Extinct deadly viruses

Buried with them was a secret. When scientists analysed DNA from the remains earlier this year, they found that one of the men had been doubly unfortunate. Not only was he violently murdered — at the time, he had been suffering from smallpox. And there was another surprise. Instead, it belonged to a remarkably different strain, one which was previously unknown, and silently disappeared centuries ago. It seems that smallpox went extinct twice. Why do some viruses disappear?

And what happens to them? As the threat posed by these tiny, primitive life forms grows ever stronger, scientists are racing to find out. A global vaccination programme pushed smallpox into extinction in the wild, although the virus still exists in two secure laboratories Credit: Alamy.

One of the most recent viruses to vanish was Sars. The earliest cases occurred in Guangdong, a coastal province in southeast China known for its many restaurants serving exotic meats.

At the time, local wet markets bustled with racoons, badgers, palm civets, doves, rabbits, pheasants, deer and snakes, which were often dispatched on the spot, mere metres from where people ate. It was common to find beheaded and disembowelled animals just lying around.

Even in the earliest days of the epidemic, it was clear how Sars had emerged. Fast-forward two years, and the virus had infected at least 8, people , of whom died. But it could have been so much worse. Like its close relative Covid, Sars had many of the necessary qualities for world domination — it was an RNA virus, meaning it was able to evolve rapidly, and it was spread through droplets expelled when breathing, which are hard to avoid.

Instead, Sars disappeared as abruptly as it arrived. By January , there were just a handful of cases — and by the end of month, the last suspected natural infection was announced. There was another outbreak a couple of months later, when it is thought to have escaped from a Beijing research lab — twice. In a nutshell, we got lucky. According to Sarah Cobey, an epidemiologist at the University of Chicago, Sars was driven to extinction by a combination of sophisticated contact-tracing and the quirks of the virus itself.

It took a global effort of surveillence and control measures to eliminate Sars Credit: Reuters. When patients with Sars got sick, they got very sick. The virus had a staggeringly high fatality rate — almost one in five patients died — but this meant that it was relatively easy to identify those who were infected, and quarantine them.

There was no extra spread from people without symptoms, and as a bonus, Sars took a relatively long time to incubate before it became contagious, which gave contact-tracers extra time to find anyone who might be infected before they could pass it on. The case of Liu Jianlun, who caught the virus before it had been properly identified, shows just how differently the Sars pandemic could have played out. The year-old specialist in respiratory medicine became infected after treating a patient at the hospital where he worked in Guangdong Province.

On 21 February , Jianlun travelled to Hong Kong to attend a wedding, and checked into a room on the ninth floor of the Metropole Hotel. Although he had been suffering a slight fever and mild respiratory symptoms for five days, he was well enough to do some sightseeing with a relative. But the following day his symptoms had worsened, so he walked to a nearby hospital and asked to be put into isolation. By then, he had already unwittingly infected 23 people , including guests from Canada, Singapore and Vietnam, who then carried the virus back to their own countries, where they spawned further outbreaks.

In the end, the WHO estimated that around 4, cases could be traced back to Jianlun , who himself succumbed to the virus. Instead of having been buried in sand, they reside within each of us, carrying a record that goes back millions of years. Then, last year, Thierry Heidmann brought one back to life. Combining the tools of genomics, virology, and evolutionary biology, he and his colleagues took a virus that had been extinct for hundreds of thousands of years, figured out how the broken parts were originally aligned, and then pieced them together.

After resurrecting the virus, the team placed it in human cells and found that their creation did indeed insert itself into the DNA of those cells. They also mixed the virus with cells taken from hamsters and cats. It quickly infected them all, offering the first evidence that the broken parts could once again be made infectious.

The experiment could provide vital clues about how viruses like H. But there are many viruses that are more dangerous than these—more infectious, far riskier to work with, and less potentially useful. Thanks to steady advances in computing power and DNA technology, a talented undergraduate with a decent laptop and access to any university biology lab can assemble a virus with ease.

The animals first became paralyzed and then died. In that case, there was a well-understood and highly desired goal: to develop a vaccine that might offer protection against future pandemics. Resurrecting an extinct virus is another matter. Still, if Heidmann had stuck to scientific nomenclature when he published his results, last fall, few outside his profession would have noticed. Heidmann is on a bit of a mission, though.

He named the virus Phoenix, after the mythical bird that rises from the ashes, because he is convinced that this virus and others like it have much to tell about the origins and the evolution of humanity.

With equal ardor but less fanfare, scientists throughout the world have embarked on similar or related projects. In the past few months, groups at Oxford University and at the Fred Hutchinson Cancer Research Center, in Seattle, have also produced results that provide startling observations about evolution and disease.

The approaches often differ, but not the goals. All of these researchers hope that excavating the molecular past will help address the medical complexities that we confront today.

Almost incidentally, they have created a new discipline, paleovirology, which seeks to better understand the impact of modern diseases by studying the genetic history of ancient viruses. Through the window, the Eiffel Tower hovered silently over the distant city. And those viruses helped make us who we are today just as surely as other genes did.

I am not certain that we would have survived as a species without them. Many people study other aspects of human evolution—how we came to walk, or the meaning of domesticated animals. But I would argue that equally important is the role of pathogens in shaping the way we are today. Look, for instance, at the process of pregnancy and birth.

That led to live birth, one of the hallmarks of our evolutionary success over birds, reptiles, and fish. Eggs cannot eliminate waste or draw the maternal nutrients required to develop the large brains that have made mammals so versatile. It may be hard to understand how organisms from that same family, and constructed with the same genes, could have played a beneficial, and possibly even essential, role in the health and development of any species. In , Robin Weiss, who is now a professor of viral oncology at University College London, found endogenous retroviruses in the embryos of healthy chickens.

When he suggested that they were not only benign but might actually perform a critical function in placental development, molecular biologists laughed. He was eager to learn whether the chicken retroviruses he had seen were recently acquired infections or inheritances that had been passed down through the centuries.

He moved to the Pahang jungle of Malaysia and began living with a group of Orang Asli tribesmen. Red jungle fowl, an ancestor species of chickens, were plentiful there, and the tribe was skilled at trapping them. After collecting and testing both eggs and blood samples, Weiss was able to identify versions of the same viruses.

Similar tests were soon carried out on other animals. The discovery helped mark the beginning of a new approach to biology. Until recently, the earliest available information about the history and the course of human diseases, like smallpox and typhus, came from mummies no more than four thousand years old.

Evolution cannot be measured in a time span that short. Endogenous retroviruses provide a trail of molecular bread crumbs leading millions of years into the past. And we do, in thousands of places throughout our genome. If that were a coincidence, humans and chimpanzees would have had to endure an incalculable number of identical viral infections in the course of millions of years, and then, somehow, those infections would have had to end up in exactly the same place within each genome.

The rungs of the ladder of human DNA consist of three billion pairs of nucleotides spread across forty-six chromosomes. The sequences of those nucleotides determine how each person differs from another, and from all other living things. The only way that humans, in thousands of seemingly random locations, could possess the exact retroviral DNA found in another species is by inheriting it from a common ancestor.

Molecular biology has made precise knowledge about the nature of that inheritance possible. With extensive databases of genetic sequences, reconstructing ancestral genomes has become common, and retroviruses have been found in the genome of every vertebrate species that has been studied. Anthropologists and biologists have used them to investigate not only the lineage of primates but the relationships among animals—dogs, jackals, wolves, and foxes, for example—and also to test whether similar organisms may in fact be unrelated.

Although it is no longer a daunting technical task to find such viruses, or their genes, figuring out the selective evolutionary pressures that shaped them remains difficult. Partly, that is because the viruses mutate with such speed. Such constant change makes it hard to develop antiviral drugs that will remain effective for long, and it has also presented a significant obstacle to the development of an AIDS vaccine. There are retroviruses like H. Because they are not inherited, they leave no trace of their history.

He has long been interested in the way complex organisms interact with viruses and adapt to them. But with these others you are looking back tens of millions of years, so it is hard to know how a virus functioned.

While Heidmann was working with the Phoenix virus in France, Bieniasz and two colleagues at Aaron Diamond initiated a similar project. Bieniasz rebuilt the youngest extinct retrovirus in the human genome—one that was still active a few hundred thousand years ago—because it had the fewest mutations. The team took ten versions of that virus we carry more than thirty and compared the thousands of nucleotides in the genetic sequence of each version. They were almost identical, but where they differed the researchers selected the nucleotides that appeared most frequently.

That permitted them to piece together a working replica of the extinct retrovirus. That is what we did. Nobody could make much sense of it. We evolved remarkably sophisticated defenses against them, and we would have done that only if their impact on human populations had been quite severe. It is eminently possible that this is not the first time we have been colonized by a virus very much like H. At the end of the nineteenth century, a mysterious series of cancer epidemics devastated American poultry farms.

One bird would fall ill and the entire flock would soon be dead. In , a desperate farmer from Long Island brought a chicken with a tumor to the laboratory of Peyton Rous, a young cancer researcher at the Rockefeller Institute for Medical Research, in New York City which became Rockefeller University.

Cancer was not supposed to spread by virus, but the bird clearly had cancer. Rous, who as a young man worked on a Texas cattle ranch, was mystified.

He extracted cancer cells from the sick bird, chopped them up, and injected the filtered remains into healthy chickens: they all developed tumors. A virus had to be the cause, but for years no one could figure out how the virus functioned. He suggested that the process could essentially run in the other direction: an RNA tumor virus could give rise to a DNA copy, which would then insert itself into the genetic material of a cell.

But he never wavered. Finally, in , he and David Baltimore, who was working in a separate lab, at the Massachusetts Institute of Technology, simultaneously discovered reverse transcriptase, the special enzyme that can do exactly what Temin predicted: make DNA from RNA.

The discovery has had a profound impact on modern medicine. It not only explained how cancer can be caused by a virus but provided researchers with the tools they needed to understand the origins and natural progression of diseases like AIDS. It also created a new field, retrovirology, and, more than that, as the Nobel committee noted when it awarded the Prize in Medicine to both Baltimore and Temin, it began to erase the tenuous borders between viruses and genes.

Retroviruses cause cancers in chickens, sheep, mice, and other animals, but their effect on humans became clear only in the late nineteen-seventies, with the identification of two viruses that cause forms of leukemia.

Retroviral proteins are particularly abundant in certain kinds of tumor cells, and scientists wondered to what degree they might be a cause of cancer. Dengue virus first appeared in the s in the Philippines and Thailand and has since spread throughout the tropical and subtropical regions of the globe, according to Clinical Microbiology Reviews.

A vaccine for Dengue was approved in by the U. Food and Drug Administration for use in children years old living in areas where dengue is common and with a confirmed history of virus infection, according to the CDC. In some countries, an approved vaccine is available for those years old, but again, recipients must have contracted a confirmed case of dengue in the past. Those who have not caught the virus before could be put at risk of developing severe dengue if given the vaccine.

Two vaccines are now available to protect children from rotavirus, the leading cause of severe diarrheal illness among babies and young children. The virus can spread rapidly, through what researchers call the fecal-oral route meaning that small particles of feces end up being consumed. Although children in the developed world rarely die from rotavirus infection , the disease is a killer in the developing world, where rehydration treatments are not widely available. The WHO estimates that worldwide, there are more than 25 million outpatient visits and two million hospitalizations each year due to rotavirus infections.

Countries that have introduced the vaccine have reported sharp declines in rotavirus hospitalizations and deaths. The virus likely emerged in bats initially, then hopped into nocturnal mammals called civets before finally infecting humans, according to the Journal of Virology.

After triggering an outbreak in China, SARS spread to 26 countries around the world, infecting more than people and killing more than over the course of several months, according to History.

The disease causes fever, chills and body aches, and often progresses to pneumonia, a severe condition in which the lungs become inflamed and fill with pus. SARS has an estimated mortality rate of 9. The virus may have originated in bats and passed through an intermediate animal before infecting people, according to Nature. The initial outbreak prompted an extensive quarantine of Wuhan and nearby cities, restrictions on travel to and from affected countries and a worldwide effort to develop diagnostics, treatments and vaccines.

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.