Dead human viruses




















If you've been tested, or you've seen video of people getting the nasal swab with that 4-foot-long Q-tip, that swab collects samples for the RT-PCR test. At the beginning of your infection and during the time you feel horrible, the assumption is and it's a really safe assumption that if you're RT-PCR positive you are infected and you are very likely to be contagious to others. At some point after you recover you are still RT-PCR positive for virus, but you might not actually be contagious anymore.

That's because some of the pieces of virus being detected may just be virus shrapnel left over from the war waged between your immune system and the virus. We don't have any SARS-Cov-2 data yet as it relates to dead bodies, but we can look at examples from other viruses again.

Typically, if infectious virus is detected for days to weeks, the genome of the virus can be detected for months to years. One study looking at how long Ebola virus might survive after death could detect the infectious virus 10 days postmortem but still detected the virus genome 10 weeks later. TA: Can we identify viruses in remains from decades or centuries ago, based on identifiable DNA or RNA as opposed to making a diagnosis based on physical symptoms?

Koci: So, the short answer here is yes. The oldest virus I know we've been able to actually detect was found in a 7, year old tooth from what is now central Germany. Researchers were able to detect and sequence the whole genome of the hepatitis B virus, or HBV, in this ancient tooth. So just a quick aside. Structurally, viruses come in two flavors: enveloped and capsid like we discussed above.

As a molecule, DNA is much more stable in the environment and can apparently survive in a tooth for thousands of years. It's unlikely that we'd be able to detect RNA viruses that far back, but depending on what happened to the body of the person when they died, maybe.

If the person was embalmed, frozen or if tissues were collected at an autopsy we could use those to identify or even diagnose viruses. In fact, people have already done that. The last great pandemic—the influenza pandemic of —came at a time before we even knew viruses were a thing.

It wasn't until the s that we figured out what viruses were, but by then that particular virus was gone. Since we didn't know what it was at the time, samples weren't collected or stored in a way that made them of any use later. So, for decades we were left speculating what may have been so different about the virus from the strains of influenza that came after it. That was until the late s, when Jeffery K. Taubenberger and a team at the Armed Forces Institute of Pathology decided to go through the tissue archive and find preserved tissue samples from soldiers who died from pneumonia-like symptoms during the pandemic.

Taubenberger and his colleagues developed methods for extracting RNA from these tissue samples something people didn't think was possible at the time and were able to pull out small bits and pieces of the influenza virus genome.

Over several years, they were able to piece together the whole genome of the influenza virus—and they used that to resurrect this extinct virus.

Koci: Yeah, I know that's most people's reaction just before they start quoting Dr. Ian Malcolm from "Jurassic Park. Looking back through history, we've had an influenza pandemic about every 30 or so years. Everyone knows about the big one in , and we're pretty sure one happened in , but we also had the Asian flu in , and the Hong Kong flu in So in the late s, most virologists were starting to brace for the next flu pandemic. We had surveillance systems and vaccines, so we assumed we were better prepared, but the pandemic was so much worse than any of the others since and we didn't know why.

There were lots of ideas about why it was worse, but no way to know if any of those ideas were right because we didn't have that virus to study in the lab. Then in the H5N1 avian flu emerged.

And while it was devastating to poultry, it was also able to infect and kill people. We had never seen a flu virus jump straight from birds to people before. Could that have been how started? Could there be clues in the virus that would tell us what to look for in new strains of flu that would give us early warning of a new pandemic strain? So the virus was resurrected to try and understand what made that pandemic worse than others in the hopes of helping us be better prepared for the next one.

Koci: This work took about eight years and a team comprised of at least three different institutions. And from all that time and effort, the biggest lesson we learned was that Mother Nature isn't giving up her secrets that easy. The hope was that there would be some flashing red-light screaming "look at me! But the real answer is more complicated than that.

There isn't one series of events or changes that might give rise to a new pandemic strain; it's the collection of several different changes coming together in just the right or wrong mix. But we still learned a lot, and several of these lessons seem like ones we're re-learning now. The virus came from birds, but it spent time evolving to infect humans in some other animal. What that intermediate host was or how long it took before it could infect people and spread from person to person we don't know, but it was clearly different enough from other viruses that our immune systems weren't prepared.

We learned that changes in the protein that the flu uses to get into our cells HA protein worked differently than most other influenza viruses, and if we moved just that gene into seasonal flu strains, they got more virulent. However, if we replaced the virus HA gene with the HA from the seasonal flu and left all the other genes the same, was just as virulent no matter which HA gene it had.

So the HA gene plays a role but all the other genes do, too. Ultimately, the lesson learned, or rather I think the lesson we were supposed to learn, was: don't be so reactionary. Stop waiting for nature to spit out a new strain and then rush to make a vaccine to it. We learned we really need a universal influenza vaccine, a vaccine that will provide protection to all strains of the flu no matter what nature decides to throw at us. We also learned we need more weapons than just vaccines.

We need more antivirals, designed to target all the different parts of viruses. And not just influenza virus but every virus we think might have pandemic potential. We have made progress on these lessons. There still isn't a universal flu vaccine on the market yet, but there are several in the latter stages of testing that sound promising. Also, we have a few more antiviral drugs today than we did 20 years ago, but clearly not enough to be ready for the next pandemic, this pandemic.

TA: Is there anything else in particular you think is worth noting to a general audience from the broader field of research into historical viruses? Koci: Nature gave us fair warning something was coming. A lot of people have been ringing alarm bells for years, but pandemic preparedness is a tough sell. When it works, nothing happens and it looks like you wasted all that money.

H1N1 did take off around the world, but it turned out to not be as nasty as we feared. That was good luck, but it's also worth noting that investments by the George W. Could that have been how started? Could there be clues in the virus that would tell us what to look for in new strains of flu that would give us early warning of a new pandemic strain?

So the virus was resurrected to try and understand what made that pandemic worse than others in the hopes of helping us be better prepared for the next one. Koci: This work took about eight years and a team comprised of at least three different institutions.

But the real answer is more complicated than that. The virus came from birds, but it spent time evolving to infect humans in some other animal. We learned that changes in the protein that the flu uses to get into our cells HA protein worked differently than most other influenza viruses, and if we moved just that gene into seasonal flu strains, they got more virulent. However, if we replaced the virus HA gene with the HA from the seasonal flu and left all the other genes the same, was just as virulent no matter which HA gene it had.

So the HA gene plays a role but all the other genes do, too. Stop waiting for nature to spit out a new strain and then rush to make a vaccine to it. We learned we really need a universal influenza vaccine, a vaccine that will provide protection to all strains of the flu no matter what nature decides to throw at us.

We also learned we need more weapons than just vaccines. We need more antivirals, designed to target all the different parts of viruses. And not just influenza virus but every virus we think might have pandemic potential. We have made progress on these lessons. Also, we have a few more antiviral drugs today than we did 20 years ago, but clearly not enough to be ready for the next pandemic, this pandemic. TA: Is there anything else in particular you think is worth noting to a general audience from the broader field of research into historical viruses?

Koci: Nature gave us fair warning something was coming. A lot of people have been ringing alarm bells for years, but pandemic preparedness is a tough sell. When it works, nothing happens and it looks like you wasted all that money. H1N1 did take off around the world, but it turned out to not be as nasty as we feared.

Bush administration into federal agencies that support vaccine research like BARDA and rapid flu vaccines, and the vaccine plant here in Holly Springs had us an H1N1 vaccine in record time. I just hope the lessons we all learn, not just scientists, stick with us for a while. I was just looking for a bottom line summary that I could give my wife during a commercial break and get back to watching our show after I was quickly able to give her the answer. For example, like if they do an autopsy on a body that just died from COVID, how long does it take for special handling procedures, or even special social distancing of the body until the virus is technically not able to infect someone else?

Very informative even to someone without medical background. Answered all my questions. The idea that a universal influenza vaccine is being developed is very reassuring. Thank you! I have studied and watch news and science programs. We in the USA failed to have informed and enforced mask , social distant, testing , tracking , isolation.

Gupta and models are similar. A idea may floor heat , crack a window in crowd room create a vent. All safety as above also. Heard immunity is bad plan. President Obama had a plan when he left office.

President Trump has been negligently. President Trump has been negligently, has weaken the nation, and should be charged for being a failure on handling this virus. I am pleased I read this. Apart from the information I am also pleased that all scientists are working together and are more than hopeful to develop a vaccine and other antiviral drugs quicker than ever before. I must say, I found it intensely disturbing that viruses can survive that long, even in a dead body.

Would it not make sense that virus victims should be cremated rather than buried? The survivors maybe could have their naturally produced antibodies extracted for use on new victims. Since its appearance, the virus has caused over five million deaths worldwide, according to Reuters. Common symptoms include fever, cough, loss of taste or smell and shortness of breath and more serious symptoms include breathing difficulties, chest pain and loss of mobility.

On Aug. In December , this vaccine became the first to be approved after a large clinical trial, according to Nature. According to WHO , the disease infected camels before passing into humans and can trigger a fever, coughing and shortness of breath in infected people.

There is no vaccine available to prevent this disease, according to the NHS. The best way to reduce the chances of infection is to wash hands regularly, avoid contact with camels and not consume products containing raw animal milk. Live Science. See all comments Don't said:. Meh said:. Comment on rabies fatality rate.

Although all warm-blooded animals are thought to be susceptible to rabies, there are strains of the rabies virus multiple bat stains strains are maintained in particular reservoir host s , with some cross over especially in the US between raccoons and skunks. Although a strain can cause rabies in other species, the virus usually dies out during serial passage in species to which it is not adapted, and non-carnivores cows, horses, deer, groundhogs, beavers AND CATS, like small rodents, are dead-end hosts.

The CDC estimates in the US, 1 million dollars per potential life saved is spent by post-exposure prophylaxis in cases of exposure to animals other than bats, canines, fox, raccoon, skunks. Hundreds of unvaccinated cats are infected with, and die or are euthanized of rabies each year -no way every human exposure to "the kitten in the park " is tracked down. Certainly, many farmers and ranchers are unknowingly exposed. Yet almost all of the people diagnosed in the US yearly, knew they were bitten by a dog when outside the US or handled a bat.

And there have been several incidences since , where people got rabies secondary to solid organ transplants. Species vary in susceptibility to various strains, humans are 'most' susceptible to canine rabies and, in the US, the silver-haired bat strain.

This is a solitary bat with infrequent human interaction, whereas we have much more exposure to big and little brown bats and Mexican free-tailed bats. Only a small percentage of any of these have rabies, -it kills them too! The virus needs to get to a nerve, so if a bite is not deep enough, or a small viral load is deposited, or the 'victim' immune system responds - an infection will never be established.

If the virus is able to get to a nerve, it attempts to travel up an axon, to the brain- again, the immune system may eliminate. As rabies is a slow virus, it can self -immunize, explaining the presence of rabies neutralizing antibodies in Amazonian Indians and others who have never been vaccinated?

The reason why a mature dog is considered immunized 28 days after its first rabies vaccination, is if it has been exposed or is 'incubating' rabies virus but the virus is more than 28 days away the vaccine will prevent infection. Although antiglobulin is given, PEP - a killed vaccine, is basically, rapid immunization. Since definitive diagnosis is made on brain biopsy, the apparent spontaneous cures or response to treatment remain unproven.

Not to diminish the threat or the misery of this disease.



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