I thought your listeners might be interested in this one day Institute of Medicine meeting on Ebola Virus. It will be webcast, and is free:
November 3, 2014 (8:30 AM Eastern)
More male bovine faecal material from the government exposed.
Putting Ebola patients into hospitals without the biological containment beds (+equipment) and training endangers the lives of the medical personnel.
The government goons don’t have to risk their lives.
There is a reason why experimental work on pathogens like Ebola is restricted to BSL-4 facilities. That reason is also operative when a human container of Ebola viruses enters an Emergency Department’s triage area.
There is also a reason why there are Infectious Disease BL-4 containment wards. And there is a reason why the Ebola cases shipped back to ‘mericuh from elsewhere went to such facilities.
Just as anything less risks researchers’ lives, so too, anything less risks medical care providers’ lives.
“”The protocols that should have been in place in Dallas were not in place, and that those protocols are not in place anywhere in the United States as far as we can tell,” National Nurses United Executive Director RoseAnn DeMoro said Tuesday night. “We’re deeply alarmed.”
Emory & Nebraska together treated five Ebola patients: no health care workers got sick. The Dallas hospital treated one Ebola patient and two health care workers contracted the disease.
And the clown from the CDC had dished out the male bovine faecal material that all hospitals can safely treat Ebola patients.
Why Frieden needs to get the boot
Dear TWiV panel;
On the last TWiV, regarding the Ebola outbreak, Alan said “I think what often gets shortchanged is that the underlying causes of a lot of these problems are not virological or technological. You know, it is fine to have a technological solution for the people who can afford it, but the reason Liberia is having this outbreak is not because there isn’t a vaccine.”
Alan further explained how “we love technological solutions for social problems,” and how “the protective equipment for preventing the transmission against Ebola is not some very sophisticated 21st century I-Phone-6 kind of device. We’re talking about rubber suits and gloves here.” Would you be inclined to say PrEP for HIV is a similar instance of an expensive pharmacological solution to a social problem that could be more easily fixed with the use of a latex condom?
Regarding Pre-Exposure Prophylaxis for HIV itself: I’m told if an HIV-positive person has the K65R mutation against Tenofovir, and the M184V/I mutation against Emtricitabine, then Truvada used for PrEP won’t work to prevent an HIV infection. I’ve also been told this kind of drug-resistant HIV is rare, because drug-resistant viruses are more difficult to transmit, and as a consequence, very few HIV strains have the K65R mutation.
And, just like the K65R mutation, the M184V/I mutation exacts a fitness and transmissibility penalty against HIV too, however, it’s more common to find M184V/I because it’s easier to develop.
So, my question is; what factors will make the rare-strain of HIV which has both the K65R and M184V/I mutations become a common-strain? And, I’m curious about what are the factors which can transform a difficult-to-transmit strain into an easy-to-transmit strain? (My intuition based on the House Finch study in the attached link, is the transmissibility will increase as virulence increases, and virulence will always increase whenever human behavior enables the virus with more opportunities to be transmitted.) If you agree this is true, it seems to me all that would need to happen in order for Truvada to be rendered ineffective as PrEP, would be for it to be used on a widespread basis by people who choose it in order to practice condomless, recreational intercourse. What’s your impression of this point of view?
In addition, as more people start to use PrEP instead of condoms for HIV prevention, I’m curious to know what you might think are the chances some new and undiscovered emerging fatal virus or microbe will be transmitted by condomless recreational intercourse again, as happened during the outbreak HIV in the early 1980s. Would you say that is likely or unlikely?
Long time listener, first time writing. I’m a grad student at MIT working on viral genomics and have been following the Ebola outbreak with great interest and trepidation.
I have a few questions:
1) A few years ago, there was a fascinating set of papers identifying Niemann-Pick C1 as the receptor for Ebola, which you covered in TWiV #166. One of these papers identified benzylpiperazine adamantane diamide-derived compounds as inhibitors of viral entry. Do you know if that result is being followed up on?
2) Contact tracing is a proven technique but is manpower-intensive. I am concerned that as the exponential growth of the current outbreak kicks in, it will be untenable to track each patient. A successful strategy used during the smallpox eradication led by Donald Henderson et al. was ring vaccination. Although there is obviously not a proven Ebola vaccine yet, I wonder if the ring strategy can be adapted in some way to the current outbreak, for example by focusing on decreasing person-to-person contact within a certain geographical areas. Could you comment on this and any other logistical strategies being used as the epidemic well and truly shifts to log phase?
3) Lastly, I’d like to reiterate Thio’s question from TWiV #304, except from the perspective of someone in the US: as a graduate student (hopefully a post-doc soon!) with training in genomics and some virology, do you have any pragmatic advice on anything I or other young scientists can do to help, either in terms of research or in the context of an aid organization?
Thanks for the great podcast!
I think you should have discussed disposable needles more.
Peter Piot showed that the first described ebola epidemic (Pattyn, S.; Groen, G. V.; Jacob, W.; Piot, P.; Courteille, G. (1977). “Isolation of Marburg-Like Virus from a Case of Hæmorrhagic Fever in Zaire”. The Lancet 309 (8011): 573.) was amplified in hospitals by use of reusable needles.
And then there’s HIV (Pepin, Jacques. The Origins of AIDS. Cambridge University Press, 2011.)
Hi Vince and friends.
I can think of one virus that eventually went airborne… The Transmissible Gastroenteritis (TGE) coronavirus of pigs was for decades confined to the fecal-oral mode of transmission – just like PEDV that is currently sweeping the Americas. However, in 1984, a respiratory variant porcine respiratory coronavirus (PRCV) was observed, first in Denmark and soon after in other European countries..The PRCV has a deletion in the spike gp (see e.g.http://www.ncbi.nlm.nih.gov/pubmed/?term=10948987). Within a couple of years this virus spread to most SPF herds in Denmark, showing the ability to spread over long distances (probably 10-50km).
Fortunately, the PRCV proved to be non-pathogenic and has effectively served as a free of charge vaccine against TGEV globally. Whether the same might happen with PEDV is still an open but very interesting question: http://wwwnc.cdc.gov/eid/article/20/12/13-1642_article
just a remark: historically, foot and mouth disease is probably the best studied virus on airborne transmission. Airborne transmission critically depends on infected individual being able to excrete an aerosol of virus and less on the ability to take up the aerosol.
Thanks to you all for your excellent discussions.
Per Have, DVM, PhD
Grand Masters of TWiV & Ebola,
I got the Epidemiologist at the hospital where I volunteer interested in TWiV. One by one your followers increase in numbers.
My understanding is that an Ebola patient has an increasing density of virus particles in the bodily fluids and cells as the infection progresses as time passes. That plus having more exposure to the bodily fluids would seem to suggest the reason mostly health care workers are at greatest risk.
Are there studies examining the rate of increasing number of virions in a patient through time?
The average number of virions it takes to cause an infection in an otherwise healthy person or animal?
Thank you to all you do!
Mary in Colorado
I was listening to last Friday’s TWIV and must say I strongly agree with Vincent regarding the flight ban issue.
One thing to keep in mind is that, in the exchange of opinions between you and your guests, there appeared to be some confusion about what the scope of the ban would actually be.
In my view, the concern is not for the US or Europe, as much as the very tangible risk that the virus would get to other less prepared countries (think Haiti for example).
Therefore what one should concentrate the discussion on is whether or not to ban travel (all travel, flight and otherwise) not so much to the US or to Europe but from each of the affected countries.
Doing so would address some if not all of Alan’s points regarding people finding alternate routes to the US.
In addition, concerning the risk of generating panic or massive flight from the affected countries, one should point out that panic is already widespread and that according to a time line published on The Guardian (http://www.theguardian.com/world/2014/oct/15/ebola-epidemic-2014-timeline) Sierra Leone has already closed its borders to neighboring countries back in July, which indicates that a travel ban might be enforceable.
I do not suggest that the flight to the US and Europe should stay open (as you say Dallas docet).
I merely suggest that all flights and other forms of travel, from the affected countries should be highly regulated.
- All routine travel should be banned.
- All travel of AID WORKERS and OTHER ESSENTIAL PERSONNEL should be allowed in and out and subjected to high levels of security (in fact the number of people going in should be increased to meet the dire need of the people on the ground).
- Food and other supplies should of course continue getting into the affected countries.
This would reduce the volume of people movement and would allow close inspection of all travel that has to occur. The result is that one would be able to CUT TO A MINIMUM the number of people that have to be kept under close scrutiny and that international efforts could then concentrate on helping the people that are most affected rather than on devising complex screening strategies at incoming Western countries airports.
In order to clarify this point and to communicate it more easily I think it is important that the emphasis is shifted from protecting the rich countries by banning people from Africa from coming in (which would only emphasize the racist undertone of this whole crisis) to protecting other countries that are even less prepared than us and keeping the epidemic contained.
In other words, as you say, the emphasis should be on the epidemiology. When you have a epidemic outbreak, the first thing you do is to contain it.
In any event, the fact that it might not work is not an excuse for not attempting it.
Caterina Strambio De Castillia
Program in Molecular Medicine
The University of Massachusetts Medical School
Hi Vincent, and other esteemed professors.
A quick note regarding LED lamps, and uv.
Generally there will be no uv, in fact you would have to design the lamp specifically to do so. I have been working on LED lamps for quite some time, and have had to include far blue, in order to accommodate coral aquariums. However I have stopped short of actual uv, on the basis that it is not needed, and might be harmful, as well as wasting energy.
That said, the far blue may well have sufficient energy to inactivate viruses, though it would not be present in a normal white LED lamp.
The weather report for weston super mare, 7:30pm 12 C, humidity 87% (rh), high temp for today, 14 C low 9C, visibility 16km, wind from the nne at 20km/h, precipitation little so far, increasing risk of showers overnight.
I hope the weather report is detailed enough to match your (Alan’s) exacting requirements!
Thanks for all the good work you do, producing the TWIx podcasts.
It’s nice to be able to answer a question for you for a change!
Let me assure you, up front, that I don’t expect that there is a good answer to my question yet. I write in hopes that there has been a good discussion.
In listening to the Ebola coverage, I noticed, once again, that there are guesses but not certainty as to the natural reservoir for Ebola virus. That got me thinking. With Ebola, we’ve got a fair number of variant genomes all of which derive from a small number of reservoirs. You have also discussed vira-genomic “archeology” in which we can track traces of viral exposures in hosts through changes in host genomes. Oops, my question just became two questions – sorry. Anyway, my questions relate to looking for reservoirs (which we don’t know) through viral genomes (which we do know).
1) In searching for reservoirs and building mammalian and avian genomic libraries, have people tried searching suspected reservoir genomes for vira-genomic traces of particular viruses? If stable reservoirs have developed, then I assume that such traces would exist. I realize that this may only apply to retroviruses and that the libraries may not, yet, have enough species “depth” to apply such vira-genomic archeology but I’m curious if anyone has begun looking in this direction.
2) Even though we might not know how all viruses’ genes function, we know that some of them have to be involved in enabling particular viruses to function in particular reservoirs rather than others. Has anyone begun looking at viral genomes for markers that might indicate fitness to particular types of hosts and, therefore, narrowing the range of particular reservoirs? I don’t know if we have deep enough genomic library to try this and it obviously wouldn’t work well in promiscuous viruses, but it might be practical in viruses with narrower preferences. I’m thinking that, in the beginning, this might be more of a meta-genomic analysis – kind of like the recent determination of human height genes – that just locates common markers without understanding why they are markers but it could be a useful tool for looking for reservoirs. Just wondering if you’ve heard of any work being done on reservoir determination from this end?
As always, thanks for your information show,
Hi TWIV team,
First off, thanks for all you do in disseminating information about virology to the world so regularly. I have tried to stay current with the TWIV episodes, but forgive me if this is a repetitive question that you have already covered. When I was an undergrad, I did a term paper on Ebola, as my interest was piqued after reading Richard Preston’s “The Hot Zone.” My question is about using viral vectors as vaccines for EBOV.
As far as I know, you have not discussed the feasibility of using viral recombinants as vaccines for EBOV. In one review (http://www.nature.com/nri/journal/v7/n7/full/nri2098.html), the authors discuss the use of viral vectors with the EBOV glycoprotein or nucleoprotein and report efficacy in non-human primate models. (p564-565) They also go on to list limitations in using these vectors in Table 2.
However, one J Virol paper notes that: “A single immunization with any construct expressing GP was moderately immunogenic against Ebola virus and protected 88% of the animals against severe hemorrhagic fever and death caused by Ebola virus. Two doses were highly immunogenic, and all of the animals survived challenge and were free of signs of disease and of detectable Ebola virus challenge virus.” (http://jvi.asm.org/content/81/12/6379.long)
Is using a viral vector like this a viable means of vaccination? From my understanding, whoever would produce it would have to just culture and isolate the recombinant viruses – but are we able to do this on a large enough scale? I suppose in theory it sounds wonderful and has data to back it up (dating from ~2008, even), but what practical implications are there that might limit the efficacy of this? Has anything been done like this before in the field?
Apologies for the lengthy email and thanks again for doing what you do.
He would seem a great guest for TWiV, interesting points on viral loads and multiple introduction
Here is a reference (alluded to by other listeners in your recent episode) for a semen sample testing positive long after acute symptoms ended. This study’s sample was taken from a convalescing Ebola patient (Sudan EBOV, not Marburg), in 2000, 40 days after onset of symptoms. The study also cites an earlier finding of the virus in semen (Zaire EBOV) after about three months of convalescence.
Please discuss accuracy of ELISA evidence compared to “real-time RT-PCR”. Is a virus infective everywhere RT-PCR can detect it (presuming a moist surface and later contact with mucus membranes)?
“Assessment of the Risk of Ebola Virus Transmission from Bodily Fluids and Fomites”
P.S. (!!) It’s a sunny morning here in San Juan, Puerto Rico.
Weather: 30°C, Wind E at 11 km/h, 70% Humidity.
I’ve been a listener of twiv (and twip ) since Dickson & Vincent appeared on Omega Tau. I am neither a native speaker nor have a formal education in your field (I am working in software quality assurance), but I keep on listening hoping that sooner or later I’ll end up with feeling that I understand more than 10% per episode 😉
Thanks for all the episodes you have already done – I could listen forever 🙂
Here’s my question: you discuss a lot about the possibility of sexual transmission of ebola, but I wonder how that could be proven considering that there are much simpler means (airborne, direct contact) and that (non-cyber) sexual intercourse would often include these. How likely would it be to find positive proof for an exclusively sexual transmission? After all, this is a horrible epidemic with uncontrollable conditions and often unreliable information.
Greetings from Germany
Anne Marie writes:
In a (fairly) recent letter, someone wrote, “One of your hosts seemed to suggest that any man exposed to the virus would immediately not be inclined towards having sex – at any time – before he gets sick, or during the long convalescence – even though he’s potentially infectious for up to 2 months.” [Emphasis added.]
I don’t believe you addressed one particular aspect of this criticism so I would love to get clarification and see if my understanding of transmission is correct. I was under the impression that if a person were up and about (so to speak) “before he gets sick,” he would not be contagious.
In other words, while it is potentially risky for people to have unprotected sex post-Ebola (and condoms are never a bad thing to promote), the virus shouldn’t be found in semen tested before symptoms occur. Am I mistaken in this?
Thanks so much! Love the show.
I saw this brilliant blog post from Pleuni Pennings (linked below) where she and her students estimate how many travelers would have to be screened at American airports to prevent one case of Ebola in the United States. The math is simple, yet shows how effective a policy (i.e. airport screening) is likely to be. The best thing about the post is that Dr Pennings gently walks the reader through the estimate. It’s easy to understand, and should help non-mathematicians to think about the current outbreak empirically.
School of Public Health
The University of Texas Health Science Center at Houston
Hello Prof. Racaniello and my favorite team of Virology professors.
One of my friends shared an article with me from the Federal Register. It seems someone has filed a patent for an Ebola vaccine. This is one of those times where you think, “why didn’t I think of that?!”
The article says, “The inventors have developed a new platform based on live or chemically inactivated (killed) rabies virus (RABV) virions containing EBOV glycoprotein (GP) in their envelope.” and “More specifically, the inventors have developed a trivalent filovirus vaccine based on killed rabies virus virions for use in humans to confer protection from all medically relevant filoviruses and RABV. Two additional vectors containing EBOV Sudan GP or MARV GP are planned to be constructed in addition to the previously developed EBOV Zaire GP containing vaccine.”
So it’s a modified rabies vaccine against Ebola. Genius if it actually works, do you agree? Of course it will work. Rabies and Ebola are in the filoviridae family. It makes total sense this would work. I hope it works. I know how I would feel if I found something like this… think I really nailed it, and then it doesn’t work and people die anyway. So here’s hoping it actually works. It’s probably not going to work LOL.
Call my head easily turned, but I eagerly expect every episode of this week in ebolavirus (not that I did not enjoy twiv before).
As a HCW probably heading off to West Africa soon (still awaiting dates and details), I have been doing my due diligence in following the outbreak since an EID deep dive I did in January, and intensified this the last months.
I have, however, found it difficult to get an overview of the actual CFRs depending on treatment regimes. I don’t think I’ve found all the cases of western HCWs in whom the infection was detected early and to whom adequate supportive measures were given. This makes it difficult for me to really make any calculations of risk in such situations.
Neither do I have the necessary knowledge to really assess the plausibilty of the proposed treatments’ or vaccines’ efficacy. Though a talk by Charles Arntzen at my hospital today was interesting and illuminating, it left me with the same questions as I had two hours before.
I would very much appreciate any information you might have on this, as it might comfort my dear mother (“no way in hell you’re going to Liberia!”).
Lovely sunny day here in Trondheim, Norway, though getting a bit chilly with 4°C. No wind, unsure about humidity.
Ps. I was disappointed not to hear anything on the Marburg case in Uganda last episode. Maybe you with the date of recording just missed it?
Pps. Sorry about the typos, wrote this on my phone.
Ppps. Oh, and concerning the cosmic weather, we’ve got a lovely aurora on now.
I have two questions for the Grand Masters of TWiV.
- For tracking Ebola, are the only flights checked the ones arriving directly from affected countries, or are all flights entering the U.S. being checked?
- Also for tracking Ebola, are the only persons being tracked the ones with direct contact with a known Ebola patient, or are contacts of contacts also being checked?
Thank you very much.
William Spindler McIntosh
no relation to my cousin, Grand Master Kathy Spindler
Professor and Friends,
Two responses to topics and comments from today’s TWiV #306:
RE: Comments about travel from, and to, the countries affected by the outbreak. Alan may be on to something.
Ebola may only be present in a few African nations, but fears over the crippling outbreak are infecting economies across the continent and may put its envy-inducing growth prospects at risk, experts said Monday…
…The World Bank warned in September that the “fear factor” of the disease could have potentially catastrophic results on economic growth…
African-economy-risks-infection-ebola, from France 24 International News website.
RE: Comments about Liberia as “…living lab…” in Jacklyn Lacey’s letter at the American Museum of Natural History…
It conjures and brings to mind, the specter of Tuskegee and the study of the natural history of Treponema pallidum. http://www.cdc.gov/tuskegee/timeline.htm
Best always, and strength to keep going.
Al Sacchetti writes:
Dear TWIV Gang
As the smartest virologists I know, I have a question (for you).
In Emergency Medicine when patients present with certain overdoses of cardiac drugs they can be treated with an infusion of a substance termed “Intralipid”. Basically it is an emulsion of lipids that we simply drip into them. The drugs themselves block certain ion channels on the myocardial cells and produce extremely low heart rates and blood pressures, frequently leading to death. Because the drugs are very lipophillic, they will preferentially diffuse off of the myocardial cells and into the fat globules of the lipid infusion. Once they release, the heart resumes its normal function. Simple physical chemistry in action, pretty cool.
My question is what would happen to an enveloped virus in the face of a lipid emulsion? Because of its shape, a virus like a filovirus would have a relatively high surface area compared to the more spherical shape of other viruses. Since the envelope itself is mostly composed of lipids, it would seem like this would make the virion itself lipophillic. So if you were to take a solution of an enveloped filoviruses and mix it with a lipid emulsion, how would the virus be distributed between the aqueous and the lipid phases? If it were to be trapped in the lipid phase, would the envelope dissolve? I do understand that the envelope contains proteins and glycoproteins to help it remain in solution in the blood, but it seems that it would still prefer a more hydrophobic environment.
Obviously this question relates to could a lipid emulsion be used to lower the viral load in an infected Ebola Zaire patient. It would be of no value to any intracellular processes, but it might limit the circulating virions by providing a chemically more preferable location for a lipophillic particle like a filovirus.
This might be just another crackpot idea, but I would be interested in your thoughts.
Thanks, still recommending the podcasts to friends and colleagues.
Alfred Sacchetti, MD
Chief Emergency Medicine
Prof V, thanks for reading my TWiV email and thanks to the entire panel for great answers to this and other questions. At the office I sent around this email to the people who had been part of the discussion in which I promised to find out the risk of picking up a used tissue:
The virologists of TWiV are in agreement that if a person touches nasal secretions (such as from a sneeze onto a surface, or blowing nose into tissue), and the secretion hasn’t yet dried, AND the person who touched it doesn’t wash or wipe off hands, then touches any of their own mucous membranes (typically the only likely ones would be eyes, nose and mouth), then yes, ebola could be transmitted.
So if you touch something that isn’t dry, don’t touch your face! It’s generally a good idea to not touch your face when out in public unless you have sanitized your hands given all the bacteria and viruses on door handles, pump handles at gas stations, etc.
Have a great week.
Sandra in Dallas/
ps- I’m glad there isn’t public transportation to my workplace so I don’t have to buy and use a laser on it…
Anne Marie writes:
I was wondering if any of the good doctors had watched the filovirus- and hemorrhagic-fever-themed episode of CSI that ran this week. I would be interested to know what all they got wrong because I am not informed enough to be able to say but it seemed pretty off for me, even given their normal flights of fancy.
- Can a virus like this be killed by “blast[ing] it with UV light and formaldehyde fog”?
- Can they test potentially exposed people for a filovirus or do they just have to wait for the end of the incubation period to know if the person has it?
- Is microbial forensics even a thing?
- Would a filovirus act by “replicat[ing] at a staggering rate, decimating the host’s cells and causing massive hemorrhage”?
- “All it takes is one infected carrier. Sneezes in line at the airport. Infecting half a dozen more.” That’s just wrong, isn’t it? If it’s a “blood-borne filovirus,” it wouldn’t be spread by sneezing to 6 people, right?
I did like the line, “A virus hunter becomes the virus-hunted,” though!
Really comprehensive document on PPE:
Dear Twiv gang,
I read that the Dallas nurse who contracted Ebola is being treated with plasma from an Ebola survivor.
Have any viruses been treated using plasma donated from animals who have repelled infections? This seems similar to anti-venom treatment for snake and scorpion bites.
I assume that the answer is “no”, but it would be interesting to hear why not.
Apparently, it’s all you mad scientists who are to blame for Ebola.
Why do people read this rag?