Species jump: when an animal virus leads to the emergence of a human disease
As we all know, the global population is currently reeling from a new virus responsible for a pandemic: SARS-CoV-2. Capable of spreading rapidly, this virus has quickly overwhelmed healthcare systems that were unprepared for such a threat. Because of its sudden emergence, this new virus is classified as “emerging.”
This article was written by students in the first year of the Master’s program in Microorganism-Host-Environment Interactions at the University of Montpellier (class of 2019–2020), under the supervision of Jean-Christophe Avarre of the French National Research Institute for Sustainable Development (IRD) and Anne-Sophie Gosselin-Grenet of the University of Montpellier.
In virology, an emerging virus is a pathogen that has recently been observed in a given population. Of animal origin, this virus has triggered an epidemic in humans, as is the case with other viruses (such as influenza viruses and Ebola viruses). This phenomenon, which allows an animal virus to infect humans and replicate there, is linked to a mechanism known as “species jump.”
What is a virus? How does it work?
Viruses are microscopic biological entities that are widespread in the environment and play a vital role in the evolution and population control of the organisms they infect.
A virus consists of a genome (its genetic information), a protein shell called a capsid, which protects the genome, and sometimes an envelope. A virus cannot replicate on its own; it must infect a cell in order to hijack the raw materials and machinery it needs to produce its own components.
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Tropism and species specificity: key viral characteristics
Infection begins when a virus encounters a cell. This encounter is initiated by proteins on the virus’s surface that recognize a specific cellular molecule, called a receptor, exposed on the cell’s surface. This recognition, which depends on the quantity and type of receptors present on the cell, determines the cell’s susceptibility to a virus. It is essential for the virus to attach itself to the cell and then penetrate it. The virus’s replication will then depend on the cell’s permissiveness, that is, its ability to allow the production of new viral particles.
These two parameters—sensitivity and permissiveness—thus define the virus’s cellular tropism, that is, its ability to preferentially enter and replicate in a particular type of cell.
The cells of an organism have their own unique susceptibility and permissiveness to a virus, which also vary from one species to another. The virus’s cellular tropism therefore also contributes to its host range—that is, the specificity of the species it is capable of infecting and in which it can replicate. Thus, some viruses have a broad host range, while others are capable of infecting only a single host species.
Species specificity therefore implies a species barrier that prevents viruses (and pathogens in general) from crossing from one species to another, thereby preventing the interspecies transmission of associated viral diseases. This barrier is multifactorial, involving physical-chemical, molecular, metabolic, and immunological factors.
Species barrier crossing leading to viral emergence
A viral emergence can manifest in various ways: it may involve the emergence of a virus in a new region, linked to a change in the virus’s or its host’s range, or the emergence of a disease in a new host species, linked to a structural change in the virus that enables it to infect that species.
Many viral outbreaks result from the transmission of viruses from animals to humans: these are referred to as zoonotic diseases or zoonoses, as was the case with AIDS, which resulted from the transmission of a virus from monkeys to humans, or with SARS in 2003, which followed the transmission of a coronavirus from bats to humans. This interspecies transmission, or species jump, implies that the virus is capable of crossing the species barrier.
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This species jump requires close contact between an animal species infected with a virus—referred to as a reservoir—and humans. The virus is generally non-pathogenic to the reservoir, and the two have coexisted for a long time. Viral replication is thus sustained in the reservoir, and large numbers of viral particles can be produced without causing harm to the reservoir.
The virus is transmitted from the reservoir to humans either directly—particularly through the ingestion of contaminated raw food or through bites—or indirectly via vectors. These vectors are often arthropods, such as mosquitoes, which carry the virus between different hosts during their blood meals.
Since the virus and its new host species have only recently begun coexisting, this species jump may be responsible for the emergence of viral diseases, as is currently the case with COVID-19.
How can a species jump occur?
For a species jump to succeed, the virus must complete four steps: come into contact with the new host species (in this case, humans), infect its cells and replicate within them, evade the host’s defenses, and spread within the population of this new host.
Contact is facilitated by the increased proximity between humans and animals, which stems in particular from the expansion of cities, the destruction of ecosystems (deforestation), and the illegal wildlife trade.
Since proximity alone is not enough, the virus must undergo certain changes to survive within its new host. Indeed, the virus must be able to bind to receptors on the surface of its new host’s cells in order to enter them and replicate by hijacking the cellular machinery. This ability to adapt is made possible in part by their very high mutation rate. The mechanism for replicating viral genetic material makes many errors that are not corrected by the “proofreading” systems common to living organisms. These mutations can lead to structural changes in the virus’s surface proteins, allowing it to bind to new types of cells and thereby altering its cellular tropism. These mutations can also enable the virus to replicate within the cells of the new host species.
The virus, when exposed to the host’s defenses (its immune system), must also develop escape strategies. To do this, some viruses directly attack the host’s defense cells, such as HIV; others “hide” by infecting cells that are inaccessible to the immune system; or they disrupt the danger signals between the host organism’s cells.
Finally, to spread within the population of the new host, the virus must be transmitted between individuals—via respiratory droplets, blood, sexual contact, or even simple direct contact between individuals. The strategy and efficiency of the transmission route will then determine the virus’s ability to spread and establish itself in the new species. Various factors related to the infected host can also influence the efficiency of transmission. For example, once established in the new host, the virus can take advantage of the host’s movements to spread. Through human population movements linked to globalization, trade, and travel, the virus can then infect individuals in another region and thus expand its range. If the spread remains localized, it is called an epidemic, but if it spreads globally, it is then called a pandemic. In cases where transmission is not possible between different individuals of the species, we refer to transmission leading to an epidemiological dead-end.
Due to humanity’s significant impact on the environment—including deforestation, poaching, and intensive livestock farming—combined with ever-increasing globalization, humans have become a major driver of the emergence of viral diseases, unwittingly facilitating species jumps that would normally occur by chance.
Jean-Christophe Avarre, Researcher in viral ecology, French National Research Institute for Sustainable Development (IRD) and Anne-Sophie Gosselin-Grenet, Associate Professor of Virology, UMR Diversity, Genomes, and Microorganism-Insect Interactions (DGIMI), University of Montpellier
This article is republished from The Conversation under a Creative Commons license. Readthe original article.