We are told that all is well. Meanwhile millions of Africans are going to die over the next five years and what comes to mind for me is Ralph Steadman.
Here's the All's Well town crier:
And this:
And finally:
Lovely. Nothing for Americans to worry/panic about. Which is true, except that the specifics of these billboards are not perfect matches to either the African experience or the basic science.
The first thing that is going to go wrong is this "21 days" claim for the time between exposure and disease development. That was always a guesstimate. This gets repeated over and over despite that it ignores the science of virus mutation.
For example, Peter Piot, Director of the London School of Hygiene and Tropical Medicine, weighed in. He was a principal investigator on the team that discovered Ebola Virus originally in 1976.
The virus is continually changing its genetic makeup. The more people who become infected, the greater the chance becomes that it will mutate ...First thing, EBOV moves that "21 days" guesstimate to 6 weeks or 10 weeks. The slower the better. When that happens, we can call the result a Piot Effect. Ebola doesn't make the change happen intentionally/deliberately; this is Biology 101's natural selection.... which might speed its spread. Yes, that really is the apocalyptic scenario. Humans are actually just an accidental host for the virus, and not a good one. From the perspective of a virus, it isn't desirable for its host, within which the pathogen hopes to multiply, to die so quickly. It would be much better for the virus to allow us to stay alive longer.
Could the virus suddenly change itself such that it could be spread through the air?
Like measles, you mean? Luckily that is extremely unlikely. But a mutation that would allow Ebola patients to live a couple of weeks longer is certainly possible and would be advantageous for the virus. But that would allow Ebola patients to infect many, many more people than is currently the case.
Second thing, the active symptom phase gets slowed from three or four days (untreated) to a week or two.
Third, EBOV goes highly contagious prior to the appearance of symptoms.
Honestly, #3 would be my choice for #1 if what we're doing is a technical risk analysis for the options. Here they're ranked for likelihood/early appearance as the virus mutates. It's easy for EBOV to get to #1.
"Going airborne" has very little to do with this. EBOV passes in human sweat and sebum/skin oil. We know this from analysis of African test swabs. The virus can remain active for at least a few minutes in sweat/sebum on common surfaces. "Airborne" would speed things up, but the saturation projections would not be very different from what is expected now.
Saturation
Saturation projections are ONLY based on current conditions. No mutation. No new medicine. No massive investment of materials/personnel.
Today, projected out 5 and 10 years using demographic analysis tools.
For saturation, we need to focus on the long term. Take today and see where it goes. It is all very well to track what happens today in West Africa. A projection for what can happen by January 20th, 2015, will do no harm. But long term saturation is what tells us the full impact and this means trying to simulate disease events for 5 and 10 years ahead.
A vaccine is not included in the simulation runs. It does not exist. We have 38 years of laboratories trying to create an Ebola vaccine. So if that effort only takes another 3 to 5 years, we will be lucky. If it takes 10 years no one should be surprised.
Doing a blocker drug is a simpler task. What the blocker does is to slow virus replication in the way it uses DNA or (in the case of EBOV) RNA. More below.
Saturation looks to spread across all of West Africa and then Central Africa. Target populations reach areas where politics/religion/superstition deny Western science. Nigeria's effort with the Patrick Sawyer event can be viewed as a delaying action. Ebola virus is obtaining every advantage, these days, and it can be expected to blanket the region within two to three years.
Total infections for equatorial Africa can go to 80,000,000 cases.
If we do not get an effective RNA blocker for Ebola and the DNA-based HIV blockers also fail for one reason or another, the total deaths in Africa can go to 50,000,000 individuals.
From a Steadman supertoon:
This is "Gus." For now let's call the black eye "Dallas." Rename as occasions warrant. (Reddened and squashed. See the original at ralphsteadmanshop.com -- the Breaking Bad collection.)
There is more bad news. Any equatorial country with slums can suffer similar EBOV contagion and saturation effects. For example, from Dr. Piot:
Do you think we might be facing the beginnings of a pandemic?One horror for India is that their clinics and visiting health care workers could easily enough spread EBOV. Similar to the actions of nuns at clinics in earlier outbreaks of EBOV in Africa.There will certainly be Ebola patients from Africa who come to us in the hopes of receiving treatment. And they might even infect a few people here who may then die. But an outbreak in Europe or North America would quickly be brought under control. I am more worried about the many people from India who work in trade or industry in west Africa. It would only take one of them to become infected, travel to India to visit relatives during the virus's incubation period, and then, once he becomes sick, go to a public hospital there. Doctors and nurses in India, too, often don't wear protective gloves. They would immediately become infected and spread the virus.
We do not have the necessary information at hand to generate a saturation simulation for India. Same time, killing 50,000,000 virtual Africans in the computer is enough e-blood for now.
And finally, EBOV is indeed unique. The test results for Infection Threshold show that 1 to 9 virons/virions/virus bodies are sufficient to generate the Ebola Hemorrhagic Fever disease.
The one viron threshold is all but unique. And of course these are tiny objects: "Each virion contains one molecule of linear, single-stranded, negative-sense RNA, 18,959 to 18,961 nucleotides in length." 970 nanometers long. Not visible in a light microscope.
Telling people that it is hard to get Ebola hemorrhagic fever is belied by the numbers coming out of Africa. The doubling cycle in their urban slums reportedly looks to be 16 days, as well as 25 days for rural areas. What could possibly be "hard to get" that goes with those numbers?
The White House needs to get on board for a reduction to optimism. Bad news is what it is.
As Ebola moves slowly toward saturation levels in equatorial Africa, less of undue optimism in statements from our public officials should be the rule.
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Good news !!
The science for applying a generic antiviral to take on Ebola had already been published. That was in the United States in 2014. We already had live testing of a similar-action drug Favipiravir/T-705 from April, 2014, with aerosol-exposed mice as well as human cell cultures:
Post-exposure efficacy of oral T-705 (Favipiravir) against inhalational Ebola virus infection in a mouse model.The Africans are expanding application of generic anti-viral medications (from HIV efforts, mainly) with reductions to the fatality outcomes. One imagines that the sooner T-705 gets out there in barrels, the better.
Smither SJ1, Eastaugh LS2, Steward JA2, Nelson M2, Lenk RP3, Lever MS2.Abstract
Filoviruses cause disease with high case fatality rates and are considered biological threat agents. Licensed post-exposure therapies that can be administered by the oral route are desired for safe and rapid distribution and uptake in the event of exposure or outbreaks. Favipiravir or T-705 has broad antiviral activity and has already undergone phase II and is undergoing phase III clinical trials for influenza. Here we report the first use of T-705 against Ebola virus. T-705 gave 100% protection against aerosol Ebola virus E718 infection; protection was shown in immune-deficient mice after 14 days of twice-daily dosing. T-705 was also shown to inhibit Ebola virus infection in cell culture. T-705 is likely to be licensed for use against influenza in the near future and could also be used with a new indication for filovirus infection.
Copyright © 2014. Published by Elsevier B.V.
KEYWORDS: Aerosol; Bioterrorism; Broad-spectrum; Ebola; Favipiravir
Reducing lethality from 70% to a range of 15% or 30% for African Ebola patients is all to the good. That does not change the base contagion statistic -- the virus continues to spread wildly among individuals who are not being treated with blocker.
(Hi there, le trump l'orange. How's ya doin'?)
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There was no way to know on October 17th that just the week prior to this diary being published, the deaths from Ebola started down in the county containing Monrovia, Liberia. Apparently the combo of effective quarantine in place (with cheap bleach sprayers) and using the HIV-connected antivirals made for big improvements.
You gotta love the local health service people in Monrovia. Their enhancement of the quarantine-in-place system are stunning. And Dr. Logan from Tubmanburg just up country for his experiment using Lamivudine/Epivir. Deaths down by 63% overall as tallied with dead body pick-ups by week in October.