To start with, I'm not a doctor. I do have access to medical journals and publications, a lot of practice and history to interpreting them, and an insatiable curiosity bug.
I'm also a hard-core science fan (anyone who reads journal publications for fun would have to be), and the F/U/D floating around out there about Ebola has been annoying me severely.
So, what follows below the squiggle of doom (or whatever it is) is a collection of topics, links, interpretations (mine), and general information on the scientific aspects of the disease.
What it is:
First off, let's describe what is happening: there is an outbreak in West Africa of a viral disease known as Ebola Hemorrhagic Fever (EHF), simplified as "Ebola" by most people who don't like near enough to the river to know the origins of the name. The virus is usually noted as EBOV in publications; specifically, this is the Zaire strain of the virus, ZEBOV, generally considered the most lethal. There's another virus, Marburg Virus (MARV), that is basically just slightly different from EBOV.
EBOV is a "filovirus", which as a lot of technical definition behind it, but simplified it means "Ebola and Marburg and an obscure virus called Lloviu that you've never heard of and has never made anyone sick". The point, really, is that EBOV is a fair bit different from other viruses you're more familiar with.
How it works:
One difference is in how it infects a cell. Structurally, you've all probably seen what EBOV looks like: a long, thin strand of string. The string is actually "hairy": EBOV has things coating the outside called glycoproteins. Like, a lot of them. Glycoproteins perform two functions: they allow the virus to attach to cells, and they also camouflage the virus from the immune system. A guy named David Sanders has been one of the primary researchers in how EBOV is structured (it resembles certain avian retroviruses, so there may be a common ancestor).
Another study determined that in order to infect a cell, EBOV has to have the glycoproteins stripped off the outside (called edosomal proteolysis). Once this happens, a receptor on EBOV is "revealed" and the virus can then infect the cell. A PBS summary says it this way:
“The previously hidden receptor rearranges itself and spring loads like a spear fishing rod,” said Saphire. “It uncoils, springs forward and penetrates the membrane, driving itself into the cytoplasm.”
It's only at this point that the body recognizes the virus as foreign and starts to attack it. The body's primary defense is to create Ebola Immuglobulin G (IgG); I think there are other antibodies, IgA and IgM, but IgG is the one that is referenced most often (I think the others disappear after infection whereas IgG provides
longer-term protection). IgG attacks the "naked" form of EBOV (I'm not sure where it binds to on the virus, but probably not the receptor site since immunity to one strain of EBOV doesn't seem to provide immunity to others).
Like HIV, EBOV attacks white blood cells first. Unlike HIV, EBOV then goes on to attack almost everything else as well, though the most well-known symptom is the inner lining of blood vessels: called the endothelium, EBOV seems to have preferential binding to it. Weakening these then causes the bleeding that gives hemorrhagic fevers their name.
Within the cell, EBOV requires a lipid (cholesterol to lay folks) transporter created from a gene called Niemann-Pick C1 (NPC1). As that linked article says, various mutations in NPC1 seem to render immunity to infection from filoviruses; prevalence of such mutations isn't really known, though some Euroean-descent populations seem to have it more than others (it's estimated to be 1 in 300 in most of Europe but, for example, 10% in Nova Scotia). Extreme mutations in NPC1 lead to a terminal disease called Niemann-Pick (where the name for the gene originates), as the body can't process cholesterol (which is actually important to function, even if that's not a justification for eating more fast food).
Death from EHF most often comes from shock/low blood pressure: generally speaking, the body has the ability to fight off the disease, but it must survive long enough to do so.
Where it comes from:
A lot of effort has gone into figuring out how people contract EBOV.
The most likely and common source seems to be bats. Bats are apparently asymptomatic carriers of the disease: they don't come down with EHF, but they also don't develop antibodies to fight off EBOV. As such, once infected, they simply carry it with them until they die. In scientific terms, this is called a reservoir species; technically, a reservoir species is an animal or insect vector for transmission. For example, mosquitoes are the reservoir species for malaria; n the case of EBOV, it's "transmission" over an extremely long period.
A lotof other animals, plants, and insects have been tested over the years; while different strains vary in how they affect different animals (for example, the Reston strain of EBOV is harmless to people but deadly to monkeys), there are certain generalities. Primates (including people) are the most susceptible to both the virus and the disease. Bats are asymptomatic carriers. Canines and mice have both tested positive for antibodies but not the virus itself (see "how we test for it" below). Pigs are unique in that the virus seems to infect their lungs and cause viral shedding (contagion) without developing other symptoms.
Due to the NPC1 connection, it's possible that mammals are the only things susceptible, and even among mammals there may be extremely limited vulnerability.
How we describe it:
Ebola is fairly deadly. Science generally refers to the official rate at which people die from a disease as the "case fatality rate" (CFR) expressed as a percentage of cases where the final outcome was death vs all cases that have had a final outcome (death or cure). The important thing to remember about CFR is that it ties back to a specific case: if person A was infected, what was the final eventual outcome of person A (cured or died)? When you read about people saying there is a "death rate" of 50% (or whatever), what they're usually referring to is "how many people are infected right now versus how many people have died so far"; this will be different from the CFR, as during an escalating outbreak (more people becoming infected more rapidly), there are (unfortunately) a certain percentage of people alive right now who won't be in the next few weeks.
The CFR for the current outbreak is about 70%; a past study (which I can't find right now) early in this outbreak of specific cases and their outcomes placed it at 67%.
Another variable you'll read about is the basic reproduction rate - R0, r-zero, r-naught. R0 is the average number of infections generated by each specific infection; when R0 = 2, each infected person (on average) infects two other people. The R0 for the current epidemic is about 1.8; historically, the R0 for EHF is usually listed as "at or under 2". For comparison, the R0 of something like Whooping Cough is about 15. An R0 of less than 1 means the disease cannot sustain itself in a population long-term.
R0 tells you nothing about the course of a disease or how long someone remains contagious: for example, the Spanish Flu had an R0 of about 2.7, not much higher than EHF, but the mechanics of the Flu are significantly different. With the Flu, you're contagious 1-2 days before symptoms exhibit and up to 5 days after they start, giving a 7-day window to infect 2.7 people (on average); with EHF, you aren't contagious at all until symptoms start but, once they do, remain extremely contagious past death or for 18-20 days (more on that later).
There's another number used to describe an outbreak, and that's the "doubling time". This is the number of days it takes to double the number of cases. Doubling time is only useful for a specific outbreak, not a disease, because it is dependent on a large number of factors. The doubling time for the current outbreak is ~28 days but has been slowing (which generally reflects the intervention of medical personnel).
All of these values, in fact, are very dependent on sociopolitical factors, the genetics of the population in question, and a number of other things. For example, the CFR for EHF reflects almost exclusively its history in West Africa, where other diseases are also widely prevalent and often co-morbid (malaria and HIV, for example). They also reflect the generally-poor living standards in the area. R0 can change with population separation, sanitation habits, etc. In fact, all of these values are descriptive rather than predictive: they'll tell you what has happened, but they can't guarantee that the same will happen in the future.
How we diagnose it:
There are two official ways to detect if someone has a EHF, one more indirect and the other direct.
The indirect method involves looking for those antibodies in the blood stream, usually IgG. The test to detect antibodies is usually an ELISA (the rapid-result tests for HIV are ELISA tests). Basically, a dot changes color when exposed to the right antibody. This is the test most often done in the field, as it is fairly rapid and easy to do. However, it's important to remember that ELISA doesn't check for the presence of a virus, just the antibodies to the virus: if your body hasn't begun producing antibodies, you may get a false negative.
The direct method takes longer to do but is more accurate. This is a reverse-transcription polymerase chain reaction (rt-PCR). PCR is the standard DNA test you see on all the crime dramas, and rt-PCR results look similar (it's the same test, but an extra step is needed to prepare the sample). Basically, the rt-PCR is used to look for actual traces of EBOV RNA in a sample; if it comes up positive, the virus must be present, but if it comes up negative, it may only mean that the virus isn't present enough to register.
In case your wondering why everyone doesn't just do rt-PCR, it's because it typically takes 24-48 hours to perform and requires some special equipment (not too special - I actually did PCR traces in my bio class in high school). But when you hear about the CDC "testing for Ebola", this is what they're doing: shipping the samples off to one of their labs and running the rt-PCR.
How we treat it:
For the most part, there's no active treatment of EHF. Treatment usually consist of preventing shock and supplying fluids to give the body a chance to fight off the infection. However, there are several techniques that may help (there is still too scant of data to say for sure).
People who survive EHF still have antibodies (remember IgG) in their blood for years afterwards; getting a blood transfusion from an EHF survivor early after onset of symptoms seems to increase survival rate.
ZMapp, which is the main "experimental treatment" you may have read about, is a set of artificially cloned antibodies (technically, monoclonal antibodies, mAbs; in fact, one of the components in ZMapp is ZmAbs, with the other being MB-003). It basically serves the same purpose as the blood transfusion, only a recovered patient isn't needed. On a random note, it's being grown in tobacco plants.
The problem with any more direct treatment is of course those glycoproteins that "mask" EBOV from the immune system. The new vaccine that Canada produced (rVSV-EBOV) is actually a similar-to-rabies virus that has been modified to induce an immune reaction against the glycoproteins of EBOV. The technique is relatively new and called "vectored immunoprophylaxis" (VIP for short) and looks extremely promising. However, it might need to be used in conjunction with something like ZMapp or some IgG production to be effective.
About that "not contagious until symptoms" thing:
There's not a lot of study on the pathology of EHF in humans, since there generally aren't many cases (thankfully) and it's not exactly ethical to infect people with it (also thankfully). However, one study was looking into the pathology of known cases and how diagnostic tools might be able to predict outcome.
The part of this study that is relevant here is that they took serial tests (ELISA and rt-PCR) for patients starting at the day of symptoms and continuing on until final outcome (cure or death). They were specifically trying to see if any of those tests could predict who would die and who wouldn't, but the graph of the results is really interesting. Here it is:
Summary of RNA copy and antigen levels of EHF cases with fatal and nonfatal outcomes. Each bar represents the arithmetic mean value, and the error bars represent 1 standard error of the mean for each time point. (A) Mean log10 RNA copies per milliliter of serum from 18 survivors and 27 nonsurvivors. The threshold of detection was 6,200 RNA copies per ml of serum and was the lowest level detected in any of the patients analyzed. For the purposes of the graph, this value was assigned to samples of laboratory-confirmed patients that had Ct values of 40. (B) Mean antigen levels determined in duplicate aliquots of those described in panel A. The positive threshold was 0.45 adjusted ODsum units at 410 nm. For samples to be considered positive, they must have had a titer of at least 1:16 and an ODsum of >0.45. (C) Mean antigen levels determined for the specimens described in panel B combined with antigen levels measured in samples from an additional 35 survivors and 62 nonsurvivors that were not tested by Q-RT-PCR (total = 89 fatal and 53 nonfatal cases).
The caption is straight from the publication, but the main point is that it shows the results of three sets of tests: (A) is the rt-PCR testing for viral RNA (and it's a log scale), (B) is an ELISA of the same people in A testing for antibodies, and (C) is the same test as (B) but includes people who didn't have the RNA test done. The graphs start at 0 days after onset of symptoms (basically, right at onset), but not all patients started testing right after becoming symptomatic. All three vertical axes identify the threshold below which a positive response can't be seen.
Now, while nothing here lists pre-symptomatic patients, even those patients who were tested as soon as they became symptomatic had extremely low levels of antibodies and virus; if we extrapolate backwards following the curves, it's likely that even one day prior to symptom onset none of the tests would have come back positive.
This fact - and other substantiation elsewhere - is why individuals who have been infected with EBOV aren't casually (is in, in a casual manner) contagious prior to being symptomatic: the level of virus at onset of symptoms is barely measurable. It's later on when you get those huge spikes in (A) - remember, it's a log10 scale, so every "number" is 10x the value of the prior - that virus starts coming out of everywhere (largely due to blood vessels breaking down) and patients are extremely contagious.
This fact is also why mandatory quarantines for people coming back from West Africa don't necessarily make sense but monitoring for symptoms (namely, fever) does: it's the onset of symptoms that delineate between "not contagious" and "contagious".
On a positive note:
Médecins Sans Frontières (MSF) International (Doctors Without Borders) had, as of mid-September, 3000 staff in West Africa. Assuming a ramp-up and a mild amount of "churn" as some people are sent out and new people replace them, it's easy to assume that twice that number have been in West Africa as some point since March. And yet, out of those potentially 6000 people, MSF only had 14 infections in the same period. That's less than 0.25%, and most of those were believed to have occurred outside their facilities (on time off).
None of the people who were quarantined due to interacting with Thomas Duncan - including the family who were in the apartment with him and the woman caring for him - came down with EHF, and we're well past when symptoms should have developed.
Resources are currently heading to West Africa to help deal with the outbreak. Some nations and regions are already starting to bring the disease under control: as of mid-October, Sierra Leone and Liberia were starting to get their outbreaks under control, and Guinea has had ups and downs; Nigeria completely stopped its progress in their country.
Things are improving, and more help is needed. But we have a lot of information and science to throw at the disease.
(This is my first diary, so please be gentle.)