# If the ebola virus were to mutate

by oneamp
Tags: ebola, mutate, virus
 P: 222 Someone of unknown academic background mentioned on a news forum that if the ebola virus were to mutate so that it spread easier, like a cold or flu, that it would necessarily lose much of its ferocity, not killing in such high numbers. Is there any fact to this? And what are the odds that ebola will mutate to proliferate easier? Is it inevitable? If it eventually spreads like a cold or flu, will we all be in a lot of trouble? Thanks
 Emeritus Sci Advisor HW Helper Thanks PF Gold P: 6,754 IDK about that statement in particular, but if a hypothetical pathogen is so virulent that it kills all of its hosts so quickly before the pathogen can spread, then the pathogen dies once the last host is dead. Over time, if the hosts develop immunity to the pathogen, then the pathogen is unable to spread, unless it can infect a host with compromised immunity to the pathogen. In order for the virulent pathogen to survive in the long term, it must mutate so that infection of a host allows time for the pathogen to propagate and not eliminate all of its potential hosts.
 Mentor P: 5,490 It's hard to say without the quote in context but I'd agree with Steamking. For an infectious disease to become a serious problem of the manner you're describing it has to be highly infectious, highly virulent and have an incubation time long enough to allow significant transfer of said disease.
 P: 222 If the ebola virus were to mutate Does this help explain why, though the virus has been known to exist for decades, we do not have a vaccine or effective treatment regimen? Because it's not likely going to make a hage impact on the first world? No tin foil hat thinking; I'm just wondering how these things work.
 P: 222 Another question: I have seen a video of a mass ebola grave, where the dead were buried. How long will these mass graves be contaminated? When someone digs up an ebola grave in the future, will they unleash the virus again?
Mentor
P: 5,490
 Quote by oneamp Another question: I have seen a video of a mass ebola grave, where the dead were buried. How long will these mass graves be contaminated? When someone digs up an ebola grave in the future, will they unleash the virus again?
No, IIRC the ebola virus can only survive a matter of days outside a living host a room temperature.
Emeritus
HW Helper
Thanks
PF Gold
P: 6,754
 Quote by oneamp Does this help explain why, though the virus has been known to exist for decades, we do not have a vaccine or effective treatment regimen? Because it's not likely going to make a hage impact on the first world? No tin foil hat thinking; I'm just wondering how these things work.
Fortunately, ebola outbreaks have been rare and confined to only certain geographical locations. The disease caused by ebola was only first confirmed in 1976 and no outbreaks have occurred in the US or Europe except from lab accidents where the virus was mis-handled.

Because of the nature of the disease and the area of its confinement, it is difficult to obtain samples of the virus to study to develop a vaccine: You need a highly secure facility just to store the virus. Certainly, if there were periodic outbreaks of ebola in the US and Europe, that would provide tremendous incentive to develop a vaccine, given that a disease like ebola could cause an untold number of deaths were an outbreak to occur in a large city. Given that its appearance is so recent, perhaps the virulence of ebola results from a mutation to a virus which was previously benign.

This is not to minimize the suffering of those who have come down with ebola, but there are many other diseases which do appear frequently in the first world for which vaccines or cures do not exist or which are becoming ineffective due to improper use. Once, before antibiotics, bacterial infections were frequently deadly, and now that antibiotics and antibacterial compounds are used frequently and indiscriminately in everything from animal feed to hand soap, the bacterial infections which we used to treat quickly are becoming so resistant that the number of effective drugs has dwindled, and some serious diseases, like TB, have strains which are resistant to treatment. It would be nice to have unlimited resources to devote to finding cures or vaccines for all infectious diseases, but we don't live in that world.
 P: 222 Thank you very much for that great answer SteamKing.
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 Quote by oneamp Someone of unknown academic background mentioned on a news forum that if the ebola virus were to mutate so that it spread easier, like a cold or flu, that it would necessarily lose much of its ferocity, not killing in such high numbers. Is there any fact to this? And what are the odds that ebola will mutate to proliferate easier? Is it inevitable? If it eventually spreads like a cold or flu, will we all be in a lot of trouble?
I didn't see a specific response to your question about possible mutation of Ebola. Coronaviruses that cause colds and influenza viruses are so virulent because they attack cells of the lungs. More specifically, they inhabit the upper portion of the lungs. This makes them exceptionally efficient at spreading from human to human via coughs and sneezes. While some can certainly spread to the bodies other organs, they generally cause their damage in the lungs.

Ebola, on the other hand, spreads principally via exchange of bodily fluids. Blood borne, it spreads quickly through the body's organs causing its grisly symptoms. It is an efficient killer but not efficient in its spread throughout a population.

The other factor that actually hinders the spread of Ebola is its incubation period. While it has a quite lengthy incubation period, up to 25 days, its victims are not contagious during that time. Compare this to influenza which has an incubation period of just 2-7 days. Short, yes, but victims are very contagious while feeling completely fine.

Can Ebola mutate to a more virulent species? Absolutely. In fact, the strain that's causing so much panic in West Africa has never been seen before. As long ago as December of 2013, the WHO and CDC knew it was a new strain.

Does this new strain have different strategies for spreading more efficiently? It would seem so given the record-setting number of cases (1300+ as of today) and the silence since April from the world's prominent health agencies. I would really like to know that the WHO and CDC are exploring the capabilities of this new strain.
 PF Gold P: 519 Here is an interesting report of experimental transmission of Zaire-Ebola virus from pig to non-human primate without direct contact. Important to note the animals were euthanized before the disease could kill them. The exact route of transmission was impossible to discern with certitude. http://www.nature.com/srep/2012/1211...srep00811.html
Other Sci
P: 1,403
 Quote by oneamp Does this help explain why, though the virus has been known to exist for decades, we do not have a vaccine or effective treatment regimen? Because it's not likely going to make a hage impact on the first world? No tin foil hat thinking; I'm just wondering how these things work.
There are a few experimental vaccines and treatments in the pipeline for ebola, but they are still in the early stages of safety testing before they can be used in the field.

 But that support hasn't been enough to bring a single product to the market. Feldmann's vaccine, for instance, consists of a livestock pathogen called vesicular stomatitis virus (VSV) in which one gene has been replaced with that for Ebola's surface glycoprotein. It gives rhesus macaques full protection against Ebola-Zaire and saved four out of eight animals when given 30 minutes after an otherwise lethal dose of the virus. But the Public Health Agency of Canada (PHAC) in Winnipeg, Feldmann's previous employer, has yet to take it to phase I safety trials in human volunteers. Profectus BioSciences in Tarrytown, New York, which is developing a similar vaccine, needs some $2 million to produce it under good manufacturing practice standards, a prerequisite for any human study. A leading drug candidate has more funding and is further advanced, but it also faces obstacles. The compound, identified by U.S. Army researchers and based on RNA interference, is in development at Tekmira Pharmaceuticals Corp., a Burnaby, Canada–based company that has a Pentagon contract worth up to$140 million to produce it. But on 3 July, the company announced that the Food and Drug Administration had put a phase I trial on hold because it wants more data and a change in the protocol to protect participants' safety. Tekmira says it expects to resolve the issue by the end of the year. Monoclonal antibodies are similarly stymied. In the \$28 million NIAID-funded project that Ollmann Saphire is leading, 25 labs from seven countries are pooling their antibodies to see which cocktail best blocks the virus. But again, none of these has entered a phase I trial. The same is true for a powerful nucleoside analog—a small molecule that's cheap to make—developed by the U.S. Army Medical Research Institute of Infectious Diseases. A promising antisense-based compound by Sarepta Therapeutics in Cambridge, Massachusetts, was put on ice after the Pentagon ended its funding in 2012.
(http://www.sciencemag.org/content/345/6195/364.full)

Likely some of the reasons these treatment candidates are advancing slowly through testing are the economic issues that you cite above.
 Sci Advisor PF Gold P: 9,493 Treatment of viral infections has always been problematic. Effective vaccines are difficult to develop [e.g., polio] and treatment is usually symptomatic - keeping the patient alive until their own body can rein in the infection. Antibiotics are ineffective against virus.
P: 23,731
 Quote by Chronos Treatment of viral infections has always been problematic.
Yes, but my understanding is that we do have some success lately - I mean things like AZT. While they don't kill the virus, they slow its replication, making it more likely our immunological system will be able to deal with the problem in time.

Or is my understanding wrong?
 Sci Advisor PF Gold P: 9,493 I agree, Borek. Slowing replication is one strategy that can be effective. Often this involves inhibiting the ability of the virus to hijack uninfected cells. The debate over whether virus are actually even alive continues. They have no innate metabolic processes, which explains why antibiotics are ineffective.
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 The team helped to find the first Ebola cases in Sierra Leone. They also immediately shipped diagnostic samples from the patients back to the U.S. and started sequencing the viruses' genomes. "We had 20 people in my lab working around-the-clock," Sabeti says. Their furious pace paid off. After just a week or so, the team had decoded gene sequences from 99 Ebola viruses. The data offered a treasure-trove of information about the outbreak For starters, the data show that the virus is rapidly accumulating new mutations as it spreads through people. "We've found over 250 mutations that are changing in real time as we're watching," Sabeti says.
http://www.npr.org/blogs/goatsandsod...ss-west-africa

CDC site on Ebola - http://www.cdc.gov/vhf/ebola/

http://www.cdc.gov/ncidod/dvrd/spb/m...spages/vhf.htm

"The genus Ebolavirus is a virological taxon included in the family Filoviridae, order Mononegavirales."
http://en.wikipedia.org/wiki/Ebolavirus
Ref: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3074192/

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

Meanwhile - Experimental Ebola Vaccine Will Be Put To Human Test
http://www.npr.org/blogs/health/2014...-to-human-test

Experimental Ebola Vaccine Also Works On New Virus
http://www.npr.org/blogs/health/2010...inst-new-virus
 Other Sci Sci Advisor P: 1,403 Here's a link to the paper referenced above: Gire et al. 2014. Genomic surveillance elucidates Ebola virus origin and transmission during the 2014 outbreak. Science. Published Online August 28 2014. doi:10.1126/science.1259657 The authors of the paper identify a "catalog of 395 mutations, including 50 fixed nonsynonymous changes with 8 at positions with high levels of conservation across ebolaviruses" which could provide a starting point for understanding what genetic changes, if any, may be driving the increased severity of the current ebola outbreak compared to previous ones. Of course, as the study is purely computational, all it can do is identify candidates and generate hypotheses, so further experimental work must be done to understand the functional effect of the mutations that the study identified. One question I had about the study, however, is when the authors write: "Mutations are also more frequently nonsynonymous during the outbreak (Fig. 4G). Similar findings have been seen previously and are consistent with expectations from incomplete purifying selection." I thought that higher rates of nonsynonymous mutations relative to synonymous mutations (i.e larger dN/dS ratios) were a sign of positive selection, but the authors are interpreting this higher dN/dS ratio as evidence of purifying (negative) selection.