Professor Dave here, let’s take a look at virus-cell interactions.
So far, we’ve learned what viruses are made of and how they’re classified.
Now, let’s talk about what happens when a virus encounters a cell.
When you get down to it, there are really only two basic types of interaction possible
between a virus and a cell, and those are called non-productive and productive, the
latter of which means that infection of the cell occurs.
It turns out that lots of things have to happen the right way and in the right order for infection
to result, so let’s get a closer look now.
As we might guess, a non-productive interaction means that the virus is not able to replicate itself.
However, there is some nuance here.
There are three possible outcomes for a non-productive interaction.
The first outcome is that the virion and its genome is completely destroyed.
99% of the time, if you take a random cell and a random virus, they won’t be compatible
and the virus just gets destroyed.
The second outcome, which is more rare, is oncogenic transformation.
This means that the virus isn’t able to make copies of itself, but it affects the
cell in such a way that it triggers uncontrolled cell division, which we typically call cancer.
An example of this is polyomavirus simian virus 40, or SV40, in rodent cells.
This DNA virus induces primary brain and bone cancers, malignant mesothelioma, and lymphomas
in laboratory animals.
The third outcome is a latent infection, where the virus enters the cell but remains dormant,
with little or no gene expression observed.
In a productive virus-cell interaction, on the other hand, new viruses are made.
These infections can fall anywhere on the spectrum between two extremes.
On one end, 100% of the cell’s resources are channeled into making copies of the virus,
which ultimately causes the cell to die.
When the cell dies, it essentially explodes and releases a slew of viruses that can then
infect neighboring cells, and the cycle continues.
This is called a lytic infection, and we looked at this process in some detail in the biology series.
On the other end of the spectrum, the cell is continually making viruses, but it doesn’t
divert as much of the cell’s resources.
This keeps the cell alive, with the rate of virus production being much slower.
This is called a persistent infection.
Some viruses fall somewhere in the middle of this spectrum, depending on what is optimal
for the lifestyle of the virus.
Now, let’s move on to the stages of the cellular viral infection cycle.
Typically, in a productive virus-cell interaction, infection happens in the following stages:
attachment, penetration, uncoating, gene expression, genome replication, assembly, release, and
maturation.
Let’s start with attachment, which just refers to when a virus sticks to a host cell.
Viruses use proteins or anti-receptors to attach in a highly specific manner to particular
receptors on the surface of the host cell.
If a cell doesn’t have the right receptors that will allow for binding, it will be a
non-productive interaction.
We should be aware that these receptors which the viruses bind to also have a normal function
in the cell, they don’t exist solely for the benefit of the viruses that hijack them.
For example, things called CD4 molecules that sit on the surface of T cells in our immune
system, help the T cells carry out their normal function, which is interacting with things
called MHC molecules, or major histocompatibility complex.
However, CD4 molecules are the primary receptor for the HIV virus, so they need these proteins
to get inside the cell.
Next up is penetration, which refers to entry of a virus or viral genome into the host cell.
There are three known mechanisms for penetration.
The first is called endocytosis, which literally means to bring something in from the outside,
or to go into a cell.
Both non-enveloped and enveloped viruses can use this method.
The second is direct injection of the viral genome into the cell, as is done by bacteriophages.
The third is direct fusion of the viral envelope with the plasma membrane of the cell.
Only some enveloped viruses do this.
We should note that in direct fusion or injection mechanisms, penetration and the next step,
uncoating, are combined into a single step.
With endocytosis, we have a separate uncoating step, which refers to changes in the virion
structure that are necessary to allow for viral gene expression.
For some viruses, this just means removal of the protective protein coat around their
nucleic acid.
For more complex viruses, uncoating may occur in several more involved steps.
The next stage of the infection cycle is gene expression.
This is where transcription, if necessary, and translation of viral mRNA occurs.
After gene expression, there will be genome replication, where progeny viral genomes are
generated.
Next there is assembly of progeny nucleoproteins.
The protein capsid must be formed, and then the genome and any necessary enzymes packaged
within it.
Second to last, we’ve got release.
For some viruses, release takes the form of lysis, in which viruses accumulate in the
cell and the cell bursts.
For others, the nucleocapsids of enveloped viruses push out through the lipid bilayer
of the cell, acquiring an envelope on the way out.
This process is called budding.
The final step is maturation, which refers to the changes in the virion required to make
it infectious.
Note that not all viruses have this step, and that maturation might occur before, during,
or after release.
Now that we’ve covered the virus-cell interaction from the perspective of the virus, let’s
move forward and discuss things from the perspective of some different types of hosts.