Petes sake...).
I totally didnt know this before I read this neat Nature review, but there are actually viruses out there that can use the histo-blood group antigens (A, B, O) as their receptors!
Noroviruses!
Apparently, Type O are the most susceptible to some kinds of norovirus infection, and Type B are the least.
Now, this might be something other kids learned in high school or something, but I dont know jack about blood groups. *shrug* So I was like "WTF! If norovirus uses blood-group antigens as a receptor, how can Type O (lacks A and B) be more susceptible??"
Like I said, this was totally news to me: 'Type O' doesnt mean your red blood cells are 'naked', it just means that there is a standard sugar, 'O'. Some people have an enzyme that makes the standard 'O' a little different with an 'A' modification. Some people have an enzyme that makes a 'B' modification. Some people have both. But if you dont have either, you keep the standard sugar, 'O'. It doesnt mean you lack the sugar entirely.
This makes perfect sense, in retrospect, but its not something I have thought about before!
So, noroviruses like the 'basic' antigens for receptors, not so much the modified ones.
Got it!
But then I was all like "WTF! How can your blood type (glycans on red blood cells) have an impact on a virus that infects your gut??"
News to me: Some people express these antigens on the epithelial cells in their mouths/GI tract. Theyre called 'secretors'.
So even if you are Type O (more susceptible), if you are a non-secretor, you are actually less susceptible!
And this is just super good news for those of you today who are Type B non-secretor. You dont get as many opportunities to poop your guts out as the rest of us. LOL! I dunno how/where/if you can be tested to see if youre a secretor or not, though.
(SUPER AWESOME online textbook that taught me this stuff: 'Essentials of Glycobiology')
Posted by ERV at 1:30 PM • 11 Comments • 0 TrackBacks
March 10, 2010
Category: Theism
Oklahomas Christian Medical and Dental Association is such a massive joke.
They brought in Donald Ewert, a clueless dork, to talk about the 'Evolution of the Immune System' Creationism.
Brought in Mr. NOMNOMNOMNOM to talk about the science/religion/ethics behind stem cell research SCIENTISTS KILLING BABBIES!
And yesterday they brought in Ellen Myers to talk about: "Did the Nazis have it correct? Part II: Euthanasia and Doctor Assisted Suicide; Will We Repeat the Past."
I had no idea who this woman was. A casual Google search turned up juicy morsels like this:
She has published papers in the Creation Research Society Quarterly and at the International Conference for Creationism. She grew up in Nazi Germany, is multi-lingual, and has a Masters degree in History.
Creationist! Nazis! Me and some friends
had to check this out!
... The following 45 minutes were quite possibly the weirdest, most irritating 45 minutes I have experienced in a very long time (hey, its been a while since Caseytits was in town).
Part of it is that Im not used to crazy old people. I dont mean crazy as in 'kooky fun!' I mean crazy in a 'tea-bagger experiencing rapid cognitive decline' way. My grandmothers were strong independent women up till the end, and very respectful of my religious/political decisions, so it took me a minute to get used to an 80 year old woman, lecturing at a medical institution, saying things like "OBAMA SAID THE US IS NO LONGER A CHRISTIAN NATION! DID YOU HEAR THAT??? GERMANY WAS A GOOD CHRISTIAN NATION UNTIL NAZIS!"
It was kinda like a 45-minute version of this.
*blink*
The one bloggable thing I got out of this event was an observation*. A difference between Radical Christian ethics and my ethics.
Read on »
Posted by ERV at 8:44 PM • 15 Comments • 0 TrackBacks
March 9, 2010
Category: Fitness
LOL!
We finally got Obesity Panacea on ScienceBlogs! YAY!
Now. *squints eyes* I gotta question for Travis and Peter as a blogwarming gift :P
Whats the deal with BMI?
Weve talked about it a lot on SciBlogs, but now weve got some Real Life obesity/exercise professionals in the house, so I wanna get the usefulness of BMI clarified.
I am under the impression that BMI is a useful tool for Average Joes/Janes to monitor their weight. Is 150 lbs healthy? Is that weight okay if you are 5 feet tall? What if youre 6 feet tall? How is Average Joe/Jane supposed to know? BMI. Certainly regular body fat analysis, and VO2 Max levels and such could be better measurements, but not everyone has access to that sort of thing. BMI is easy.
What I hear regularly (and have already seen on Obesity Panacea), is Average Joes/Janes saying the BMI scale is useless because according to it they are overweight/obese, but they are as healthy as a horse! You know, The Rock is obese according to the BMI scale!
Average Joes/Janes are not 6'4" 275 lb professional wrestlers on steroids.
I fail to see how BMI fails for Average Joes/Janes.
I consider myself an Average Jane. To be considered BMI 'overweight', I would have to gain 35 pounds. To be that weight but keep my current body fat percentage, only 5 of those 35 lbs could be fat.
There is no way I could do that without steroids. No friggen way.
To get into the 'obese' range, Id have to gain almost 70 pounds! Only ten of that could be from fat.
No way could I be considered 'BMI overweight' or 'obese' and still be as healthy as I am right now!... Unless I was on steroids.
On the other hand, 2010 Abbie is the same weight at 2004 Abbie... but Ive pulled my body fat percentage down about 10%. So there are points where BMI is not a helpful measurement.
But I think as a general measure for Average Joes/Janes, its fine.
But I am not, in any way, an expert on this topic.
So I would like to hear Travis and Peters take on this issue.
:)
Posted by ERV at 1:00 PM • 42 Comments • 0 TrackBacks
March 4, 2010
Category: Immunology • XMRV
Two things I didnt intend on writing about on ERV more than a few times, but turned into repeat guests: XMRV and Vpu.
Theyve finally come together.
Susceptibility of xenotropic murine leukemia virus-related virus (XMRV) to retroviral restriction factors
Know how I was talking about
intrinsic immunity yesterday?
Well, some scientists wondered how the heck XMRV was replicating in humans (especially human PBMCs), when other murine gammaretroviruses are restricted in humans because of our intrinsic immunity: Tetherin, APOBEC, Trim5. So they set out to investigate what effect (if any) these human antiretroviral proteins have on XMRV.
RECEPTOR: First things first. If a cell doesnt have the receptor XMRV needs, then it cant infect a cell. The cell doesnt have the right lock for XMRVs key. But what if you give XMRV the key to locks on every cell (VSV-G)? Can XMRV infect anything, then?
Nope.
XMRVs can infect some cells a little better with the VSV-key, but it doesnt make a huge difference. This means that there is something else restricting infection and cell tropism. A greater pressure than something as simple as receptor, and present in every cell... Intrinsic immunity!
APOBEC3G: This protein does not prevent the production of babby viruses. But, the babby viruses are mutated beyond repair, and are thus noninfectious. But not every APOBEC works on any retrovirus, and some retroviruses have figured out ways to interfere with APOBEC (HIV-1 Vif).
Well, human APOBEC3G does not like MLV (XMRVs ancestor). It shuts that mo-fo down. Weirdly, though, APOBEC3G is found in high levels in human PBMCs... but infectious XMRV was found in human PBMCs... The resulting viruses should have been duds.
So, they tested whether human APOBEC3G can mess up XMRV. Um... it could. Human APOBEC3G knocked XMRV infectious offspring levels down to MLVs crappy levels. Hmm.
TETHERIN: These experiments are so cool! Okay, first of all, XMRV is restricted by tetherin. That is, you get really really shitty viral production off of infected cells that express human tetherin (or tetherin from a couple non-human primates). Now, HIV-1 has Vpu to counteract tetherin, right? So they added Vpu to XMRV infected cells, and voila! Tons of XMRV.
Furthermore, XMRV does not appear to have any obvious way of countering this host restriction. Yes, HIV-1 has Vpu. But viruses related to HIV-1 (HIV-2, SIVs) counter tetherin a different way-- with the envelope protein. Well, you dont need a complex retrovirus for Env, maybe XMRV counters tetherin that way?
Nope. HIV-1 with Vpu deleted replicates really shitty in human cells. If you add in XMRV envelope... HIV-1 with Vpu deleted still replicates shitty. Hmmm.
TRIM5alpha: Human TRIM5alpha messes up the structural proteins of regular MLV so it doesnt uncoat properly. So, they wanted to see if human (and twelve non-human primate) TRIM5alpha can screw with XMRV too...
It cant!
This is the one innate immunity hurdle that XMRV can clear, while MLV cannot. Its odd, because XMRV-MLV structural amino acid sequences are super similar (95%), and TRIM5alpha has to interact with specific amino acids to work, but, eh, XMRV can do it.
But it still doesnt entirely make sense why the Reno group could find infectious XMRV in PBMCs. Evolutionarily, it shouldnt be there. Well, rather than screaming about how Judy Mikovits is a liar and a fraud, Harriet et al reacted in another normal, scientifically acceptable way-- by proposing some putative explanations, and excitedly waiting for future results. Their entire discussion was a pleasure to read.
In fact, the last author on this paper is Dr. Kate N. Bishop, also the last author on the second XMRV paper from the UK. Ignored the WPIs frantic wailing and claims everyone is incompetent but them, and kept doing science.
*tips hat to Dr. Bishop*
Neat science in this paper, Ma'am.
Posted by ERV at 6:00 PM • 6 Comments • 0 TrackBacks
March 3, 2010
Category: HIV/AIDS
Your immune system is like an onion ogre parfait.
Its has lots and lots of layers.
You have intrensic immunity-- Abilities every single one of your cells has to defend itself from viruses. VpuTetherin would be a good example of this, as would APOBEC and Trim5a. Pick a cell in your body-- it can make these proteins. Doesnt have to be a special immune cell.
Then you have innate immunity-- Certain immune cells are not specific for any particular pathogen, but they can identify patterns that are 'wrong'. They see things your body knows aint right, like double-stranded RNA (your body doesnt make that!) or unmethylated bits of DNA made up of mostly Cs and Gs (your body doesnt have that!), or bacterial proteins like flagellin (mammals dont have flagella that look like bacterial flagella!). These cells dont care what virus is making the double-stranded RNA (HIV-1, rotavirus, respiratory syncytial virus), it just knows that double-stranded RNA is wrong, and that happens to be a step in these viruses life-cycle. Only immune cells can see pathogens this way, and respond accordingly.
And then theres adaptive immunity-- This is the one you all are probably most familiar with. These immune cells evolve in the face of infection to be specific for that pathogen. Very generally, Cytotoxic T-cells evolve to specifically target and kill host cells infected with the pathogen, and B-cells evolve to make antibodies specific for the pathogen, to neutralize them or make them easier for your immune system to see-->kill.
All this specific immune response takes time to evolve (couple weeks). Viral vaccines use weak/dead viruses to prime your adaptive immune response. Thus when you are exposed to a real, harmful virus 'in the wild', your body has a cheat-sheet for how to get rid of the virus. Your response is stranger and faster than if you had never gotten the vaccine.
To bring this back to HIV-1, we might be screwed when it comes to making a CTL vaccine (or, if we dont do it quick we are screwed). HIV-1 is figuring out how to pick our locks at a population level.
Okay, well, what about antibodies, then? What about a vaccine that revs up B-cells instead of T-cells?
Well, a series of papers have been coming out of a lab in the Netherlands that makes me think we might be screwed on that front too.
And once again, its all evolutions fault.
Read on »
Posted by ERV at 11:00 AM • 36 Comments • 0 TrackBacks
March 1, 2010
Category: HIV/AIDS
HIV-1 deniers-- They love Orac. They love Tara. Even like haunting the Hoofnagle brothers a bit.
They dont like ERV.
Never have.
*sad face*
I really cant figure out why. (I bet its cause Im mean and kannut com00nicates scienz).
Three years ago, today, I posted a challenge to HIV-1 Deniers. A simple test of basic HIV-1 literacy and competency. Three years ago... and it only has three comments. One from a supporter, one from me, and one from an HIV-1 Denier... who didnt answer the question. Just linked to the nutty Perth Group and hoped something Perth said stuck (nothing on the linked page was related to The Challenge, sry).
Alllllll those HIV-1 Deniers stalking Silvia... allllll those HIV-1 Deniers blabbing on other science blogs... they have no idea what that picture is. Dont know what it is, so cant figure out what it means. Stock-standard image that is in a million HIV-1 publications, they dunno what it is.
But they know HIV-1 doesnt cause AIDS. Or it doesnt exist. Or something.
Maybe expecting people with such passionate opinions be even modestly educated on the topic they are so passionate about is too much to ask.
So here is an even easier challenge. Ill even include some links to make this really, really fucking easy.
HIV-1 DENIERS! EXPLAIN THIS:
293T cells were transfected with an infectious molecular clone of HIV-1, where EGFP was inserted between env and nef. The resulting viruses contain genomes that contain the EGFP gene, thus the EGFP gene is permanently inserted in the host genome after infection.
This is what happens to cells 'infected with HIV-1' (raw image)
This is what happens to cells that only get media off untransfected 293Ts (raw image)
If HIV-1 does not exist:
- How did the EGFP gene get into the PBMCs genome?
- Why are these cells now producing EGFP, as well as progeny virions that can go on to infect new cells and turn them green?
- Why are all those EGFP positive cells going to be dead tomorrow, while the not-green cells are snug as bugs in rugs?
Posted by ERV at 6:00 PM • 41 Comments • 0 TrackBacks
February 26, 2010
Category: Douchebaggery! • Science Outreach
Boy, do I have egg on my face!
After I just made fun of the absurdity of Chris Mooneys 'building bridges with antivaxers' or 'ladders to heaven' or 'rope swings to Creationists' or whatever strategy, Mooney is named a Templeton Foundation 'fellow'.
Like most of you, my initial response was "What a douche."
But then I realized-- This is THE answer to my prayers.
All these years I have been so goddamn frustrated with the level of stupidity coming out of religious institutions regarding HIV-1.
But there was nothing I could do about it because Im not nice and Im a stoopid scientest tat dunt commoonikates gud.
Now that The Master Science Communicator and Bridge Engineer is in A Position of Power, Mooney can solve all of my problems!!!!!
The GameMaster Pope will start telling everyone to use condoms to stop the spread of HIV-1!
Fundamentalist Christians in the US will stop trying to kill HIV(+) homosexuals in Africa!
Fundamentalist Christians will stop holding up Anti-HIV funding because it might go towards family planning clinics or needle exchange programs!
Fundamentalist Christians will stop promoting their failed 'abstinence only' anti-HIV plan, recognizing that their 'moral authority' has limited real-world applications.
Fundamentalist Muslims will stop killing HIV-1 advocates in Africa!
The Red Sea will part, manna will fall from the heavens, bridges will be built between the real world and lunatics, now that Chris Mooney is a Templeton Fellow!
He can now show us all how its done!
*grins like a Cheshire cat and waits*
Posted by ERV at 4:30 PM • 42 Comments • 0 TrackBacks
Category: XMRV
Study from the Netherlands:
Prevalence of xenotropic murine leukaemia virus-related virus in patients with chronic fatigue syndrome in the Netherlands: retrospective analysis of samples from an established cohort
CFS/ME patients plus age/sex/neighborhood matched controls (patients brought in friends that lived in the same area-- environment might play a role).
32 ME/CFS patients
43 controls
0 XMRV present in PBMC, using reagents verified in this paper (integrase) and this paper (gag- the same ones WPI used).
Cut/Paste summary:
A limitation of our study is that the numbers of patients and controls in our study were relatively small. Based on these low numbers, the upper limit of the 95% confidence interval is a prevalence of 9% for the patient group and 7% for the control group, as calculated according to Eypasch et al (by the formula p=3/n).18 Although we cannot formally rule out a role of XMRV, our data cast doubt on the claim that this virus is associated with chronic fatigue syndrome in the majority of patients...
... Technical aspects are unlikely to explain the difference in XMRV positivity rate between our data and their data...
... It is possible that the study of Lombardi et al has unravelled the viral cause of the chronic fatigue syndrome outbreak, but it seems unlikely that their study demonstrates a viral association for sporadic chronic fatigue syndrome cases, such as those we tested, or represents the majority of patients.
Now, this paper demonstrates the scientifically acceptable, normal way scientists bitch-slap one another (SPOILER: It doesnt involve calling other scientists frauds):
In conclusion, we found no evidence for a role of XMRV in the cause of chronic fatigue syndrome in Dutch patients. Over the past decades we have seen a series of papers prematurely claiming the discovery of the microbial cause of chronic fatigue syndrome. Regrettably, thus far none of these claims has been substantiated.
Still no XMRV in Europe.
Posted by ERV at 12:00 PM • 20 Comments • 0 TrackBacks
February 25, 2010
Category: HIV/AIDS
From building bridges with anti-vaxers to building bridges with animal liberation maniacs, Chris Mooneys 'building bridges' plan is revolutionizing the way scientists interact with insane people!
Its even changing the playing field with HIV-1 Deniers.
Long-time readers know I have relatively little patience with HIV-1 Deniers. Everyone involved with HIV Denial, from the 'professional scientists' to the 'Average Joe snake-oil salesman' are complete and utter morons. So, frankly, they are only good for one thing: lulz.
So while I like writing about the latest HIV-1 findings on ERV, I rarely actively engage HIV Deniers. I just laugh at them.
Now, that is a Very Bad Move, according to Mooney. HIV-1 researchers should be building bridges with HIV Deniers:
Instead, I believe we need some real attempts at bridge-building between medical institutions--which, let's admit it, can often seem remote and haughty--and the leaders of the anti-vaccination HIV Denial movement. We need to get people in a room and try to get them to agree about something--anything. We need to encourage moderation, and break down a polarized situation in which the anti-vaccine HIV Denial crowd essentially rejects modern medical research based on the equivalent of conspiracy theory thinking, even as mainstream doctors just shake their heads at these advocates' scientific cluelessness. VaccineHIV skepticism is turning into one of the largest and most threatening anti-science movements of modern times. Watching it grow, we should be very, very worried--and should not assume for a moment that the voice of scientific reason, in the form of new studies or the debunking of old, misleading ones, will make it go away.
This is what happens when you try to build bridges with HIV Deniers:
Read on »
Posted by ERV at 2:00 PM • 119 Comments • 0 TrackBacks
I'm a graduate student studying the molecular and biochemical evolution of HIV within patients and within populations. I also study epigenetic control of ERVs.
