At a Maryland country fair in 2017,
the prize pigs were not
looking their best.
Farmers reported feverish hogs with
inflamed eyes and running snouts.
But while fair officials worried
about the pigs,
the Maryland department of health was
concerned about a group of sick fairgoers.
Some had pet the pigs, while others had
merely been near their barns;
but soon, 40 of these attendees would
be diagnosed with swine flu.
More often than not, sick animals
don’t infect humans.
But when they do, these
cross-species infections,
or viral host jumps,
have the potential to produce
deadly epidemics.
So how can pathogens from one species
infect another,
and what makes host jumps so dangerous?
Viruses are a type of organic parasite
infecting nearly all forms of life.
To survive and reproduce, they must move
through three stages:
contact with a susceptible host,
infection and replication,
and transmission to other individuals.
As an example, let’s look
at human influenza.
First, the flu virus encounters
a new host
and makes its way into
their respiratory tract.
This isn’t so difficult, but to survive
in this new body,
the virus must mount a successful
infection
before it’s caught and broken down
by an immune response.
To accomplish this task,
viruses have evolved specific interactions
with their host species.
Human flu viruses are covered in proteins
adapted to bind with matching receptors
on human respiratory cells.
Once inside a cell, the virus employs
additional adaptations
to hijack the host cell’s reproductive
machinery
and replicate its own genetic material.
Now the virus only needs to suppress
or evade the host’s immune system
long enough to replicate to sufficient
levels and infect more cells.
At this point, the flu can be passed on to
its next victim
via any transmission
of infected bodily fluid.
However, this simple sneeze also brings
the virus in contact with pets,
plants, or even your lunch.
Viruses are constantly encountering
new species and attempting to infect them.
More often than not, this ends in failure.
In most cases, the genetic dissimilarity
between the two hosts is too great.
For a virus adapted to infect humans,
a lettuce cell would be a foreign and
inhospitable landscape.
But there are a staggering number
of viruses circulating in the environment,
all with the potential to
encounter new hosts.
And because viruses rapidly reproduce
by the millions,
they can quickly develop random mutations.
Most mutations will have no effect,
or even prove detrimental;
but a small proportion may enable the
pathogen to better infect a new species.
The odds of winning this destructive
genetic lottery increase over time,
or if the new species is closely related
to the virus’ usual host.
For a virus adapted to another mammal,
infecting a human might just take
a few lucky mutations.
And a virus adapted to chimpanzees,
one of our closest genetic relatives,
might barely require any changes at all.
It takes more than time and genetic
similarity
for a host jump to be successful.
Some viruses come equipped to easily
infect a new host’s cells,
but are then unable to evade
an immune response.
Others might have a difficult time
transmitting to new hosts.
For example, they might make the host’s
blood contagious,
but not their saliva.
However, once a host jump reaches
the transmission stage,
the virus becomes much more dangerous.
Now gestating within two hosts,
the pathogen has twice the odds of
mutating into a more successful virus.
And each new host increases
the potential for a full-blown epidemic.
Virologists are constantly looking for
mutations
that might make viruses such as influenza
more likely to jump.
However, predicting the next potential
epidemic is a major challenge.
There’s a huge diversity of viruses
that we’re only just beginning to uncover.
Researchers are tirelessly studying the
biology of these pathogens.
And by monitoring populations to quickly
identify new outbreaks,
they can develop vaccines and containment
protocols to stop these deadly diseases.