Are there any examples of viruses that have jumped from reptile to human?

Are there any examples of viruses that have jumped from reptile to human?

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I know that there are plenty of examples of zoonosis occurring from reptiles to humans that involve bacterial pathogens, (e.g. Salmonella) but are there any instances of viruses being transferred from reptiles to humans?

If applicable, for this question, I am only interested in reptilian viruses "jumping" from reptiles to humans, not the capacity of reptiles to serve as reservoirs for non-reptilian viruses that could potentially infect humans.

Q&A: New Tool Ranks Viruses by Their Risk of Jumping to Humans

Jef Akst
Apr 9, 2021

W ell before the world began grappling with the COVID-19 pandemic, researchers were already looking out for potential outbreaks from emerging diseases—and trying to stop them. A major hurdle in doing so is understanding which viruses in animals are most likely to make the jump to people. A new, interactive web-based tool, published April 5 in PNAS, uses 32 risk factors and data on more than 500,000 samples taken from nearly 75,000 animals, along with public records of virus detections in wildlife, to rank the chances of spillover among 887 viruses.

Project leader Jonna Mazet, an epidemiologist and disease ecologist at the University of California, Davis’s School of Veterinary Medicine, spoke with The Scientist about the “SpillOver” tool that she and her collaborators developed.

The Scientist: Tell me about how this project got started.

Jonna Mazet: For more than a decade, I have been the PI and leader of the PREDICT Consortium, which is a very large group of scientists and laboratorians and public health professionals working in more than 35 countries around the world to strengthen systems to identify viruses of concern before they spill over and make people sick. And in doing that work, we were strengthening the systems, but we were also discovering viruses, and we wanted to understand and put some information for the policymakers around the risk of the viruses we were finding.

I think we were a little surprised and disappointed to find that no good information was in the scientific literature about really how to rank these viruses. So we had to start that effort as we were building the systems and as we were discovering viruses. This is a culmination of that huge collaborative project that included at least 400 individuals in the PREDICT project as well as experts from around the world in virology, ecology, epidemiology, and other disciplines.

TS: How did you build the SpillOver tool, and how does it work?

JM: We did intensive literature reviews, and we also mined the minds, if you will, of the scientists and individuals working on the PREDICT project. And then we collated all of the risk factors we could identify as . . . bits of risk in all the scientific papers that have talked about viral spillover risk and even spread. . . . We added to those ones that we were finding in the PREDICT project, because for the most part, the ones we could find in the literature were only around virology and didn’t include the host, the environmental risk component for exposure, or any of the ecology. . . . And then we reached out to scientists all over the world that were working at the top of their fields in this specific area of zoonotic disease and virology and spillover, and we asked them to rank those risk factors that we had identified as well as rank their expertise.

So, for example, if a virologist was ranking one of the virology-oriented risk factors, they may rate themselves as an expert. But if they were looking at one that was more in the ecology realm, they might rate themselves a little lower in their expertise. And we use their rankings as well as their self-assigned expertise to then look at all of the risk factors and put together a program—equations, basically—to come up with a weighted score for each risk factor. And then we used that to then find the data for all of the known zoonotics that were found first in wildlife and transmitted to people as kind of a gut check of our ranking system to see if it was working. And then once we found that the tool looked to be functioning very well for historical spillovers, we then ranked the viruses that the PREDICT project found.

See “Predicting Future Zoonotic Disease Outbreaks”

TS: Where did SARS-CoV-2 rank?

JM: When we were first working on this, obviously there was no SARS-CoV-2 that we knew of—it existed, but it hadn’t been identified yet. So initially, it wasn’t even in our system, but of course as we were coming to put the final touches on the manuscript and the tool, we did add SARS-CoV-2 . . . with all other viruses that were coming out in the literature and in GenBank and GISAID and others.

When we added SARS-CoV-2, it ranked number two of the known zoonotics—[second to Lassa virus, found among rodents in West Africa and which causes hemorrhagic fever in people]. That’s ranking for its ability and likelihood to spill over again, and it has a bit of a nod to pandemic potential with our risk-ranking system. And I think that’s very telling. . . . Obviously, it’s a terrible virus that’s caused the pandemic, so it should rank very highly, as it does. And the reason that it’s not ranking even higher as number one is that it hasn’t been studied, until it spilled over.

Our goal is to actually rank viruses and study them before they spill over, so that we have them ranked on a watch list, so that countries that have these viruses can create watch lists and do the surveillance and risk mitigation before they spill over. As more and more information is coming out about the host and the distribution of SARS-CoV-2—it’s obviously worldwide in people but we’re interested in its distribution in wildlife and the potential reservoir hosts—I think it might even go up to number one.

SARS-CoV-2 jumped from bats to humans without much change

Credit: MacLean OA, et al. (2021), Natural selection in the evolution of SARS-CoV-2 in bats created a generalist virus and highly capable human pathogen. PLoS Biol 19(3): e3001115. CC-BY.

How much did SARS-CoV-2 need to change in order to adapt to its new human host? In a research article published in the open access journal PLOS Biology Oscar MacLean, Spyros Lytras at the University of Glasgow, and colleagues, show that since December 2019 and for the first 11 months of the SARS-CoV-2 pandemic there has been very little 'important' genetic change observed in the hundreds of thousands of sequenced virus genomes.

The study is a collaboration between researchers in the UK, US and Belgium. The lead authors Prof David L Robertson (at the MRC-University of Glasgow Centre for Virus Research, Scotland) and Prof Sergei Pond (at the Institute for Genomics and Evolutionary Medicine, Temple University, Philadelphia) were able to turn their experience of analysing data from HIV and other viruses to SARS-CoV-2. Pond's state-of-the-art analytical framework, HyPhy, was instrumental in teasing out the signatures of evolution embedded in the virus genomes and rests on decades of theoretical knowledge on molecular evolutionary processes.

First author Dr Oscar MacLean explains, "This does not mean no changes have occurred, mutations of no evolutionary significance accumulate and 'surf' along the millions of transmission events, like they do in all viruses." Some changes can have an effect for example, the Spike replacement D614G which has been found to enhance transmissibility and certain other tweaks of virus biology scattered over its genome. On the whole, though, 'neutral' evolutionary processes have dominated. MacLean adds, "This stasis can be attributed to the highly susceptible nature of the human population to this new pathogen, with limited pressure from population immunity, and lack of containment, leading to exponential growth making almost every virus a winner."

Pond comments, "what's been so surprising is just how transmissible SARS-CoV-2 has been from the outset. Usually viruses that jump to a new host species take some time to acquire adaptations to be as capable as SARS-CoV-2 at spreading, and most never make it past that stage, resulting in dead-end spillovers or localised outbreaks."

Studying the mutational processes of SARS-CoV-2 and related sarbecoviruses (the group of viruses SARS-CoV-2 belongs to from bats and pangolins), the authors find evidence of fairly significant change, but all before the emergence of SARS-CoV-2 in humans. This means that the 'generalist' nature of many coronaviruses and their apparent facility to jump between hosts, imbued SARS-CoV-2 with ready-made ability to infect humans and other mammals, but those properties most have probably evolved in bats prior to spillover to humans.

Joint first author and PhD student Spyros Lytras adds, "Interestingly, one of the closer bat viruses, RmYN02, has an intriguing genome structure made up of both SARS-CoV-2-like and bat-virus-like segments. Its genetic material carries both distinct composition signatures (associated with the action of host anti-viral immunity), supporting this change of evolutionary pace occurred in bats without the need for an intermediate animal species."

Robertson comments, "the reason for the 'shifting of gears' of SARS-CoV-2 in terms of its increased rate of evolution at the end of 2020, associated with more heavily mutated lineages, is because the immunological profile of the human population has changed." The virus towards the end of 2020 was increasingly coming into contact with existing host immunity as numbers of previously infected people are now high. This will select for variants that can dodge some of the host response. Coupled with the evasion of immunity in longer-term infections in chronic cases (e.g., in immunocompromised patients), these new selective pressures are increasing the number of important virus mutants.

It's important to appreciate SARS-CoV-2 still remains an acute virus, cleared by the immune response in the vast majority of infections. However, it's now moving away faster from the January 2020 variant used in all of the current vaccines to raise protective immunity. The current vaccines will continue to work against most of the circulating variants but the more time that passes, and the bigger the differential between vaccinated and not-vaccinated numbers of people, the more opportunity there will be for vaccine escape. Robertson adds, "The first race was to develop a vaccine. The race now is to get the global population vaccinated as quickly as possible."

Peer reviewed Experimental study Animals

In your coverage please use these URLs to provide access to the freely available articles in PLOS Biology: http://journals. plos. org/ plosbiology/ article?id= 10. 1371/ journal. pbio. 3001115

Citation: MacLean OA, Lytras S, Weaver S, Singer JB, Boni MF, Lemey P, et al. (2021) Natural selection in the evolution of SARS-CoV-2 in bats created a generalist virus and highly capable human pathogen. PLoS Biol 19(3): e3001115. https:/ / doi. org/ 10. 1371/ journal. pbio. 3001115

Funding: DLR is funded by the Medical Research Council (MC_UU_1201412) and Wellcome Trust (220977/Z/20/Z). OAM is funded by the Wellcome Trust (206369/Z/17/Z). SLKP and SW are supported in part by the National Institutes of Health (R01 AI134384 (NIH/NIAID)) and the National Science Foundation (award 2027196). PL acknowledges funding from the European Research Council under the European Union's Horizon 2020 research and innovation programme (grant agreement no. 725422-ReservoirDOCS), the European Union's Horizon 2020 project MOOD (874850), the Wellcome Trust through project 206298/Z/17/Z (The Artic Network) and the Research Foundation -- Flanders (`Fonds voor Wetenschappelijk Onderzoek -- Vlaanderen', G066215N, G0D5117N and G0B9317N). MFB is funded by a grant from the Bill and Melinda Gates Foundation (INV-005517) and by NIH/NIAID Center of Excellence in Influenza Research and Surveillance contract (HHS N272201400007C). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

Competing Interests: The authors have declared that no competing interests exist.

Disclaimer: AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert system.

AI model examines virus spread from animals to humans

Glycan diversity. The image shows a glimpse of glycan diversity, showcasing several classes of glycans from various kingdoms of life. Credit: Daniel Bojar

A new model that applies artificial intelligence to carbohydrates improves the understanding of the infection process and could help predict which viruses are likely to spread from animals to humans. This is reported in a recent study led by researchers at the University of Gothenburg.

Carbohydrates participate in nearly all biological processes—yet they are still not well understood. Referred to as glycans, these carbohydrates are crucial to making our body work the way it is supposed to. However, with a frightening frequency, they are also involved when our body does not work as intended. Nearly all viruses use glycans as their first contact with our cells in the process of infection, including our current menace SARS-CoV-2, causing the COVID-19 pandemic.

A research group led by Daniel Bojar, assistant professor at the University of Gothenburg, has now developed an artificial intelligence-based model to analyze glycans with an unprecedented level of accuracy. The model improves the understanding of the infection process by making it possible to predict new virus-glycan interactions, for example between glycans and influenza viruses or rotaviruses: a common cause for viral infections in infants.

As a result, the model can also lead to a better understanding of zoonotic diseases, where viruses spread from animals to humans.

"With the emergence of SARS-CoV-2, we have seen the potentially devastating consequences of viruses jumping from animals to humans. Our model can now be used to predict which viruses are particularly close to "jumping over." We can analyze this by seeing how many mutations would be necessary for the viruses to recognize human glycans, which increases the risk of human infection. Also, the model helps us predict which parts of the human body are likely targeted by a potentially zoonotic virus, such as the respiratory system or the gastrointestinal tract," says Bojar, who is the main author of the study.

In addition, the research group hopes to leverage the improved understanding of the infection process to prevent viral infection. The aim is to use the model to develop glycan-based antivirals, medicines that suppress the ability of viruses to replicate.

"Predicting virus-glycan interactions means we can now search for glycans that bind viruses better than our own glycans do, and use these "decoy" glycans as antivirals to prevent viral infection. However, further advances in glycan manufacturing are necessary, as potential antiviral glycans might include diverse sequences that are currently difficult to produce," Bojar says.

He hopes the model will constitute a step towards including glycans in approaches to prevent and combat future pandemics, as they are currently neglected in favor of molecules that are simpler to analyze, such as DNA.

"The work of many groups in recent years has really revolutionized glycobiology and I think we are finally at the cusp of using these complex biomolecules for medical purposes. Exciting times are ahead," says Bojar.

Transmission of Avian Influenza A Viruses Between Animals and People

Influenza A viruses have infected many different animals, including ducks, chickens, pigs, whales, horses, and seals. However, certain subtypes of influenza A virus are specific to certain species, except for birds, which are hosts to all known subtypes of influenza A viruses. Currently circulating Influenza A subtypes in humans are H3N2 and H1N1 viruses. Examples of different influenza A virus subtypes that have infected animals to cause outbreaks include H1N1 and H3N2 virus infections of pigs, and H7N7 and H3N8 virus infections of horses.

Influenza A viruses that typically infect and transmit among one animal species sometimes can cross over and cause illness in another species. For example, until 1998, only H1N1 viruses circulated widely in the U.S. pig population. However, in 1998, H3N2 viruses from humans were introduced into the pig population and caused widespread disease among pigs. More recently, H3N8 viruses from horses have crossed over and caused outbreaks in dogs.

Avian influenza A viruses may be transmitted from animals to humans in two main ways:

  • Directly from birds or from avian influenza A virus-contaminated environments to people.
  • Through an intermediate host, such as a pig.

Influenza A viruses have eight separate gene segments. The segmented genome allows influenza A viruses from different species to mix and create a new virus if influenza A viruses from two different species infect the same person or animal. For example, if a pig were infected with a human influenza A virus and an avian influenza A virus at the same time, the new replicating viruses could mix existing genetic information (reassortment) and produce a new influenza A virus that had most of the genes from the human virus, but a hemagglutinin gene and/or neuraminidase gene and other genes from the avian virus. The resulting new virus might then be able to infect humans and spread easily from person to person, but it would have surface proteins (hemagglutinin and/or neuraminidase) different than those currently found in influenza viruses that infect humans.

This type of major change in the influenza A viruses is known as &ldquoantigenic shift.&rdquo Antigenic shift results when a new influenza A virus subtype to which most people have little or no immune protection infects humans. If this new influenza A virus causes illness in people and is transmitted easily from person to person in a sustained manner, an influenza pandemic can occur.

It is possible that the process of genetic reassortment could occur in a person who is co-infected with an avian influenza A virus and a human influenza A virus. The genetic information in these viruses could reassort to create a new influenza A virus with a hemagglutinin gene from the avian virus and other genes from the human virus. Influenza A viruses with a hemagglutinin against which humans have little or no immunity that have reassorted with a human influenza virus are more likely to result in sustained human-to-human transmission and pose a major public health threat of pandemic influenza. Therefore, careful evaluation of influenza A viruses recovered from humans who are infected with avian influenza A viruses is very important to identify reassortment if it occurs.

Although it is unusual for people to get influenza virus infections directly from animals, sporadic human infections and outbreaks caused by certain avian influenza A viruses and swine influenza A viruses have been reported.


In August of 1978, a medical photographer at Birmingham Medical School developed smallpox and died. She infected her mother, who survived. Her workplace was immediately above the smallpox laboratory at Birmingham Medical School. Faulty ventilation and shortcomings in technique were ultimately implicated.

Investigators then re-examined a 1966 smallpox outbreak, which was strikingly similar. The initial 1966 infection was also a medical photographer who worked at the same Birmingham Medical School facility. The earlier outbreak was caused by a low-virulence strain of smallpox (variola minor), and it caused at least 72 subsequent cases. There were no deaths. Laboratory logs revealed variola minor had been manipulated in the smallpox laboratory at a time appropriate to cause the infection in the photographer working a floor above.

Common Cold Can Protect Against Infection by COVID-19 Virus

Exposure to the rhinovirus, the most frequent cause of the common cold, can protect against infection by the virus which causes COVID-19, Yale researchers have found.

In a new study, the researchers found that the common respiratory virus jump-starts the activity of interferon-stimulated genes, early-response molecules in the immune system which can halt replication of the SARS-CoV-2 virus within airway tissues infected with the cold.

Triggering these defenses early in the course of COVID-19 infection holds promise to prevent or treat the infection, said Ellen Foxman, assistant professor of laboratory medicine and immunobiology at the Yale School of Medicine and senior author of the study. One way to do this is by treating patients with interferons, an immune system protein which is also available as a drug.

“But it all depends upon the timing,” Foxman said.

The results will be published today (June 15th, 2021) in the Journal of Experimental Medicine.

Previous work showed that at the later stages of COVID-19, high interferon levels correlate with worse disease and may fuel overactive immune responses. But recent genetic studies show that interferon-stimulated genes can also be protective in cases of COVID-19 infection.

Foxman’s lab wanted to study this defense system early in the course of COVID-19 infection.

Since earlier studies by Foxman’s lab showed that common cold viruses may protect against influenza, they decided to study whether rhinoviruses would have the same beneficial impact against the COVID-19 virus. For the study, her team infected lab-grown human airway tissue with SARS-CoV-2 and found that for the first three days, viral load in the tissue doubled about every six hours. However, replication of the COVID-19 virus was completely stopped in tissue which had been exposed to rhinovirus. If antiviral defenses were blocked, the SARS-CoV-2 could replicate in airway tissue previously exposed to rhinovirus.

The same defenses slowed down SARS-CoV-2 infection even without rhinovirus, but only if the infectious dose was low, suggesting that the viral load at the time of exposure makes a difference in whether the body can effectively fight the infection.

The researchers also studied nasal swab samples from patients diagnosed close to the start of infection. They found evidence of rapid growth of SARS-CoV-2 in the first few days of infection, followed by activation of the body’s defenses. According to their findings, the virus typically increased rapidly for the first few days of infection, before host defenses kicked in, doubling about every six hours as seen in the lab in some patients the virus grew even faster.

“There appears to be a viral sweet spot at the beginning of COVID-19, during which the virus replicates exponentially before it triggers a strong defense response,” Foxman said.

Interferon treatment holds promise but it could be tricky, she said, because it would be mostly effective in the days immediately after infection, when many people exhibit no symptoms. In theory, interferon treatment could be used prophylactically in people at high risk who have been in close contact with others diagnosed with COVID-19. Trials of interferon in COVID-19 are underway, and so far show a possible benefit early in infection, but not when given later.

These findings may help explain why at times of year when colds are common, rates of infections with other viruses such as influenza tend to be lower, Foxman said. There are concerns that as social distancing measures ease, common cold and flu viruses — which have been dormant over the past year — will come back in greater force. Interference among respiratory viruses could be a mitigating factor, creating an “upper limit” on the degree to which respiratory viruses co-circulate, she said.

“There are hidden interactions between viruses that we don’t quite understand, and these findings are a piece of the puzzle we are just now looking at,” Foxman said.

Reference: “Dynamic innate immune response determines susceptibility to SARS-CoV-2 infection and early replication kinetics” by Nagarjuna R. Cheemarla, Timothy A. Watkins, Valia T. Mihaylova, Bao Wang, Dejian Zhao, Guilin Wang, Marie L. Landry and Ellen F. Foxman, 15 June 2021, Journal of Experimental Medicine.
DOI: 10.1084/jem.20210583

Nagarjuna R. Cheemarla, a postdoctoral associate in Foxman’s lab, was first author of the study, which was carried out by a team of Yale scientists in the Departments of Laboratory Medicine, Immunobiology, and Genetics.

Other Yale authors included Timothy Watkins, Valia Mihaylova, Bao Wang, Marie Landry, Dejian Zhao, and Guilin Wang.

We put this question to Cambridge University Researcher Ed Hutchinson.

In the case of flu, you've got the fact that flu will spread from organism to organism so although we're worried particularly about a human virus, or a virus of livestock as well, it actually starts off as a virus in waterfowl. Things like ducks, where it's not really a pathogen at all - it just lives in there and gets along with them. That doesn't really tell you where a virus has come from. We know that they can spread from organism to organism.

In the first place viruses probably evolve as just bits of the genetic sequence which just get out of hand and start copying themselves, moving to places they shouldn't and acquiring more and more abilities along the way. There are quite a few examples of this where thing start jumping around inside genomes eventually will get the ability to jump from cell to cell as well.

Chris - In the answer to what came first, chicken or the egg, the virus-cell situation has to be the cell came first, the virus came later?

Ed - Remember, the defining feature of the virus is that it's absolutely dependent on taking over a cell to work. Without a cell the virus isn't going to do anything at all.

Family relations

The International Committee for the Taxonomy of Viruses has approved the naming of more than 40 coronaviruses. The vast majority of these infect animals. The COVID-19 outbreak has brought the number of identified coronaviruses that infect humans to seven. Four of these are community acquired and have circulated through the human population continually for a very long time.

The other three – SARS-CoV, MERS-CoV and SARS-CoV-2 – appear to have jumped to the human population more recently. Worryingly, these three result in a high mortality rate.

All coronaviruses are zoonotic. They start off in animals and can then, following mutation, recombination and adaptation, be passed on to humans.

Many animal coronaviruses cause long-term or persistent enzootic infections: they infect animals in a particular locale or during a particular season. At the same time, these animal coronaviruses have co-evolved and adapted with their reservoir host over a very long time. For this reason, the zoonotic coronaviruses don’t typically cause symptoms in their reservoir host. Even if they do, symptoms are very mild.

The worry, though, is that these extended periods of animal coronavirus infection – together with a high recombination rate with other viruses as well as a high mutation rate – increase the probability of a coronavirus mutant developing the ability to jump to another host.

There is speculation that when an animal coronavirus enters this new host, the severity of the disease is significantly increased at the start of a new round of adaptation between the coronavirus and the new host. It is speculated – but not yet proven – that only after a very long period of adaptation and co-evolution could the new host adapt enough to the virus to be able to fight it off more effectively. This would result in milder symptoms.

The seven human coronaviruses have been reported to have domestic and wild mammals as intermediate and amplifying hosts. This means that they transitioned into humans via a few other animals after originating probably in bats and rodents.

The four community-acquired human coronaviruses – meaning that they are acquired or arise in the general population – typically cause mild cold-like symptoms in humans. Two of them, hCoV-OC43 and hCoV-229E, have been responsible for between 10% and 30% of all common colds since about the 1960s.

Even though these coronaviruses cause infections throughout the year, spikes in infections occur during the winter and early spring months. As with other respiratory viruses, such as the influenza virus, the reasons for this are not entirely clear. This group of human coronaviruses typically infects all age groups multiple reinfections are common throughout the lifespan of humans.

Why viruses are sneaky

The basic biology of viruses contributes to their capacity to cause disease. Most human viruses replicate almost instantaneously and in huge numbers. As a result, mutations arise at a high rate in the genetic code of a virus. This allows the virus to adapt quickly to an adverse environment, such as the human immune system or drugs. It may also allow a virus to jump from an animal host to humans.

Some viruses establish a chronic infection, which extends the potential for transmission. After acute illness, Ebola virus hides for many months in parts of the body that generate weak inflammatory responses, such as the sexual organs, the brain and/or the eye.

And although human immunodeficiency virus (HIV) may cause an acute illness, there is usually a long delay between infection and the onset of any disease. Consequently infected people may pass on HIV for years before being aware that they carry the virus.

Mosquitoes are responsible for the most viral transmissions. from

There are no specific drugs for most dangerous human viruses. This is in part because viruses are a fast growing and diverse group, with no common drug targets to exploit, as has been possible with antibiotics for bacteria.

But another challenge relates to the viral life cycle, which uses the infected person’s cell machinery. Drugs that target the growth of viruses therefore have effects on the person’s cell, which may result in drug side effects.

Also, the capacity of a virus to adapt implies the potential to develop resistance to a drug. Drug treatment for HIV infection involves a combination of drugs with different actions to address this problem.

Despite the many challenges associated with dangerous viruses, research continues to yield even more innovative solutions. The World Mosquito Program, run out of Monash University, is one example. This program is based on the discovery that a safe and natural bacteria, Wolbachia, stops viral growth in the mosquito. Insects in regions endemic with mosquito-borne diseases are being infected with Wolbachia to break the transmission cycle.

Ultimately, the cunning strategies used by dangerous viruses are no match for the wide breadth of human ingenuity.


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