Health

Understanding zoonotic diseases: ‘How we interact with environment drives spillovers’

The scope and scale of deforestation and opening of new interfaces with forests and wildlife increases the chances of spillovers, says health expert Prashanth NP

 
By Ishan Kukreti
Last Updated: Thursday 07 May 2020

Is the novel coronavirus disease (COVID-19) a zoonotic disease? What makes it possible for viruses to jump from animals to humans? 

Down to Earth spoke with Prashanth NP, health equity cluster lead, Wellcome Trust DBT India Alliance Fellow Institute of Public Health, Bangalore to understand what events cause viruses to cross over from one species to another. Edited excerpts:

Ishan Kukreti: Could you explain in detail the factors which make it possible for viruses to jump from animals to humans and also, from humans to humans?

PNP: Typically, spillover events occur when a virus is able to find a new host outside of its typical reservoir hosts.

Such spillover events are most likely to happen when virus comes in contact with human hosts, or when it is able to undergo mutation that established it within human hosts.

In either case, increased physical interfaces that allow human-animal biological material exchange or animal-animal interactions allows multiple strains of viruses to cross over from one species to another. It creates an ideal situation for such spillover events. 

IK: Has there been an increase in the human-to-human transmission of viruses? Why do you think that is the case?

PNP: The scope and scale of deforestation and opening of new interfaces with forests and wildlife increased the chances of spillovers. The way we interact with our environment has certainly increased the exposure to newer pathogens.

It has, in fact, allowed us to come closer to pathogens that would have otherwise not come into contact with large populations.

The Kyasanur Forest disease in southern India, for example, was restricted to tiny pockets in a small town in western Karnataka. But today, it is reported from several states along the Ghats.

Some of the recent work we have done in terms of predicting possible locations where KFD could occur has to do with rapid land-use change. Plantations and deforestation are occurring at a rapid scale.

Deforestation is not often driven by local communities who live among / close to forests, but by powerful interests in far-away cities. We must realise that in some sense, the interfaces and spillovers are as much a consequence of our extractive practices and economies as much as they are a matter of obscure genetic exchange between reservoir hosts and new host species.

Further, the sudden socio-demographic changes, inward and outward migrations into / out of remote areas in response to economic shifts brings newer and unfamiliar populations into these areas. They could drive new ways of interaction with the environment that could further increase risk of spillovers. 

IK: Does the difference in human and animal immunity systems make us more vulnerable to zoonoses? 

PNP: Humans and animals don't have very different immune systems. Pathogens merely look for hosts that allow them to sustain spread and thrive.

In fact, an adapted pathogen is one that does not immediately kill. Take the example the classical (vivax) malaria or HIV/AIDS. In the latter, the jump from possible primate host to humans did not undergo too ‘high’ a mutation given relative similarity in the two systems.

Moreover, the chronicity ensures that the pathogen continues to thrive. The ones that cause a greater number of deaths tend to die out unless they adapt by further mutations,

Such mutations, however, do not always give an advantage to the pathogen. That said, within human beings, the differential immunity due to other co-morbid conditions could shape differences.

For example, it’s been argued that human-to-human transmission of germs may have shaped human history. Limited exposure to some pathogens that the invaders (Europeans) had long-term exposure to drove mortalities among the indigenous Americans in the modern colonisation of the Americas.

In this case, a large immunologically naive population and one that was also possibly nutritionally unprepared, suffered higher mortality from other populations that were immunologically better prepared.

That, however, is not the case anymore because globalisation means that flu strains and pandemics such as COVID-19 spread in a matter of months.

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IK: What enables a virus to become airborne in its transmission? Are there cases where the human-to-human transmission of a virus was airborne — not through respiratory droplets, but aerosols?

PNP: For a virus to become airborne, it needs to be able to survive in fairly adverse environments. The pathogens that cause viral, bacterial and fungal diseases such as measles, tuberculosis and chickenpox have developed that ability.

They are also affected by various environmental factors. Legionella pneumonia, for example, is spread by air-conditioning systems. In the case of COVID-19, while in-situ/laboratory settings have demonstrated that the virus could survive in aerosols, current evidence suggests that this is not the primary route of transmission.

IK: Studies have found evidence of SARS-CoV-2 on aerosol particle. But the understanding so far is that these are not infectious. Could you explain when viruses on an aerosol particle become infectious.

PNP: Studies like these are important. Our understanding of the disease is still improving. However, the ability to demonstrate viral particles in aerosol is insufficient to show airborne transmission.

It is still likely that crowded spaces could multiply chances, so could certain conditions seen in surgical/medical procedures.

That said, the likelihood of large-scale airborne transmission is unlikely in open areas unless the crowd size, number of infectious people etc are added to the context. Fomites (surfaces) seem to be more efficient transmitters of infection than free-floating aerosols. 

IK: Why is treating zoonoses such as SARS, MERS and now COVID-19 so difficult? 

PNP: Primarily because these are ‘new’ infections where the pathogen has not co-evolved with the host (like in the case of tuberculosis). That said, we must remember that the infection fatality rate (not case fatality) is still quite small.  

For every 100 people who get infected, 99 are recovering fully. About 30-50 do not even realise that they were ill. 

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