I have something that I think atleast vaguely relates - it’s a bit hard to explain, but I’ll give it a try:
I simply can’t stand patterns that look like… uhm the inside of beehives, hexagons I guess but it applies to other “clustered holes” too.
I have no idea why I feel this way, but it simply repulses me. Happens when I’ve baked eggs too, they leave this cell like pattern on the pan that I simply can’t stand.
I’ve even seen it once, in a muffin after taking a bite and I had to throw the rest away.
Have you worked directly with live Ebola virii? Do you find that you feel under extra pressure at work because you are working with items that are potentially very dangerous? Did you have to go through security backgroung checks befor you could work in your labs, and do you have to deal with officially secret documentation. i.e. did you have to sign whatever the US version of the UK’s “Official Secrets Act” befor you could start this job?
Cheers, Bippy
Hrrm. I know one tech is leaving shortly for the FBI academy. I’ll be leaving in July and I imagine we’ll lose one or two other people. There is also the UT-Health Science Center just north of the facility where I work I know they have a microbiology program. So they will probably hire someone this summer too.
Check here, that’s the personnel department at the foundation. There are some ‘scientific support staff’ aka lab monkey postings. And like I said, I know of two job openinings in the next 6 months.
The pay is crap, but with 2 years of experience you should be a lab associate 1 which should pay more than a lab technician (which ironically I leave 2 weeks before I get promoted).
Cyn: I’m not sure how large of a scar, I just remember reading about smallpox vaccine scars being large.
Anyhoo. Getting back to the topic about the small pox vaccine. Here’s my take on it.
Soviet scientists worked on using smallpox as a bioweapon during the cold war. Which means they probably heavilly mutated the small pox genome. Now, the question I have that nobody can answer is: does the current small pox vaccine offer protection against a mutated weaponized strain of small pox? Because, if there has been enough mutation to the surface proteins in the small pox virus the vaccine won’t generate antibodies appropriate to the weaponized version. HOWEVER, if ALL weaponized small pox vials have been accounted for, then we don’t need to worry about this.
See, it’s a 3 part problem.
Do terrorists have access to small pox?
Do they have wildtype or mutated/weaponized small pox?
Does the small pox vaccine work against weaponzed smal pox?
#2 we don’t know the answer to and #3 the only way we can find out is if people who have the vaccine start dying from small pox.
And now I think I just freaked a lot of people out.
Silentgoldfish: Let me try to explain it how I understand it.
SIV and HIV are VERY similar viruses, the differences being that SIV infects cells expressing monkey CD-4 and HIV infects cells expressing human CD-4. However because of this difference, there is almost no chance of a human being infected by SIV. Which makes it reasonably safe for humans to work around.
Now, there are several stages to drug/vaccine research.
You start by doing experiments in cell lines (immortalized cell lines – cells that don’t suffer from the gradual degradation of their DNA during replication) to see if your basic theory works. You spend this time perfecting your experimental protocol. This is basically where you find out the mechanics of setting up the experiment, how many cells, how much virus, type and concentration of media and all that good stuff.
Next you move onto ‘wild type’ cells. Cells isolated from living creatures. Because working with artifical cell lines only tells you so much information. You need to see how cells that exist in nature–not manmade–react to your treatment.
The work I do involves transfer of SIV between different types of cells. Both types of cells I can isolate from primate blood then I can simulate a transfer of virus from one type of cell to the other in culture dishes. This tells you IF your protocol is likely to work in an organism. You find out if your treatment will kill the cells and you can determine the proper concentrations for best results. With enough good data and a good enough justification you can move into animal models.
Now at this point: All you know is that your protocol SHOULD work, and it doesn’t kill the type specific cells you’re working with. You still have no idea how an organism as a WHOLE will react to your treatment, nor the best way to deliver the treatment or the amount needed for a full animal.
Now the FDA comes into play.
See, getting to clinical trials is DAMN hard. And generally costs tens of millions of dollars. There’s a reason why those brand name drugs are so damned expensive when they come out, that’s because a research drug company probably lost 50 million dollars developing it (and has maybe a year or two left on the patent for the drug). And if you are working on a vaccine, or a method of blocking the spread of HIV between cell types, any human you test it on where the treatment fails just died. Because you now gave them HIV.
With me so far?
Now, we go back to SIV. SIV is VERY similar to HIV. Many of the anti HIV drugs also work on SIV, the is remarkable similarity between the two virus genomes. Also it is much easier to run experiments on primates than it is on humans.
So, if you start working on experiments with SIV on primate cells and get good results you should be able to get permission to run experiments on primates. Now, if your data is good the similarity between both HIV and SIV, and the similarity between other primates and humans means what works in the primate has a HIGH chance of working in humans.
You should still run tests on cells isolated from humans to make sure your treatment does work the same on human cells as primates. But with the proof that your protocol works in primates, you have every reason to believe it will work on humans.
I hope that makes sense.
The short answer to your question is: Yes, we can and do get blood samples from humans. However, to me at least, it makes more sense to procede through an animal model to make sure the protocol is safe and has a high degree of working before you jump into running tests on humans. I’d rather be responsible for the deaths of non-human primates than humans should my protocol not work in vivo (or vitro… I never could remember the difference).
Basically it’s a device used to deliver a small electric shock to a small back of cells.
Think of it like one of those adapters you get with modern electronics. There’s this large box that you plug into the well socket and it can deliver various electic pulses. Typically around 1-2 kiloVoltes and a few miliAmps. So, it’s nothing particularly dangerous.
Connected to the ‘adapter’ is a small tray. This tray is where you place the cuvette. The Cuvettes are what holds the cells we want to porate. They are around 1.5 inches tall and maybe .5 inches square. They are made of plastic, except on two sides where are metal–to conduct current.
To the cuvette you add a mixture of low salt media, cells and plasmid DNA. Plasmid DNA is a chunck of DNA containing 1 or more genes that is circular. You then place the cuvette in the tray, close it and press the ‘pulse’ button. Then the machine sends that small electric pulse through the cuvette and shocks the living hell out of the cells. When you do this to cells you create holes in their membranes (little pores if you will, hence electroporation). With the holes in the cells you can now have the plasmid DNA freely pass into the cells.
You’ve now just inserted viable DNA for a specific gene or set of genes into a group of cells! By using this technique you can introduce new characteristics to cell line. Now, almost all plasmids you use will have an extra gene on them. These genes code for, in bacteria, resistances to SPECIFIC antibiotics. This means you can then take your ‘transformed’ bacteria and put them on a agar plate with the same antibiotic that they have the resistance to from the plasmid and all of the bacteria WITHOUT the resistance gene will die. This way you make sure that and cells you continue to work with have the plasmid. We call this keeping them ‘in selection’. You can do similar things with mamalian cells.
And unfortunatly, no baboons are allowed in the virology labs. Especially considering the machines are roughly the same volume and weight as 4-5 year old notebook computers and cost 5-10k
I have NO training to work around/with the monkeys. And to be honest I don’t want to get near them. All requestions for blood samples are done through the docs in the hospital. They have animal handlers that collect the monkey and vet techs that help draw the blood.
I work with HIV/SIV. When I started work it was very strange to spend 6 or so hours in the BSL-3 suited up working with virus. It got worse when I started doing a lot of work with HIV, especially the strain I used. I later ran viability assays on the cells I infected with HIV. After 2 weeks after initial infection barely 20% of the cells remained alive. I don’t want to think what that virus would do to my T-cells should I get exposed to it.
Since I work at a facility that has one of the half dozen BSL-4 facilities in the nation I’m sure the did a fairly detailed background check. I do not do classified government research. The lab I work in is funded by NIH grants, all grant information isn’t classified and is available on the web. Anyone bored enough to read the grant applications could figure out most of what I do.
Velma:
We haven’t had much problems with protesters. In the year and a half I’ve been here there hasn’t been a peep. Before I started people were laughing at one protester who locked himself up in a cage by the front gates to “signify the crulety being done to those nobel creatures”.
Except he kinda missed a few key points: The vast majority of the baboons are in outdoor corrals that are larger than some football stadiums. None of the animals are housed in cages so small they can’t run around and all of the housing cages have stuff for them to climb on and swing off of. Heck, even the squeeze cages we use to transport the animals from where they are housed to the vets had porportionally more space in them.
But most importantly. And this is key here folks. He forgot to bring water into the cage with him. In late july… in texas. All of the various housing areas for the primates have easilly operated drinking fountains for the monkeys so they can always have access to clean, relatively cool water without wasting much water.
One thing I should point out, baboons eat EVERYTHING that can’t out fight them. Including the grass and trees that were origionally on the corrals they were housed in. Which I find bizzare given the huge volume of food they go through.
Oh yeah, I forgot the second half of Velma’s question.
Personally, I can’t stand non-human primates. They are loud, smelly and unbelievably VIOLENT creatures. Some of them like to fight, and you can tell which ones do because they have had their tails ripped/chewed off.
I also don’t work directly with the animals so, no I don’t form any attachments. In college I worked with mice and killing and harvesting organs from a couple, it never bothered me.
As for how we deal with the protesters… I’m not sure. All I know is that this is texas and security is handled by ex- airforce security officers.
CRorex you are the first person ‘in the know’ whom I’ve heard call them virii. Am I that far out of the loop? Is this the new terminology? What is your degree in? What exactly are you doing? At first I thought you were doing protein purification (same as me) but now I’m lost.
tsarina, I’m probably the other person you’re thinking about. I too am a Microbiologist (from MSU thankyouverymuch!).
I’m not even sure if I’m using the right words anymore.
Virion refers to a single viral particle. And never is used outside of textbooks from what I can tell.
Virius is generally used when dealing with one serotype of virus.
Virii I think is used when you’re talking about a wide range of different viruses (either multiple pathogens or serotypes).
That virology course was now almost 4 years ago and the terminology I use every day is utterly bizzare. We use the names of the isolates ie CL8 is “clone 8”. 027 is “oh-two-seven” 170 is “one-seventy” HIV-NL4-3 is “N L four DASH three”.
I don’t think it’s new terminology. I think there once were some rules of english governing which word to use when, but we’re dealing with scientists and virii is a pain in the ass to say.
I’ve got a BA in Biology, just general biology. I focused my studies in immunology, virology and microbiology. Which was a pain in the ass. I’ve got enough biology credits for 2 bio majors
I’m also doing some preliminary drug screening. Mainly toxicity, determining effective dosage and trying to determine which part of the virion the compound inhibits.
90% of my experiments are running infections and seeing how the production of antigen is impacted by the various treatments.
Influenza samples would be easy to obtain. The 1918 pandemic certainly shows that the flu can mutate into a lethal strain. So, why hasn’t anyone weaponized the flu?
And what’s the big deal about West Nile? I’m reasonably sure that I had it(studpidly took in sick bird at time the virus was being reported in the area. Bird died in 24 hours. I got sick shortly after.). The experience was less severe than the average cold or flu.
How difficult would it be to engineer and introduce an organ specific, human specific, luciferase virus? It could be the look of the 21st century! You could be the father of designer virus fashion!
Considering how easy genetic engineering is currently there are much worse thing you can do than to recreate the 1918 flu.
One of the reasons why the flu virus spreads so easilly is in it’s genetic structure, it has 8 small gene segments that aren’t well regulated. That, with the high mutation rate associated with the virus means it mutates at an increadable rate. This is why we need a flu vaccine every year, and why the vaccine doesn’t always work.
Now, I’m not too famaliar with the flu virus. But I’m thinking that the specific structure of the genes (the flu virus has a protein that is responsible for collecting 8 gene segements and building a virion around them) would make it quite difficult to splice in genes for a deadlier virus.
The other problems are with the incubation time and ease of transmission with the flu virus. You can have flu virus in you for several days before you start feeling sick, in the mean time you’re spreading the virus to everyone you’re coming into contract with. For a bioweapon I’m guessing this is a bad thing. It’ll spread too quickly and you won’t be sure your side will be affected by it.
As for west nile:
Like with chemical exposure researchers have determined the LD50 (lethal dose to achieve a 50% death rate) for virus. The more pathogenic strains of Ebola have LD-50’s of 1 viral particle.
With more benign pathogens it would take a large amount of initial exposure to cause death.
Also the functionality of your immune system plays a role in how sick you become.
Our immune system is broken into two parts: Cell-mediated (t-cell/b-cell and antibody resonce) and humoral (macrophage/something I can’t rembmer --basically immunecells that eat pathogens)
Now, some pathogens, there is a hemmoragic fever that makes for a really good example, cause different levels of damage depending on how sever each response is. With the hemoragic fever (which I can’t remember which one is it, I think Denube) if you body generates a strong cell mediated responce you’ll die. That’s because the virus grows in your lungs and with a strong enough immune responce killer T-cells (T-cells that kill cells infected by pathogen) will basically destroy your lungs.
So, I imagine that you exposure to West Nile might have something to do with low initial exposure to the virus coupled with a more ‘proper’ immune response.
Either that or you already had a headcold and just associated that with West Nile.
Without running your blood serum looking for West Nile antibodies nobody will be able to tell.
As for tailoring viruses. It’s quite easy now. Gene therapy for years has worked on the principle you can use specifically tailored retroviruses (viruses that need to intergrate their DNA into a host cells DNA to replicate) can be directed to target cells either by treatment (inhale the virus to get it to the lungs) or by changing the receptors on the virus to ONLY respond to marker protiens found in the tissue type you want to effect.
If you know the proper biochemistry and you have the correct genes it’s just a matter of cutting and pasting genes in the virus. It’ll take maybe a month and a few hundred dollars, but it shouldn’t be much effort.
My medical biochem class is discussing HIV right now, and I feel I have just enough knowledge to be dangerous (not as in to cause harm, but in misunderstanding things).
Our professor emphasized that although SIV and HIV are related, SIV is not fatal in primates. To me, that seems as though it would invalidate some work done with SIV. Or, are virologists looking at the SIV-primate system and comparing it with the HIV-human system, to make the latter more like the former (ie not fatal)?
I’m not quite a micro person . . . I’ll graduate in May (crosses fingers) with a degree in biomedical engineering, but I decided to be hard-core and pick up a second major in biochem. And I spent a year as an undergrad assistant in a genetics lab.
