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Coronavirus: Human and Animal Health Are Two Chapters in the Same Book

Coronavirus: Human and Animal Health Are Two Chapters in the Same Book

A scientist examines the result of a plaque assay, a test that allows scientists to count how many flu virus particles are present in a mixture. Photo: CDC/Unsplash.

Humans are quite likely to overcome the new coronavirus within the next few months, but that moment will only signal the end of a chapter in a larger book about the relationship between humans and animals. Our present coronavirus outbreak is certainly not the last. There will be more such outbreaks in future, more such public health emergencies, and to anticipate them, we need to understand the different ways in which humans and animals interact, and how their health affects each other on this shared planet.

Researchers have reported the discovery of new coronaviruses since the 1960s. To date, we know of seven coronaviruses that infect humans. Each virus is a new beast. For example, even though the SARS virus and the new coronavirus (SARS-CoV-2) are genetically about 70% similar, the new virus kills less but spreads more, forcing researchers to develop new defences suited to it.

We believe SARS-CoV-2 probably came from bats because the virus’s genes are 96% similar to those of a coronavirus isolated from horseshoe bats. However, without any documented evidence of direct transmission from bats to humans, researchers believe there could have been an intermediary animal such that the virus jumped from bats to the animal and from the animal to humans. One candidate is pangolins, since a protein pangolins make in their bodies resembles one the virus makes to the tune of 99%.

Once the new coronavirus began human to human transmission, it could’ve adapted better to surviving in the human body. Researchers are still working this one out.

Recently, a tiger at the Bronx Zoo in New York contracted the disease, presumably from a zookeeper. This is weird because viruses can infect a body only if it’s adapted to survive in that body; each pathogen has its own way of evading the host’s immune response. So it seems implausible that a virus capable of infecting humans can also infect tigers.

Scientists are looking for answers to these and other questions to fully understand the new coronavirus as well as to help prevent other zoonotic diseases – diseases transmitted from animals to humans – waiting in our future just like what we learnt from older viruses prepared us to deal with the new one better.

For example, rabies – which affects the central nervous system – is caused by a neurotropic virus. The virus has to travel from the site of an infected animal’s bite via the peripheral nervous system (unlike many viruses that travel through the body in the blood) to reach the central nervous system. In effect, the virus has to keep moving outside the bloodstream, so it evolved mechanisms to hijack the transport system.

There is a protein called p75NTR on the tips of peripheral neurons, and it binds to a substance called the nerve growth factor (NGF). After binding, the NGF is enclosed in a vesicle (bubble) and transported to the central nervous system. The rabies virus behaves exactly like the NGF, and binds to p75NTR and reaches the central nervous system with ease.

The Bacillus anthracis bacteria have evolved a similarly unique mechanism. These bacteria cause anthrax, which affects cattle, buffalo and horses. Humans acquire the disease from the affected animals but it is not lethal.

Inside the body of a living host, the bacteria exist in their vegetative form, growing and multiplying. But when they’re outside and exposed to relatively larger quantities of free oxygen, the bacteria create a protective structure around themselves called a spore, which is resistant to heat, cold, acidity, desiccation and radiation. This way, the bacteria can endure for many years at a time.

Animals can contract anthrax either by inhaling or ingesting the spores. Death is often sudden, with blood often seen oozing out of the poor animal’s natural orifices. Animals that have died this way are never cut open for necropsies because the disease could easily be transmitted to humans and other animals from the infected carcass. Instead, the animal is simply cremated.

Some pathogens need a vector to carry them from one species to another. A classical example is the Kyasanur forest disease, whose vector is a tick. Once the causative virus enters a tick, the tick stays infected forever, and passes on the virus to its offspring through its eggs. When the ticks get on monkeys and small wild mammals, they become infected by the disease. Humans contract the disease from a tick bite or when they come in contact with an infected monkey. However, the virus doesn’t jump from humans to humans (at least not that we know of).

Human-made stressors like deforestation and encroachment into wildlife habitats play important parts in accelerating the spread of this disease. A farmer succumbed to it in Karnataka on March 30, 2020, and five others had reportedly tested positive in the region.


Also read: The Seven-Decade Transnational Hunt for the Origins of the Kyasanur Forest Disease


In all these diseases, humans were the dead-end hosts; the viruses didn’t jump from humans to a different animal species and wreak havoc among them. And with the exception of the virus that causes the Kyasanur forest disease, and some others, the pathogens caught humans’ attention when they became infectious and in some cases lethal. Some prominent examples of such zoonotic viruses include the SARS virus, the MERS virus, the ebolavirus, the Nipah virus and, of course, the new coronavirus.

As it happens, most of these viruses came to humans from bats, possibly thanks to bats’ antiviral response. These flying mammals have a strong immune response but their inflammatory mechanism is not good enough to drive the viruses away altogether. Additionally, when viruses invade a bat’s body, the bats’ cells release a molecule called interferon alpha, which signals to other cells that they should enter an ‘antiviral state’. So altogether viruses are able to replicate faster without damaging their host. Humans on the other hand don’t possess a similar antiviral mechanism.

When humans disrupt their habitats and environment, these bats become more stressed and spill more viruses into their saliva, potentially infecting more animals and humans as a result.

As it happens, humans’ environmental habits alone aren’t to blame. Many disease-causing pathogens have of late been becoming more resistant to antimicrobial drugs, either by developing the corresponding mutation or by acquiring ‘resistance’ genes from external sources. This way, a drug that was once effective against this or that microbe is likely to have become less effective, if not entirely impotent. Since in most cases the same classes of medically important antimicrobials are used to treat both humans and animals, both animals and humans contribute to antimicrobial resistance.

Humans could help transport ‘resistance’ genes from pathogens in an animal’s body to a different pathogen in the human body, such as by eating uncooked contaminated meat. A wide range of animal species used in food production — such as poultry and pigs – further complicates the use of antimicrobial drugs in animals.

As the human population continues to grow, industrialise and change the face of the planet, our ecosystems and biodiversity deteriorate, promoting the emergence of zoonotic infectious diseases. Since about 75% of emerging infectious diseases are zoonotic, it’s human that human and animal health experts work together in the spirit of the ‘one health’ concept. ‘One health’ is a trans-disciplinary approach that recognises the relationship between people, animals and the environment, which they all share. So if we’re to successfully control zoonotic diseases, we should also understand human and animal health together instead of separately.

Niranjana Rajalakshmi is a veterinary microbiologist.

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