At a Maryland country fair in 2017,

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the prize pigs were not looking their best.
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Farmers reported feverish hogs with inflamed eyes and running snouts.
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But while fair officials worried about the pigs,
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the Maryland department of health was concerned about a group of sick fairgoers.
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Some had pet the pigs, while others had merely been near their barns;
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but soon, 40 of these attendees would be diagnosed with swine flu.
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More often than not, sick animals don’t infect humans.
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But when they do, these cross-species infections,
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or viral host jumps,
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have the potential to produce deadly epidemics.
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So how can pathogens from one species infect another,
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and what makes host jumps so dangerous?
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Viruses are a type of organic parasite infecting nearly all forms of life.
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To survive and reproduce, they must move through three stages:
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contact with a susceptible host, infection and replication,
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and transmission to other individuals.
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As an example, let’s look at human influenza.
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First, the flu virus encounters a new host
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and makes its way into their respiratory tract.
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This isn’t so difficult, but to survive in this new body,
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the virus must mount a successful infection
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before it’s caught and broken down by an immune response.
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To accomplish this task,
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viruses have evolved specific interactions with their host species.
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Human flu viruses are covered in proteins
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adapted to bind with matching receptors on human respiratory cells.
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Once inside a cell, the virus employs additional adaptations
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to hijack the host cell’s reproductive machinery
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and replicate its own genetic material.
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Now the virus only needs to suppress or evade the host’s immune system
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long enough to replicate to sufficient levels and infect more cells.
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At this point, the flu can be passed on to its next victim
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via any transmission of infected bodily fluid.
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However, this simple sneeze also brings the virus in contact with pets,
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plants, or even your lunch.
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Viruses are constantly encountering new species and attempting to infect them.
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More often than not, this ends in failure.
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In most cases, the genetic dissimilarity between the two hosts is too great.
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For a virus adapted to infect humans,
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a lettuce cell would be a foreign and inhospitable landscape.
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But there are a staggering number of viruses circulating in the environment,
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all with the potential to encounter new hosts.
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And because viruses rapidly reproduce by the millions,
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they can quickly develop random mutations.
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Most mutations will have no effect, or even prove detrimental;
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but a small proportion may enable the pathogen to better infect a new species.
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The odds of winning this destructive genetic lottery increase over time,
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or if the new species is closely related to the virus’ usual host.
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For a virus adapted to another mammal,
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infecting a human might just take a few lucky mutations.
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And a virus adapted to chimpanzees,
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one of our closest genetic relatives, might barely require any changes at all.
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It takes more than time and genetic similarity
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for a host jump to be successful.
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Some viruses come equipped to easily infect a new host’s cells,
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but are then unable to evade an immune response.
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Others might have a difficult time transmitting to new hosts.
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For example, they might make the host’s blood contagious,
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but not their saliva.
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However, once a host jump reaches the transmission stage,
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the virus becomes much more dangerous.
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Now gestating within two hosts,
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the pathogen has twice the odds of mutating into a more successful virus.
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And each new host increases the potential for a full-blown epidemic.
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Virologists are constantly looking for mutations
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that might make viruses such as influenza more likely to jump.
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However, predicting the next potential epidemic is a major challenge.
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There’s a huge diversity of viruses that we’re only just beginning to uncover.
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Researchers are tirelessly studying the biology of these pathogens.
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And by monitoring populations to quickly identify new outbreaks,
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they can develop vaccines and containment protocols to stop these deadly diseases.
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