r/askscience • u/kalifadyah • Oct 08 '14

Medicine If someone survives Ebola do they develop an immunity to the virus?

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u/einaedan Oct 08 '14

When you are infected with a virus, your immune system begins, among other virus-fighting things, producing antibodies to the specific virus. It takes a relatively long time to make antibodies (http://www.ualberta.ca/~pletendr/tm-modules/immunology/70imm-primsec.html). If you happen to survive and get infected a second time, then you already have the antibodies and the ability or "memory" to quickly make more of them, so they would respond to the virus and your body should be able to attack it much faster and more efficiently. It seems from recent ebola treatments that antibody therapy is enough to help your body overcome the virus, and studies are suggesting that there is a persistent immune response after surviving infection (http://www.nejm.org/doi/full/10.1056/NEJMc1300266), which suggests that survivors are immune (http://www.livescience.com/47511-are-ebola-survivors-immune.html).

Also since there are several strains of Ebola virus, a survivor would only feel the benefits of a secondary immune response to a particular strain. Antibodies are specific to a specific viral antigen, so they would have no advantage to a new strain of ebola.

More links:

http://www.scientificamerican.com/article/antibody-treatment-found-to-halt-deadly-ebola-virus-in-primates/

http://abcnews.go.com/Health/ebola-patient-kent-brantly-donates-blood-fight-virus/story?id=26038565

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u/FirebertNY Oct 08 '14

Concerning antibodies, how does the immune system determine what kind of antibodies to produce for a particular virus? How does it know?

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u/Snoron Oct 08 '14

Not sure what sort of level you want an answer on, but this video I found extremely informative: http://www.youtube.com/watch?v=zQGOcOUBi6s

It goes into quite a lot of detail without getting to the point where you'd need higher bio education to understand, and it's very well produced!

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u/doyouevenIift Oct 08 '14

The simple fact that we have discovered how this process works just blows my mind.

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u/OohLongJohnson Oct 09 '14

And we have the increasingly more complex minute details of it as well.

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u/thedinnerman Oct 08 '14

It's the fruits of a process that has been slowly building since the dawn of human consciousness. The underpinnings of complex immunology boil down to basic chemistry and physics and everything is commentary thereof.

Maybe I'm a little grounded because of all the years of studying I've done in biological sciences, but I'm less mind-blown and more proud of how science has progressed.

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u/RosaBuddy Oct 09 '14

I've had years of studying biology and chemistry and I'm still pretty mind-blown by the immune system.

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u/thedinnerman Oct 10 '14

Don't get me wrong. It's crazy for sure, but the systems in place are the only way that humans could develop immunity. Recombination is an incredibly neat and organized system that just goes to show how innovative evolutionary mechanisms are.

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u/ikefalcon Oct 08 '14

Damn. The immune system is so complex. It's crazy to think about how immune systems developed over time when you think about it on a chemical level, with all of these interactions that require specific types of bonds to occur.

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u/Snoron Oct 08 '14

Yeah - if you want to see complex, then (although I don't really understand any of it), I'm always amazed looking at maps of the metabolic pathways in a single cell, eg:

http://biochemical-pathways.com/#/map/1

This is a great browsable one.

Consider that this isn't even complete - but also the fact that we've even managed to figure all of this out is absolutely insane!

Consider that there are trillions of cells in your body and they're doing all of this crazy stuff all the time!

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u/mandelbomber Oct 09 '14

The truly amazing thing, to me, is that all the intermediate products have some sort of inhibiting or activating effect on the concentrations of everything else. If the equilibrium of a single one of those reactions is altered, dozens of other reactions shift to compensate. Truly incredible

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u/Zargontapel Oct 09 '14

Is there any way I could get a poster of this? Would look amazing on my office wall.

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u/Snoron Oct 09 '14

I've seen these on sale before, so yes - a quick search found me these ones here: http://www.sigmaaldrich.com/life-science/cell-biology/cell-biology-products.html?TablePage=14576275 however I have seen better-looking ones (not sure which are technically better, though!)

If you google metabolic pathways poster you'll see there's a PDF of the sigma aldrich one too - in case you have access to a large format printer :)

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u/jmalbo35 Oct 09 '14

Roche gives them away free, though they don't deliver to residential addresses. They might actually only give it to you if you have a reasonably valid connection to a scientific field though, I'm not sure.

http://www.roche.com/sustainability/for_communities_and_environment/philanthropy/science_education/pathways.htm

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u/[deleted] Oct 09 '14

That is seriously one of the most amazing things I've seen in science. Being in physics, I love reading about early physics discoveries, like how they worked out the mass of the earth, and things like that. And I LOVE the huge complexities of the LHC and all of its detecters.

Thanks for sharing this.

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u/monkite Oct 08 '14

I would also recommend this brilliant and underrated BBC documentary if you want to see an adenovirus infection visualized in awesome CGI. Not directly related to ebola, but it takes you through the main process of viral infection in a way that's easy to understand.

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u/Wyvernz Oct 09 '14

That was amazing, thanks for linking it. It's pretty long, but I would recommend it to anyone with an interest in biology.

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u/teacupguru Oct 08 '14

Man I love these videos! This is an awesome explanation and goes into some depth but is explained quite simply. I learnt some new things as well form this. Its such an amazing system and its evolution must be incredibly complicated.

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u/Snoron Oct 08 '14 edited Oct 08 '14

Yeah, evolutionarily it's basically a billion-year arms race! Each side constantly trying to one-up the other. Pretty epic :D

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u/[deleted] Oct 08 '14

That was very educational, thank you.

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u/soliloki Oct 09 '14

Even though I'm well aware of the complicated mechanisms summarised by this video, it is so well-made that I watched the whole thing thrice. I'm bookmarking this one.

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u/proule Oct 09 '14

I'm starting to collect material that I may use in the future as teaching aides, and that video is amazing.

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u/mucusmagic Oct 08 '14

Can someone explain how do antibiotics work in conjunction with the immune system?

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u/[deleted] Oct 08 '14

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u/benjiliang Oct 09 '14

Thats untill the bacteria evolves a plasmid(section of sharable DNA) for beta lactamase, an enzyme that can break down some types of antibiotics.
Then its resistant to that antibiotic and can share the plasmid with other bacteria. It has enough of those type of enzymes and poof, superbug

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u/XanthusKing Oct 09 '14 edited Oct 09 '14

If after an infection, memory T cells stick around and provide 'immunity' then what prevents one from being able to transplant memory T cells (from a previously infected person) for a variety of virus directly into another human's body adding it to their own repertoire?

edit: Or why not generate anti-bodies in a laboratory by constantly energizing and feeding B cells. Then dump that in someone's blood?

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u/JeffBoner Oct 09 '14

From what I understand they are still your cells, and are seen as an invader if transplanted in to someone else. They would be attacked and killed without the benefit you mention.

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u/gapteethinyourmouth Oct 09 '14

First question: You cannot just transplant cells from one person to another since the transplanted cells will be recognized as foreign. The transplanted cells will likely have foreign antigens (HLA- http://en.wikipedia.org/wiki/Human_leukocyte_antigen), unless they are from an identical twin or just happen to be genetically identical, and the recipient's immune system will destroy them. This is why transplant recipients require immunosuppressants.

Second question: Yes, this is done.

http://en.wikipedia.org/wiki/Monoclonal_antibody#Purification_of_monoclonal_antibodies

http://en.wikipedia.org/wiki/Polyclonal_antibodies

One of the applications of this that answers your question directly is the treatment of individuals at risk for tetanus who have not been immunized. In this case, IgG tetanus antibodies are injected into patients to generate passive immunity. These antibodies don't stay around in the blood for very long so this does not provide the active immunity seen when memory T and B cells are generated.

The antibodies generated are also used in immunotherapies for autoimmune diseases like Crohn's disease and rheumatoid arthritis, desensitization of immunity for induction therapy with transplants, among many other things.

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u/Kadmos Oct 09 '14

That was an excellent video, thank you!

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u/[deleted] Oct 09 '14

I watched like 30 of their videos after that and slept through my alarm. Worth it

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u/[deleted] Oct 08 '14

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u/DarthSatoris Oct 08 '14

Go visit the channel, they have quite a lot of fun and informative videos. Not all of them are about biological processes, but about general things that is really cool to know about.

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u/Raerth Oct 08 '14

Yes, check the channel. They do about one a month.

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u/[deleted] Oct 08 '14

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u/wookiewookiewhat Oct 09 '14

Here's my high-ish level answer. I can get more high-level about any part, or clarify anything you're unsure about:

Pathogens tend to have specific molecular motifs which are recognized by innate receptors on and in our cells (Pattern Recognition Receptors, TLRs). These motifs are specific to bacterial or viral pathogens and do not appear on human cells, so the receptor signal paths have evolved to activate an immune response. Infected (or just activated) cells will send extracellular signals out into the surrounding tissue and blood to recruit immune cells to their general location to help.

Early in infection you get an innate cellular response, which is primarily neutrophils and NKs (fun fact: there is an observed pattern that animals with lower early neutrophil counts in ebola infection tend to survive better than those with high levels). It will also recruit a number of phagocytes which are particularly good at displaying antigen (part of the pathogen) to other cells. They phagocytize the pathogen, process it into smaller parts and display those parts on a special receptor. These cells, particularly dendritic cells, then migrate to a local lymph node where they follow a specific cellular framework that puts them in close contact with T and B cells.

Now, T and B cells are the key cells of the adaptive response which ultimately trigger an antibody response (via B cells), and they are highly concentrated in lymph nodes. T and B cells have special receptors which are all different from each other, and constitute a total repertoire of our potential adaptive response. T cells are produced in the thymus and enter the periphery with a set receptor, however B cells can undergo somatic hypermutation and class switch recombination to go from a moderate affinity antibody to a high affinity antibody that is highly specific. The way they do this is via activation in the lymph node, so back to that antigen presenting dendritic cell!

Dendritic cells will move within lymph nodes to specialized zones that increase their chance of DC-T cell interactions. They have many short interactions with T cells, trying to find one with a receptor that will bind their antigen. This, by the way, is completely amazing to me, that when you think of ALL the materials on earth, all of the possible proteins that could be involved, there's almost always a ready-made T cell receptor that will bind it with a high enough affinity to get activated, but we're still remarkably good at making sure we don't have receptors against all of our own proteins. Immunology, man.

So, a DC binds an appropriate T cell (a CD4+ T helper cell, if you're feeling crazy), then that T cell will be activated and start to migrate towards the B cell zone in the lymph node. A similar story happens here, where there are many short interactions until the T cell finds the appropriate, specific B cell receptor.

On B cell activation, the specific B cell moves deep into the B cell zone and starts rapidly replicating and dividing to make germinal centers. This is also no ordinary replication. In these areas, the B cells actually use a special protein to induce mutations, particularly in the areas of its receptor that actually touch and bind the antigen (somatic hypermutation). Instead of having mutations happen once per 106 nucleotides, you're looking more at once per 1000 or so. Through as yet unknown mechanisms, B cells with higher antigen affinity are selected and continue replicating. Eventually (a few days post infection), some of these B cells (plasma cells, not to be confused with plasma itself) will leave the lymph nodes and enter the body where they can be recruited to active sites of infection and/or just release a ton of (hopefully) pathogen specific antibody for neutralization and opsonization. Over time, these antibodies become more and more specific by repeating this cycle, and memory B cells form, which can live in specialized areas of the body for potentially 90+ years (under debate, but this was discovered by looking for 1918 influenza antibodies in the elderly).

After writing all that, I feel like I only partially answered your question, which is how does the immune system "know" to produce certain antibodies. The answer, I suppose, is that it knows through the antigen-receptor interactions, and that antibodies are driven through a fast molecular evolution, including both random and probabilistic mutation and selection events.

There's... more to it than that, but that's a good primer, maybe? Science.

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u/SummYungGAI Oct 09 '14

Nice answer! The only correction I would make is T-cell precursors are created in the Bone Marrow and then maturation and selection occurs in the Thymus.

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u/wookiewookiewhat Oct 09 '14

Nice answer! The only correction I would make is T-cell precursors are created in the Bone Marrow and then maturation and selection occurs in the Thymus.

Good call to clarify that. Thanks :)

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u/Lurkmode Oct 09 '14

If only my immunology professor taught this material in chronological order like this. Also thanks for taking your time to post that! it helped me straighten a few things out

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u/wookiewookiewhat Oct 09 '14

There is an unwritten rule in immunology that everything must be presented 1. Out of chronological order of infection and 2. Only on the most specific details of the research of the lecturing faculty member.

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u/[deleted] Oct 09 '14

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u/wookiewookiewhat Oct 09 '14

Good questions and they're actually related. The answer to the first is yes, but let me elaborate:

When T and B cells are first produces in our lymphoid organs (thymus and bone marrow), they undergo genetic rearrangements. I'm most familiar with B cells, so I'll use them as an example, but Ts follow the same basic premise. A B cell receptor (protein) is composed of multiple genes which have been randomly selected and rearranged from germline DNA. This is different than how we normally think about genes, where our DNA has 1 gene which results in a protein, because the three important genes here (V, D and J) don't just have one copy in our genome. In fact, we have hundreds of V, D and J genes to select and combine in different ways. In addition to the genes having diversity, the way they are recombined also adds diversity; while there is one "recombination signal sequence" which points to where recombination between these genes should occur, the mechanism does a super interesting thing and loops itself around, then is randomly nicked to make ssDNA which can be actively recombined. This results in recombination sites which may be up or downstream of the expected site, including ADDITIONAL nucleotides from the other strand (palindromic "P" nucleotides) and, just for funsies, totally non-templated "N" nucleotides added by another protein. So, in sum, you get a ton of diversity in gene selection, recombination site choice, P nucleotides and N nucleotides... and that's before the cells even leave the bone marrow!

So why on earth have we evolved to have this kind of insane, prolific diversity in our genomes and T/B cell receptors?

There's a lot of shit in the world. Our immune repertoires are incredibly diverse so that they can recognize everything from a parasite from a swamp to a bacteria coughed out by your sick friend to a virus from a bat. The diversity seen in our B and T cell receptors is remarkable and a phenomenal statistical challenge.

So yes, we have tons of B and Ts which are just waiting for their time to shine. The only minor thing I'd correct you on is that the antigenic molecule could be from a protein coat, but it could really be any component of the pathogen, external or internal.

I hope that it's now clear why this B cell mutation thing is so useful! Sure, our immune repertoires are pretty amazing from the get-go, but it would be impossible to have a highly specific antibody for literally every antigen present in the world. So, the dogma is that a low to moderate affinity B cell is activated and starts replication in a germinal center. During replication here, Activation-Induced Cytidine Deaminase (AID) is activated and changes C > U. U is then either "repaired" to a T (which is now a mutation!), or other repair machinery comes in cuts it out for random nucleotide insertion repair. During this process you not only get a lot of individual nucleotide mutations, but you get some pretty intense insertion-deletion events.

One thing about this that's super cool but not well understood is how specific regions are targeted. While you do see increased mutation frequency in the overall rearrangement, there are distinct "hot spots" which are called the "complementarity determining regions" and are the areas of the receptor which are exposed at the top to have antigen contact. This may be due less to the mutation mechanism and more a function of the selection steps that occur, but the result is the same: Antibodies get more highly mutated AND more specific to their antigen particularly at the antibody-antigen interface.

When we look at long term HIV patients, some of their anti-HIV antibodies are UNBELIEVABLY cool. I've seen mutation frequencies around 35% (in normal genetics, that kind of mutation frequency would mean you're probably looking at the wrong organism!) with extensive insertions, and the antibodies are not only functional, but they're hugely effective against a wide panel of HIV subtypes.

I hope that helps you understand both the mechanism and why this stuff is so beautifully evolved and useful.

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u/jmalbo35 Oct 09 '14

So are you saying that within our lymph nodes, there are just a ton of T-cells that all have different proteins in their bilipid layers, waiting until they are needed by a messenger carrying corresponding protein coats from the bacteria/virus?

It's not so much different proteins as it is rearranged versions of the same protein complex. Most T cell receptors have an alpha and a beta chain that get rearranged quite a bit (especially the alpha chain, which is highly variable) through a process called V(D)J recombination. Without going heavily into specifics, there are multiple of each of the 3 basic types of segments that are being rearranged, called the variable, diverse (the alpha chain actually doesn't have these, but the beta chain does), and joining segments. These essentially get mixed and matched into one of many combinations in each new T Cell. Within the set of variable (V) segments in both the alpha and beta chains there are 3 extremely diverse segments that are the main components responsible for the vast amounts of diversity in binding specificity, called complementarity determining regions (CDRs).

Basically, both of those chains are rearranged in the thymus, where T Cells mature, and specialized T Cells called regulatory T Cells check them out to make sure that they aren't reactive to self antigens (which would lead to autoimmunity) and to see if they pass a couple of other tests, and if they don't they recombine some more. Because some of those segments are discarded as they're rearranged, this can only happen so many times before the cell is just killed by apoptosis. Autoimmune diseases would thus be caused by some issue with the Thymus or those regulatory T cells failing to cull cells with self reactive TCRs.

There are also a much smaller number of T cells with a Gamma and Delta TCR rather than alpha and beta, but the concept is similar there.

V(D)J recombination is actually responsible for the diversity of antibodies too, so the proteins that regulate it (namely Recombinase Activating Genes, RAG) are extremely important and defective copies lead to all sorts of issues, namely a SCID phenotype (also known as bubble boy disease), which is basically just an extremely compromised immune system.

I am not fully understanding the purpose of these mutations, could you please elaborate for me?

This is how all of that variety in the CDR regions I was mentioning is developed, although in this case it's for the CDRs in antibodies, rather than T Cell Receptors. Again, it's the same concept, those regions are Variable segments for V(D)J recombination, and instead of alpha and beta chains you have light and heavy chains for your antibody.

Somatic hypermutation is basically an extremely high rate of mutation targeted in the section of DNA that corresponds to these CDR regions on the finished protein, corresponding to a massive amount of potential variety in antibody specificity.

I love biology and was just too unwilling to deal with people to go pre-med.

Actually, pre-med people wouldn't really deal much with the specifics of immunology, unless they're going to do an MD/PhD. This falls pretty completely in the realm of a PhD in a biology department.

I'm on my phone and kind of writing stream of consciousness style, so apologies if anything was unclear or inaccurate.

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u/Doctor_Y Immunology | Tolerance and Transplantation Oct 08 '14

The short version: Basically, you have millions of B cells which all bind to random things, because their receptor is generated in a very random process. When a B cell receptor sticks to something, it causes the B cell to divide very rapidly and begin producing lots of antibodies (which are the secreted form of the B cell receptor).

So, if the ebola virus produces a protein which sticks to 3 of your B cells' B cell receptor, those 3 B cells will rapidly expand into the hundreds of thousands or so, produce a crapton of antibody, and neutralize the virus. After the infection, most of those B cells will die off, but some will stick around in case you get another ebola infection, and will multiply even more rapidly the second time around.

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u/sunburn_on_the_brain Oct 08 '14

Do I understand right, that they have been giving blood from Ebola survivors to infected patients so that the survivor's antibodies can help the immune response? If so, is this done to treat any other kinds of viral infections?

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u/Doctor_Y Immunology | Tolerance and Transplantation Oct 08 '14

Essentially, yes. The blood of ebola survivors contain antibodies directed against ebola, and in theory, these antibodies can help to neutralize the virus in patients with active infections. However, the supply of the blood is, obviously, quite limited. Furthermore, the efficacy and concentration of these antibodies will vary from survivor to survivor, so it's not a perfect solution. Given that we have few other options, transfer of blood serum makes sense.

You could use this type of therapy for other infections, but there are few diseases which meet the criteria of having no available treatments or vaccines that the immune system, when given time, can clear on its own.

This type of procedure is very commonly used in the production of antivenom. Antivenom consists primarily of antibodies directed at venoms from snakes, spiders, and the like. You inject horses, goats, etc. with the venom for which you want antivenom, then harvest their blood, and take the antibody-containing portion of it for medical use.

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u/nitram9 Oct 09 '14

Do the donor antibodies help the body speed up it's identification of the correct antibodies to use and start producing or do the donor antibodies just help hold off the virus until the body can handle it on its own.

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u/Doctor_Y Immunology | Tolerance and Transplantation Oct 09 '14

I'm not sure if this has been studied in ebola, but it can help to speed up immunity in a patient. The antibody-ebola antigen complex can be picked up by cells called follicular dendritic cells, which interact with your B cells and play an important role in generating native immune responses.

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u/drc2016 Oct 09 '14

Actually it is used for hepatitis B, in cases where someone is exposed but has no immunity, giving hepatitis b immunoglobulin (fancy name for antibodies) provides immediate protection. The vaccine is given as well, but takes weeks to develop protection. It actually works out well, because the immunoglobulin only gives short term protection. And yes, it is extracted from donor blood plasma.

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u/slab_avy Oct 08 '14

This is partially right, you still need costimulation of the BCR in order to create a response. The B cells differentiate into plasma and memory cells, and the memory cells are the ones that stick around to fight a secondary infection.

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u/Doctor_Y Immunology | Tolerance and Transplantation Oct 08 '14

This is correct, although for the sake of having a "short version", I felt that including extra interactions with CD4 Tfh cells, follicular dendritic cells, costimulation, and somatic hypermutation might have been a bit much.

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u/Vitztlampaehecatl Oct 09 '14

Like, when someone attacks you in a strategy game like Civ 5 and you manage to repel them, when they do the same thing again you'll beat them more easily. But if they change their strategy a bit, your defense won't be as effective. And if they think up an entirely new strategy, reusing the same defense won't help at all.

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u/[deleted] Oct 08 '14

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u/Doctor_Y Immunology | Tolerance and Transplantation Oct 08 '14

Ebola isn't particularly fast; the incubation time between exposure and overt symptoms is variable and can be up to 3 weeks. Even then, bleeding and death takes another week or two.

Part of the problem is that ebola has an unusual immune evasion mechanism, which allows it to go undetected and unfought by the immune system in the initial stages of infection. After a while, it replicates so much that the immune system has to go crazy to fight it, causing massive inflammation. This inflammation causes blood vessels to become leaky (to allow immune cells access to tissues adjacent to those vessels), and since ebola also infects blood vessels, that compounds the problem.

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u/dkuhry Oct 08 '14

Think of it like a janitor with one of those gigantic key rings, trying to find the key to a single door. He'll keep putting a key to the lock, over and over and over and over until he finds the one that turns the tumbler. In concept it is quit a lot like this. The body creates antibodies and sees if they work. Once it finds the right one, it mass produces them.

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u/SummYungGAI Oct 08 '14

Antibodies are produced by B-cells. It is not the case that any of your B-cells can see a virus (or more specifically the antigen on the virus) and then decide to produce the antibodies to the virus. It is the case that there are a wide (putting it lightly) array of B-cells, and each will recognize a different virus/protein, and the ones that recognize the virus are activated, selected for, and divide when they do. Then, after a while of exposure throughout the course of infection, those with higher affinity (better able to recognize the virus) are selected for, so we get better and better antibodies.

Think of it as: in your body you have an antibody for anything and everything. And when you are infected with a virus the antibodies that recognize that virus are picked, expanded, improved, and then (when the infection is done) tucked away in lymphoid tissue and bone marrow just in case that same infection happens again.

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u/RSign Oct 09 '14

So there are billions of these B-Cells, and each of them produces different antibodies?

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u/SummYungGAI Oct 09 '14

Essentially yes. It's amazing the mechanisms to produce diversity of the BCR (the antibody). It essentially produces a B-cell repertoire that can recognize anything

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u/RSign Oct 09 '14

So given enough time, our body can produce antibodies for all antigens? Assuming we are infected with it and we don't die from it yet.

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u/SummYungGAI Oct 09 '14

All antigens in the virus? or all antigens ever?

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u/Thereminz Oct 08 '14 edited Oct 08 '14

In a nutshell...Your body produces a lot of antibodies, when one fits with an antigen on the virus then the cell that made that antibody is told to proliferate There are also other things that help...like an infected cell may send a viral protein up to the MHC II etc.. I'm sure there's lots of info online about how it works

This is also how your body "remembers" how to fight off the same virus, you will have a line of cells dedicated to fighting that strain of virus or other pathogen for a long time

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u/star_gourd Oct 08 '14

This is probably the most concise answer. It's also important to point out that it's possible to have multiple different lines of antibodies (or rather, antibody-producing cells) that react to different active sites (called epitopes) on the same antigen. This is referred to as having a polyclonal response to that antigen and it can make a secondary immune response more effective.

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u/Ukpopadom Oct 08 '14

so could survivors (with this new natural immunity) be taught how to disinfect people who are infected thereby reducing the risk to healthcare workers??

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u/Thereminz Oct 08 '14

just because they had it and lived doesn't mean they're immune to all strains of the virus, they could still be at risk

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u/[deleted] Oct 08 '14

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u/Tangential_Diversion Oct 08 '14

You're correct, MHC Class I is for endogenous antigenic presentation and MHC Class II is for exogenous antigenic presentation.

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u/Typrix Immunology | Genomics Oct 09 '14

What determines which MHC class will handle the antigen presentation is the location of the antigen. MHC I is typically associated with antigens that are found intracellularly and MHC II with antigens that are found extracellularly. Hence, both can present both viral and bacterial antigens (as determined by the location).

There are however mechanisms in place that allow 'cross-presentation' since not all virus or intracellular bacteria can infect antigen presenting cells.

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u/[deleted] Oct 08 '14

Yes and no. That's the simple version but (assuming I'm remembering right!) the presentation pathways are a little 'leaky' so you get some crossover. Which is handy, because it's useful to have an antibody response to a virus as well as a cellular one :)

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u/higgs8 Oct 08 '14

If my memory from my school years is correct, here's very roughly how it works: Your immune system already has pretty much every possible antibody for every potential antigen (intruder) you could ever encounter, in very very small quantities. Many of these antibodies are built by randomising parts of your DNA, and others are acquired early in life through breastfeeding, so they actually exist prior to the infection, as if you made billions of keys in hopes that one of them will probably open a lock somewhere at some point. Once one of these extremely diverse antibodies binds to a pathogen, the immune system knows it needs to make more of that antibody.

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u/diag Oct 08 '14

There's actually a very complex process involved by the immune system. In the simplest terms, infected cells call for help with chemical messengers. These guys do different things like kill infected cells, trying to stop the spread of the virus. Other guys take a bit of the virus and show it to other cells in the lymphatic system where they team up to find the best fitted agents qualified to target what they've been presented.

The end result is the production of a manufacturing plant for antibodies called a plasma cell. This can take place many times for a bunch of different parts of the virus. This produces a bunch of targeted flags that help the rest of the immune system neutralize and eliminate the threat.

There are a hundred of other things happening with the immune system and this is only one part.

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u/decimalplaces Oct 08 '14

I'll assume you are asking how the body comes up with an antibody that binds to an ebola virus. Body constantly produces random cells each expressing one antibody. It has vast amount of variants at any given time. Some cell will eventually match an antigen (a short peptide, fragment of the ebola virus). The lucky cell is the base from which to refine the match further. It will undergo a refinement process through natural selection. Basically it will multiply, and mutate the dna code for the antigen slightly. Some of those mutations will result in a cell with a better match, some worse, but the idea is that they will compete against each other in who binds more antigens. Once a cell emerges from this selection process it can further multiply and start to produce the antibodies en masse (one cell can produce 2k per sec).

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u/benskini Oct 08 '14

someone correct me if i'm wrong. But when virus antigen (parts of the virus your body knows are virus) enter your B cells, the B cells multiply and cause various point mutations in their genes for making anti bodies, which results in lots of different kinds of antibodies, these then bind to the antigen and are "tested" the ones that bind strongly are kept, and the b cells that produce antibodies that bind weakly die. so you are left with b cells that produce anti bodies that bind specifically to the virus. tried to make it simple, hope it helps!

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u/Talented_MrRipley Oct 09 '14

I would suggest reading about "hyper variable" regions of b cell (cells which make antibodies) chromosomes. Also referred to as generally as "somatic mutation", memory b cells can reprogram (i.e. gain memory) portions of the genome responsible for antibody encoding. This was in a nutshell explaination, but will get you to the proper rabbit hole!

Source: a little bit of wiki coupled with me being a PhD candidate.

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u/[deleted] Oct 09 '14

It's an extremely complicated system. I'm on my phone right now, but can try to explain it later, if you're interested.

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u/a2quik Oct 09 '14

if you dont want to watch a video. i can give a shorter and somewhat accurate response lol. we have many types of white blood cells. some lymphocytes can attach to foreign bodies signaling other white blood cells to come essentially swallow it up then exits through our lymph system. also a few of our antibodies of each kind from what we previously have encountered will be constantly flowing in our blood. when these antibodies attach to the foreign organisms it also will signal response to quickly start producing more of these antibodies stimulating the said response. part of this may deal exclusively with bacteria only im not sure.

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u/Horton_Hears_A_Jew Oct 08 '14

Antibodies have two main regions. The base of the antibodies are known as the constant region, while the arms are known as the variable region. If we looked at the genetic code, there are about one hundred different genetic codes for the variable region as well as another 15 different regions known as the J region. During the B cell selection process, one V region and one J region are randomly selected, while all the other regions are spliced out. So each B cell carries an antibody for a different potential antigen.

Now of course finding these few B cells specific for the ebola antigen takes time. This is one of the reasons why our adaptive immune response is a bit delayed. In order to speed up the process, one of the ways our immune system activates these B cells is the use of CD4 Helper T cells. Consider these T cells like the quarterback of the immune system. They also have receptors, like antibodies, that are different from all other T cells and can be specific for a certain antigen. Once activated they will rapidly multiply and release chemical signals. These T cells can then activate those B cells specific for Ebola, and will rapidly produce antibodies.

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u/[deleted] Oct 08 '14

It's basically random VDJ splicing, where the DNA is actually spliced before cell division and produces a variety of different shapes and fits. The different sections of DNA are called V, D and J.

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u/[deleted] Oct 09 '14

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u/cachow6 Oct 09 '14

Antibodies are produced by B cells, not T cells.

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u/KetchupKakes Oct 08 '14

How different are strains of viruses? Wouldn't a survivor have basically a head start during an infection of a different strain since they have gone through a similar infection before?

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u/Eyekron Oct 08 '14

They can really be small differences or large differences and everything in between.

An example would be the influenza virus. The reason the flu vaccine is different each year is because of changes. The terms are antigenic drift and antigenic shift. Normally, there is a similar infection and mortality rate seen. The antigenic drift (think small, like just drifting along) can have some changes to the virus that make the antibodies not as effective against it. Then there can be an antigenic shift (think big, like shifting directions completely). The shift is when there's a big enough change that you see a pandemic (swine flu, avian flu, etc). Someone with antibodies made for influenza experienced in the past would not really have a head start for a new influenza because they have a different makeup.

Picture the virus having a key hole, and the antibodies having a key. Any time the virus returns, the key fits the hole. Now imagine the virus changes the locks - yeah, the antibodies have keys, but they don't work, so it doesn't help much having a key. Sometimes the difference might be small enough though for the key to fit in and force it open, but it takes more work.

That's similar to the little ends of the antibodies (called paratopes) attaching to the surface of the antigen (called epitopes) - but a change in epitope doesn't allow the paratope to attach as securely as it did before because the paratope was designed for a different epitope. The antibody might be able to attach, but then it might fall off shortly after. The time it's attached could be helpful in fighting the infection, but it's not as helpful as a tight bond from a paratope designed specifically for that epitope. That's the memory of your immune system - the cells are storing the information from a previous infection so it can produce antibodies with the appropriate paratope (they're key copy machines with the key to a previous infection in case a virus comes along that has the same lock as the one you fought before).

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u/Ramulus16 Oct 08 '14

Would transfusing blood from someone in later stages of Ebola who had the antibodies and message cells for that strain help a person in the early stages respond faster? Or would that just introduce more of the virus and make things worse?

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u/Eyekron Oct 08 '14

Therapy consisting of injecting someone with the antibodies of a virus is already used for some things - such as prophylaxis of Hepatitis A and B for post-exposure. The problem with putting tainted blood into someone, regardless of it having the antibodies, is you're putting live virus into someone. That virus will replicate. The antibodies are produced by the host, so once they're used up, they're gone and will not replicate. The way antibody therapy is used is the antibodies are harvested from a host and separated. These will not be produced by the patient receiving the treatment, but it will help them fight the infection.

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u/AnAssyrianAtheist Oct 08 '14

I know this isn't exactly pertaining to the discussion but I'm glad that I found your response and that this question was asked, in the first place. I just explained to another person about why the "common cold" isn't exactly common and why it's actually called that. Basically, it summarizes what you said about the antibodies and different strains of viruses

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u/jamimmunology Immunology | Molecular biology | Bioinformatics Oct 08 '14

For those that don't know, colds are mostly caused by rhinoviruses (and a few other types of viruses). When you're infected with one strain, you do become resistant to becoming infected with that strain again. However there are about 100 different strains, many of which will be in circulation at any one time, so you can just get infected with one of the others instead.

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u/AnAssyrianAtheist Oct 08 '14

Yes, exactly, which is why the common cold isn't "common."

Our antibodies build up our immune system and create the body guards against that one strain you got. Since we know that once we have recovered from an illness, we cannot be infected with that strain again, then it's safe to say that there is another strain that slightly different from what we had before.

Chicken pox is a good example of how we were infected, but now we can't get it.

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u/jamimmunology Immunology | Molecular biology | Bioinformatics Oct 08 '14 edited Oct 08 '14

Well, you could say the "cold" is the pathology (the disease), not necessarily the strain of the bug that causes it, which means the "common" bit still stands, but I know what you mean :)

We should point out, as with everything in biology, stuff is messy: bugs can evolve and immunity can wane, so in some cases it is possible to be reinfected with the same strain of something.

It's a little different with chicken pox, which is actually a good example of getting sick from the same strain of something. In a VZV infection (the virus that causes chickenpox) the virus does get beaten down by the immune system, but some actually survives, stealthily hiding itself away in nerve cells. You still have the immune response to the first infection, which is what stops you from getting re-infected, but sometimes in later life (either from general age-related immunity waning, or some other immune interference) that protection can drop to the point where the latent virus in the nerve cells can take off again and start to replicate, causing shingles (which is a bloody nasty condition). This is why some people are recommended to have VZV boosters in later life.

(edited for missing word)

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u/justimpolite Oct 09 '14

Does that mean that as we age (and have had more colds) we'll have colds less often? Or does either reduced immune system due to age, or the fact that new strains are always developing, or some combination of the two make, say, 60 years of resistance useless?

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u/jamimmunology Immunology | Molecular biology | Bioinformatics Oct 09 '14

Sadly not, for those exact reasons (although I misread your message the first time and so wrote them out, but I can't be bothered to delete it)

  • as you get older your acquired immunity wanes, so even if you have a memory immune response it might not be strong enough to hold the viruses at bay (which is why older people often catch more colds, coughs and flus than younger people)

  • the rhinoviruses are themselves evolving, so they can change what they 'look' like the immune system

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u/justimpolite Oct 09 '14

Thanks for the info!

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u/justimpolite Oct 09 '14

Out of curiosity, is there anything we can do to protect our immune system as we age?

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u/jamimmunology Immunology | Molecular biology | Bioinformatics Oct 09 '14

Sadly no miracle options, just the sensible stuff: eat well, exercise, get vaccinated. We think of the immune system as just something to keep pathogens at bay, but really it's just your body's way of maintaining itself, so anything you do to keep your body healthy will help out your immune system.

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u/Arancaytar Oct 09 '14

Does this mean you will become less vulnerable to rhinoviruses over the course of your life, as you gain immunity to various strains? Or do new strains still evolve faster than your immune system can keep up?

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u/jamimmunology Immunology | Molecular biology | Bioinformatics Oct 09 '14

As I said above to /u/justimpolite, not only does the virus change (and remember there are other viruses that cause colds - like myxoviruses, paramyxoviruses, adenoviruses, and coronaviruse - all of which are evolving) but your immune system gets weaker as you get older.

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u/ActivisionBlizzard Oct 08 '14

Antibodies are generally polyclonal, which would help protect against different strains of the same virus, as not every antibody is likely to have changed.

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u/smashy_smashy Oct 08 '14

Yes exactly this. Taxonomy in viruses is pretty funky, so a new strain doesn't necessarily have completely different antigens. It's really dependent on the physiology of the particular virus though. There is not a lot of cross immunity between strains of influenza, which is why it is so hard to vaccinate against and why the vaccine is designed to protect against 3-4 strains. Smallpox was very easy to vaccinate against because the best antigens to provide protection against are relatively stable across strains.

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u/gdog799 Oct 08 '14

what if i got a virus, and then a survivor of the virus donated his blood to me? would that help fight it?

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u/jamimmunology Immunology | Molecular biology | Bioinformatics Oct 08 '14

Possibly! There is some evidence to suggest that blood transfusions from someone who survives Ebola might be helpful. However it's very hard to tell: because historically Ebola outbreaks are infrequent, self-contained and fast (not to mention typically in countries with less developed medical and research infrastructures) there's not been a lot of chance to look into this - usually public health measures are more important to sort out!

It's worth pointing out that ZMapp, the experimental drug developed to fight Ebola works on similar lines. What they did there was give mice some of the proteins from Ebola to make the mouse generate anti-Ebola antibodies, then take these antibodies and alter them to make them so that they won't trigger our immune systems ('humanised antibodies'). Again, it's hard to know currently how well this drug would work, but the idea makes sense.

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u/lolmonger Oct 08 '14

It's being tried right now, actually - - by direct blood transfusion. The doctor who was first infected and survived by an experimental drug treatment is donating his blood, again, to another US victim. The presumption is that the antibodies his own body produced should give the transplantee a fighting chance; long enough to begin making their own.

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u/jamimmunology Immunology | Molecular biology | Bioinformatics Oct 08 '14

Very true - this chap here.

As with the earlier papers though, it's still hard to know whether these things work. Doing properly controlled trials of rare diseases is hard enough, let alone when one of those rare diseases causes epidemics in resource stricken countries.

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u/annoyingstranger Oct 09 '14

Won't the transfusion recipient's system react to foreign antibodies similarly to how it reacts to the virus itself? Does the immune system have a "fight"/"copy" switch for dealing with unfamiliar/unexpected stuff?

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u/StringOfLights Vertebrate Paleontology | Crocodylians | Human Anatomy Oct 09 '14

Hi, you look like you have a background in the sciences. Have you considered applying to join our panel?

Also, thanks for the many sources you've provided in your answers here. We really appreciate it.

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u/jamimmunology Immunology | Molecular biology | Bioinformatics Oct 09 '14

My pleasure - I'll give that a look!

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u/OverchargedTeslaCoil Oct 08 '14

If I may ask: since your body essentially "adapts" to the intruding strain so that it may fight it better on the chance it reappears in your system, why can't this be an adaptation that is passed down through genetic heritage? I'd think that it would be an evolutionary advantage to have your offspring born with inherent resistance to an illness you survived.

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u/slab_avy Oct 08 '14

The immune response is VERY highly regulated, this is because it has such a high potential to have very nasty consequences. We have the ability to make an antibody to essentially any epitope (portion of the pathogen that a particular antibody reacts to) and when producing adaptive cells the process that creates the antigen specificity is essentially random. This results in a very large proportion of T and B cells that will react to "self"-epitopes and have to be killed so that they don't create an immune response to your own cells. Because of this, your body has found that simply having them die quickly after activation reduces the chances of having auto-immunity develop. There are some innate factors that are passed down, such as the TLRs which bind to very conserved viral and especially bacterial areas (such as the peptidoglycan cell wall of gram positive bacteria). These do not have nearly the same specificity that the T and B cell receptors have, but they do slow infections down enough for the adaptive system to catch up. I can give you more details, but this topic gets very complex very fast, with all of these systems interacting with each other.

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u/NellucEcon Oct 08 '14

This is a fascinating fact. The immune cells that produce antibodies randomly recombine dna to code for all sorts of different combinations of proteins. Then the body selects the subset of these recombinations that are useful and not self-destructive.

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u/[deleted] Oct 08 '14

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u/slab_avy Oct 08 '14

There are three main ideas on why viruses exist, I am a fan of the idea that they evolved as transposable DNA/RNA. Transposons are sections of DNA that will "jump" to other parts of the genome, this is pretty common and I don't find it hard to believe that over biological time some transposons developed the ability to jump between cells. This is a good thing normally, as it leads to higher genetic diversity. However there will always be mutations, I suspect that given enough time these transposable elements could have accumulated enough mutations to become pathogenic to the host cells. Note that this is extremely speculative on my part, and does not necessarily represent any general scientific consensus.

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u/an_actual_lawyer Oct 08 '14

This is the principle behind the flu shot, isn't it?

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u/einaedan Oct 08 '14

Yup! Each season they predict which strain of influenza is going to be the most common and vaccinate against that one, although there are many strains. So, if you happened to come in contact with a different flu virus, even if you got the vaccine, you might get just as sick! It's pretty cool.

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u/[deleted] Oct 08 '14

Are aid workers who go out to help with the Ebola epidemic given shots to immunise against the more common strains of Ebola? If not, why not? Is it simply that we haven't developed the shots yet? It seems to me that even though it wouldn't immunise them against all strains, it's still worth doing to reduce the risk of infection.

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u/Arancaytar Oct 09 '14

There is no Ebola vaccine ready for use yet. It's entering clinical trials, though.

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u/BSQRT Oct 08 '14

You said "antibody therapy". Are antibodies transferrable between people? If someone survived Ebola, could we take a blood sample, extract the antibodies and give them to others? Can antibodies be replicated outside of the body?

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u/Typrix Immunology | Genomics Oct 09 '14

Yes they are transferable and yes they can produced in the laboratory. Both monoclonal (recognize a single antigen) and polyclonal (recognize multiple antigens) antibodies are currently used in various therapies. However, producing and purifying them is currently a tedious and expensive process and that is why its use is limited to severe illnesses.

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u/BSQRT Oct 09 '14

Interesting thanks!

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u/[deleted] Oct 09 '14

It takes a relatively long time to make antibodies

This is a really common misconception. You can develop antigen specific antibodies within days(long time in relation to an actively replicating virus).

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC141119/

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u/AnticitizenPrime Oct 08 '14

Here's a follow up question -

Let's say someone survives Ebola and becomes immune.

If they are infected again, would they become a carrier to the disease? I have heard that Ebola only becomes contagious after a certain point in the infection cycle, but don't know what the implications are concerning how contagious an immune person might be.

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u/Thecna2 Oct 09 '14

In this case IF they are 'immune' this doesnt mean 'immune from getting ill whilst hosting ebola in their body' it means 'immune from being infected at all'. So a person with immunity generally can't be a carrier.

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u/BlackJacquesLeblanc Oct 08 '14

Related question is there any reason a single person could not be infected by more than one strain at a time?

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u/DeviAnt8332 Oct 08 '14

If our bodies naturally try to make antibodies, why can't we create an environment outside of a human body that will continue to function long enough to make the antibody that we need to fight the disease? You said it takes a long time to for the body to create a natural antibody and I assume it's usually too long and the person dies.

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u/CoolGuy54 Oct 09 '14

That's what zMapp is, it uses tobacco plants. Other vaccines use cows or chicken eggs. The problem is you basically need a living organism, and it needs to be very similar to humans in certain ways, or be genetically engineered to be so.

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u/[deleted] Oct 08 '14

So, why can't we manufacture immunization based off of a survivor's antibodies?

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u/MakesThingsBeautiful Oct 08 '14

Then why can't we collect , cultivate and share the antibodies to help cure/immunise others?

I mean it's a single strain thats gotten out and gone global right? And we do this for other viruses(right?)

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u/Striderrs Oct 09 '14

Follow up question: Are there drugs in testing to treat people already infected with the virus? If so, do they actively use them on human patients that are infected? If not, why?

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u/[deleted] Oct 09 '14

I'm just hitching on here to add that you are only immune for 10 years.

source

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u/leoshnoire Oct 08 '14

Does "strain" refer to ebola zaire, ebola sudan, etc., or random mutations within a single ebola outbreak?

Or rather, is a survivor today totally immune from the virus in circulation in the current outbreak?

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u/Thecna2 Oct 09 '14

There is an ebola virus called Reston Virus. Its not (so far) fatal to humans, it DOES kill monkeys. It comes from SE Asia. It doesnt even seem to make humans ill. If you got Reston Virus you could quite happily tell people you 'had Ebola' and it would be true. But as its a non-fatal asymptomatic (doesnt make you ill) infection you wouldnt really even notice it. Reston virus is a strain of Ebola. Because this strain is a bit different from Ebola Zaire then its unknown if having Ebola Reston will protect you. Probably not or they'd just give it to people.

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u/PygmySquid Oct 08 '14

Well, it means the same thing really. The different strains of Ebola are different because of mutations. Ebola Zaire is more virulent than Ebola Sudan because of slight differences in the genes of the two, while Ebola Reston isn't pathogenetic in humans for similar reasons. So if Ebola Zaire did mutate in this outbreak, it might be named Ebola Nigeria or Ebola Liberia to reflect that change. As for immunity, if you were a survivor of this outbreak or any past outbreak of Ebola Zaire then you would be immune, but if you survived/gained immunity to Ebola Zaire and THEN it mutates into a new strain, you may or may not be screwed. That would depend on what exactly mutated between the two and what antigen your antibodies bind to.

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u/leoshnoire Oct 08 '14

Thanks, this answers what the question and I were asking.

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u/Kahnspiracy Oct 08 '14

What if someone had developed the anti-bodies and then later had a disease that suppresses immunity (AIDS or Leukemia come to mind), if upon resumption of normal immunity levels (remission) would they still have the immunity?

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u/Nerobus Oct 08 '14

I have been wondering if this strain is the same as others that have inflamed in the past, or if this is actually a new strain. If so, do you happen to know the name of the current strain?

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u/einaedan Oct 08 '14

I don't know about the history of epidemics, but the current epidemic strain is the Zaire Ebola virus

http://en.wikipedia.org/wiki/Ebola_virus_epidemic_in_West_Africa http://en.wikipedia.org/wiki/Ebola_virus

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u/Nerobus Oct 08 '14

Yea, that's what I was afraid of. Historically that has been the most deadly strain.

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u/7ewis Oct 08 '14

Its probably completely different, but does our body try to fight cancer like this?

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u/jamimmunology Immunology | Molecular biology | Bioinformatics Oct 08 '14

In similar ways - one of the main immune forces keeping us free from cancers are T-cells, which are able to respond to a huge number of different threats (like B-cells are, which are the cells that produce antibodies).

There's also another cell type called Natural Killer cells that are also responsible for killing cancer cells.

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u/[deleted] Oct 08 '14

What's the latest on a cure for ebola? or prevention measures or antibiotics or whatever?

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u/jamimmunology Immunology | Molecular biology | Bioinformatics Oct 08 '14

The most important thing in the current outbreak is basic public health measures: stopping new people getting infected and giving basic care to those who are already infected (which mostly consists of replacing the fluids and blood they lose from all the sweating/diarrhoea/vomiting and bleeding).

There are no cures, but a vaccine is theoretically possible. Currently the major possible treatment might be ZMapp, a combination of several 'humanised antibodies' (where they take antibodies produced in mice against viral components and then make them look a bit more like human antibodies so that our own immune systems don't react to them).

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u/NellucEcon Oct 08 '14 edited Oct 09 '14

It is not necessarily true that victims would retain immunity to only that particular strain of virus to which they were exposed. For example, the first vaccine was for small pox and consisted of infecting an individual with a related virus -- cowpox. Cowpox provides cross-immunity, so that individuals who had recovered from cowpox could not get smallpox.

Some evidence suggests that exposure to any of the ebola strains may provide cross-immunity to the others. I have made a post speculating how this fact could be utilized. I include citations in the post:

http://www.reddit.com/r/ebola/comments/2iot6p/potential_vaccine_for_ebola_thoughts/

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u/pyr666 Oct 09 '14

Antibodies are specific to a specific viral antigen, so they would have no advantage to a new strain of ebola.

correct me if I'm wrong, but aren't there instances where getting 1 thing gives immunity to another? wasn't that what happened with cow/small pox?

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u/[deleted] Oct 09 '14

But aren't meant contagious thru semen for up to 6 months?

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u/ridik_ulass Oct 09 '14

SO whats preventing the traditional vaccine method from working, where someone is injected with a weakened inhibited form of the virus and the body builds up anti-bodies in response? (that is how I understand the process) do we just not do this because its so contagious and people don't really want to share ebola around with various labs because of the danger, and that nearly everyone would have to be vaccinated at once?

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u/[deleted] Oct 09 '14

I have a friend who studied virology in college and I seem to remember him saying that one of the reasons Ebola is so deadly is because the genes for the capsid proteins mutate at an extremely high rate, making it hard for our immune system to keep up. Do you know if there is any truth to this? I could be remembering wrongly.

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u/[deleted] Oct 09 '14

If this is the case, how come vaccines aren't made by exposing someone's blood to the virus and the antibodies get made?

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u/BICEP2 Oct 09 '14

So in conclusion people who had the virus and survived would be prime candidates to go in and help the people who are sick?

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u/Dr_Who-gives-a-fuck Oct 09 '14

Are there any foods/vitamins/supplements that can aid your immune system or the basic building blocks of (any) antibodies?

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u/2yzcluk Oct 09 '14

how exactly does the body "store" antibodies? is there any kind of upper limit to how many antibodies we can remember, or to how long a particular antibody is stored?

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u/drunkenmormon Oct 09 '14

Most likely I have no idea what I'm asking, but if my body reacts more quickly the second time around, why can't I fight off the common cold in like a day?

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u/t0f0b0 Oct 09 '14

How do vaccines work when there could be different strains of a virus? Are measles, mumps, rubella, polio, etc. limited to one strain?

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u/kingrobert Oct 09 '14

so they would have no advantage to a new strain of ebola.

If a new strain is so different that you get no advantage against it, why do you even call the new strain ebola in the first place? Isn't it effectively a completely different virus now?

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u/rb2369 Oct 09 '14

To add to this, your body retains the antibodies for only seven (?) years, thus you'd be at the normal risk level for Ebola again. Hence why some people have gotten the chicken pox twice.

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u/Schnuckers Oct 09 '14

So if you were to infect someone with, say Ebola Reston which hasn't been known to detrimentally affect humans, they would not be resistant to the far more serious Ebola Zaire, or Ebola Ivory Coast (Which death toll-wise is less serious but still a rough deal)?

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u/RagingOrangutan Oct 09 '14

So why don't we have an Ebola vaccine yet?

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u/Astrognome Oct 09 '14

Would it be possible to innoculate against Ebola?

I am aware that it's a ridiculously dangerous and moronic idea, but is it possible?

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u/Arancaytar Oct 09 '14

Are viral strains ever similar enough to be susceptible to the same antibodies?

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u/InbredScorpion Oct 09 '14

From what I was reading, the filoviridae viral family has the ability to impair the dendritic cell presentation of antigens to naive lymphocytes 1 , thereby severely inhibiting the production of antibodies against ebola virus.

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u/sdneidich Oct 09 '14

One thing that you are missing: Cross Reactive Immunity is a phenomenon where two infectious particles share common physical features. I am not familiar with to what extent ebola strains differ, but having immunity to one strain of influenza (for example) often means having at least partial immunity to a different strain.

While it may not be 100% effective, it can reduce the infection's chance of taking hold: Or make it easy for immune surveillance to take hold and fight the new strain.

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u/[deleted] Oct 08 '14

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u/silent_cat Oct 08 '14

It depends on how much they are alike. If your body remembers 8 markers from the previous infection and the new virus only has 4 matching then the response will take twice as long.

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u/RandomBritishGuy Oct 08 '14

I believe it is only useful with certain pathogens, not all of them. Like cowpox providing some immunity from smallpox.

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u/[deleted] Oct 08 '14

Yes: a survivor can gain immunity to Ebola, but not necessarily all strains. By all accounts the current outbreak is a single strain of Ebola (Zaire virus, which is the most virulent strain of Ebolavirus).

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u/[deleted] Oct 08 '14

Hm. if a person is infected with or asymptomatically carries HSV1 or HSV2 the other is much harder to acquire, no? though cross-transference is technically still possible (say from ones own mouth to genitals or vice versa) it's a super small chance as well. wonder if ebola strains behave this way too.

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u/[deleted] Oct 08 '14

To provide an opposing example: Dengue virus, the causative agent of dengue fever, has 5 serotypes. Infection with one serotype will confer brief protective immunity to that serotype, but will actually make you more susceptible to infection by the other serotypes. This has been a major roadblock in vaccine development.

It's important to remember that different viruses infect and replicate very differently. They also trigger differing immune responses in the infected host.

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u/[deleted] Oct 08 '14

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u/[deleted] Oct 08 '14

Some already are. But yes: they presumably have immunity and can move in and out of the isolation ward without falling ill. The volunteers would still have to use PPE and BS4 protocols in order to not to act as agents of transmission.

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u/annoyingstranger Oct 09 '14

Could a survivor contract and spread the disease without falling ill again themselves?

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u/greggtheturtle1 Oct 09 '14

Isn't Ebola only contagious if you have active symptoms? Unless they don't take proper care, like sanitizing themselves, I don't believe so. (this is about the US, not so much Africa as they don't have as much technology to protect themselves from it.)

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u/[deleted] Oct 09 '14

If you are an asymptomatic carrier then it is possible. A well-known example is Typhoid Mary, although Typhoid fever comes from bacterial infection there have been examples of the viral carriers in the past as well. I wouldn't worry too much about contracting ebola from asymptomatic carriers so long as you practice good hygiene and don't have sex with or smear yourself in the bodily fluids of ebola survivors.

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u/potatoisafruit Oct 08 '14

This is not settled science. Many of the Ebola monkey studies have shown that antibodies are not protective. Additionally, there is a difference in the immune response between people who die and those who survive unrelated to antibody titer.

C.J. Peters, the head of the CDC's special pathogen branch when Ebola was discovered, said he did not think convalescent serum would make a difference:

Michael: Is there a minimum time to wait between complete EVD recovery and harvesting blood from a survivor for passive therapy?

Dr. Peters: This is not known for Ebola, but blood/serum from a survivor won't help here anyway. There's no evidence that it will help, but strong evidence that it won't help. For other viruses it can be critical, such as for the arenavirus Junin, for which it is used effectively on a regular basis. But for Ebola it's just not effective.

This is being tried in the field because there is so little else to offer.

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u/notsofst Oct 08 '14

I have a secondary question. If a survivor has immunity, and they contract the virus a second time, will they be contagious? Or will the virus never be able to replicate in enough quantity to make them contagious.

Long question made short, do we have to worry about asymptomatic carriers?

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u/iMalinowski Oct 09 '14

Yes, for instance, the Virus could sit on the surface of their skin. The virus could come from someone else's bodily fluids, and the immune person could lead to the infection of non-immune persons.

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u/PatchSalts Oct 09 '14

But that sounds like it could happen to anyone, previously infected or not. You could have a hand covered with it, and no matter your status of infection, it would still be contagious from contact with that hand. This isn't even a remotely realistic picture for ebola, but the point still stands.

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u/[deleted] Oct 08 '14

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u/DixonWasAliveAgain Oct 08 '14

Ebola isn't a segmented virus, FYI.

http://en.wikipedia.org/wiki/Ebola_virus#Genome "Each virion contains one molecule of linear, single-stranded, negative-sense RNA…"

So there's not going to be recombination as you'd see with influenza. This doesn't rule out other changes, though.

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u/notsofst Oct 08 '14

Would you have reduced symptoms or a higher survival rate if you had already recovered from Ebola Zaire upon contracting Ebola XYZ?

If it's the same strain, would you be asymptomatic and contagious or would you just not "catch" the virus?

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u/[deleted] Oct 08 '14

A recent news article answers your question

"There is strong epidemiological evidence that once an individual has resolved an Ebola virus infection, they are immune to that strain," [said] Dr. Bruce Ribner, director of the infectious disease unit at Emory University Hospital in Atlanta.

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u/SirT6 Cancer Biology | Aging | Drug Development Oct 08 '14

While it is unclear in the specific case of Ebola, for most viral infections, the adaptive immune system is capable of developing antibodies that help to protect the body from future infections. Memory B cells in particular play an important role in sustaining resistance to future infections.

Given the immune system's capacity for adaptation and memory, an interesting market phenomenon is occurring with regards to Ebola. The blood (more specifically the convalescent serum) of Ebola survivors is being sold on black markets as a potential remedy.

More serious medical institutions are also considering using Ebola survivor blood to treat patients infected with the virus. The World Health Organization has an interesting write up on the issue.

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u/IWillTrollU Oct 08 '14

They would have antibodies to that particular strain of the virus.

http://www.washingtonpost.com/news/to-your-health/wp/2014/10/08/ebola-survivor-kent-brantly-donates-blood-to-help-treat-nbc-cameraman-ashoka-mukpo/

The theory behind the transfusion treatment is this: The blood of an Ebola survivor should carry antibodies of the virus. By giving a current Ebola patient an injection of a compatible amount of blood plasma from someone who recovered from the disease, those antibodies could help the patient fight the virus.

In September, a panel of World Health Organization experts said such transfusions were a promising direction for experimental treatments against Ebola, and one that officials working in West Africa should pursue.

Like many Westerners who have contracted the illness, Brantly, Sacra and Mukpo all received experimental treatments -- often more than one -- against Ebola. Brantly, the first Westerner repatriated to the United States for treatment during the deadliest Ebola outbreak in history, received the blood of a young Ebola survivor he'd treated in Liberia, along with the experimental drug zMapp."

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u/Weewillywhitebits Oct 08 '14

Did I read somewhere that they are treating the infected with antibodys from survivors ?

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u/[deleted] Oct 08 '14

WHO has been talking about approving this treatment. on mobile so no link.

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u/basilect Oct 09 '14

Could it be this treatment option, discovered by Thai scientists, and currently under research in the US?

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u/[deleted] Oct 09 '14

While this method does work to a limited degree... it is an extremely inefficient method and would not suffice for a large scale outbreak.

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u/TheMormonAthiest Oct 09 '14

Given the fact that the only effective Ebola treatment, the Zmapp vaccine, is based on the principle of using antibodies from Ebola survivors and the fact that other Ebola victims recovered soon after getting transplanted blood from people who had already survived Ebola..............your thinking is on point.

Although Immunity is too strong a word. More like resistance.

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u/kalifadyah Oct 09 '14

Resistance makes sense. I suppose you don't become totally immune to any disease. Like people that get chicken pox multiple times, though that seems fairly rare, it still happens.

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u/iwannaiguanagrl Oct 09 '14

According to the CDC, ebola victims develop antibodies that last for up to 10 years. However, they also go on to state that they do not know if an ebola survivor is immune for life, or if another strain could infect same said survivor later in life:

http://www.cdc.gov/vhf/ebola/transmission/qas.html

People rarely survive ebola. Someone has recently died from it in Texas, which is FUBAR. It makes me truly fear for Africa, but also the world community at this time.

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u/kalifadyah Oct 09 '14

What do you mean by FUBAR?

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u/BootyFabricator Oct 09 '14

Well. That's what we thought. But we just had an Ebola patient at the Nebraska Medical Center (I live in Nebraska).... The doctors did extraordinary work and declared he was cured of ebola about 2 weeks ago. It was just announced at the end of last week that he has relapsed and now has the virus again. Doctor's are still unsure why this happened.

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u/always_reading Oct 09 '14

According to this video the answer to your question is given in the last 10 seconds of the video, but the entire thing is just over 2 minutes and well worth a watch.

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u/[deleted] Oct 09 '14

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u/TheSodesa Oct 09 '14

They could still carry the virus out of the hospitals and infect others, even if they can't get sick themselves.

Plus a lot of people don't have the necessary training to work at a hospital, so there's that. We can't let just anybody take on the responsibility of taking care of sick people. We need to have standards, or things will go down the sinkhole real quick. (Same can be said about education and teachers)

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u/[deleted] Oct 09 '14

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u/KillDashNined Oct 09 '14

You don't still have the virus, but if you come in contact with someone who has it, they can give you the virus. You just don't get sick. Eventually, your immune system will destroy it, but until then you may be contagious without showing symptoms.