Pathophysiology of herpes | Infectious diseases | NCLEX-RN | Khan Academy

Pathophysiology of herpes | Infectious diseases | NCLEX-RN | Khan Academy


– [Narrator] When we’re talking about the pathophysiology of a disease, we’re trying to figure out how
that disease causes symptoms. So in the case of herpes,
or the herpes simplex virus, we’re trying to figure out
how the virus infects cells, and causes symptoms. So let’s take a look at
this skin cell over here, this is a cell that may live on your lips, and here’s the nucleus, I’m gonna draw it dotted so we can see what’s going on inside. And in there there’s going to be some DNA. And I’ll draw it like this
even though DNA is a lot more tightly wound than it is here. Then I’ll label these things
so this dotted line here, I mentioned was the nucleus. Or we can also refer to it
as the nuclear envelope. And then on the inside, this guy is our cell’s DNA. It’s our own DNA or our nucleic
acid that lives in there. Now let’s imagine this
cell’s going to be infected by the herpes virus so
I will use this triangle to symbolize herpes, and so this triangle or this
virus will come and attach on to the cell membrane here. And within the cell, the
herpes has its own DNA. The viral DNA that exists
as well as some proteins that are in here and I’ll
explain in a few minutes what these proteins help it do. But just realize first
off this green border, the triangle on the outside, is a nucleocapsid. This helps the virus inject
the DNA and the proteins into the cell, like we’ll see in a minute. Right here we’ve got some proteins, as I’ll mention in a few minutes. These help incorporate the viral DNA into the human or host DNA. And finally this yellow strand right here is the viral DNA. So this is the DNA of
the herpes simplex virus. And so our first step here
is that the nucleocapsid has proteins that help
inject the viral DNA and these proteins into the human cell. Which means that as I’ll draw right here, is to inject viral DNA. So once we do that, let
me just draw our cell again over here. Now the viral DNA will
be inside of the cell. And with it will be these viral proteins that the nucleocapsid injected as well. So at this point, the viral DNA will use these
proteins to inject itself or incorporate itself, which is a better word, into the human DNA here. And so our next step is
that we will incorporate viral DNA using these proteins. And so what you’ll end up getting, and I’ll bring in another
sample of the cell right here, so this is the cell
we’ve been working with, is the human DNA here but
now it’s also attached to the viral DNA. Now at this point, this cell that now is under the control of the herpes virus, because the viral DNA is now in the brain or the nucleus of the cell, this cell can do two things. And I’ll draw that right here. Here’s one path that we can take, and then here’s another path we can take. So I’m trying to draw
all this like a cycle, go let’s complete this
cycle and talk about this step right here, which after we’ve
incorporated the viral DNA, we will start to mass
produce the herpes virus, which, as I’ll draw this cell again, over here, you’ll begin to see a lot
of these nucleocapsids being formed again and so
they’re going to swell up in the cell. These guys will also have their own copies of the viral DNA. And you might not be able to see it but I’ll just mention the
protein is there as well. And in fact this occurs
at such a crazy extent that the cell can’t handle
that type of viral production. And so what’ll end up happening is that the cell will rupture. It’ll pop open. So I drew this cell here
but let’s draw another one. Up over here, and I’ll really exaggerate this, there’s going to be so many
of these viral nucleocapsids that are filled with DNA and proteins that the cell will not
have any more nutrients for it to fortify its cell membrane or for it to grow on its own. And so what’ll end up happening is that the cell membrane
will fracture open, like that, it’ll pop, it’ll burst, and you’ll begin to have an
exodus of these viruses out here which then allows you
to restart the cycle. And because the cell popped
open here, or ruptured another term for rupture is lysis, the name of this phase
for the herpes life cycle is the lytic phase. This is the lytic phase. And that’s in contrast
with what’s happening here. Instead of killing the cell, what you’ll see happening
is that the herpes virus will remain dormant, and so what you’ll get
are two of these cells, so there’s one here,
and here’s another one. So the virus just kind of takes a backseat and allows the human
cell to grow on its own. So here the virus will
reproduce with the cell, and this relatively more
dormant phase of the virus, or the herpes virus life cycle is referred to as the lysogenic, the lysogenic phase. That’s just to emphasize
that the cell is able to undergo the lytic phase, or undergo lysis of the cell, that’s why lysogenic
meaning able to cause. So it has that potential but
it’s currently not doing that. It’s just going along for the ride. And for the time being, the herpes virus is dormant. Meaning it’s at rest
and not mass producing its viral nucleocapsids,
proteins, or its DNA. Now an important thing
about herpes is that it likes to be dormant
in nerve cell bodies, and the term for nerve cell bodies is ganglion. So I’ll write ganglion here. Or if you’re talking
about multiple ganglions, there’s no such word as ganglions so instead we say ganglia. And in fact we know what
specific ganglion or ganglia herpes likes to go into
the lysogenic phase in, and that depends where it occurs. So remember herpes labialis is herpes that occurs on the lips, on the inside of your cheeks, or even on the tip of the tongue, so it’s oral herpes. That tends to go and become dormant in the trigeminal ganglion. The trigeminal ganglion
which is a cranial nerve that helps you feel touch on your face. So that’s for herpes labialis. Now for herpes genitalis, there are several ganglia that the herpes can become dormant in, and we group them together and call them the lumbosacral ganglia, which is a reference to the spinal cord. It can be in the lumbar
or the sacral region of the spinal cord, so somewhere in there. But recall because this is lysogenic, or able to cause lysis, these cells are able to pick right on up and enter the lytic phase. There are a couple of things
that are known to cause that. Sunlight is one thing that’s
been noted in some people to induce the lysogenic cycle to convert into the lytic cycle. Decreased immune function
is another known cause. But what these all boil down to is that anything that’s
an overload of stress, and that can also
include emotional stress, can trigger a lysogenic virus to enter the lytic phase. Which is such an interesting concept because the herpes virus
must be able to read how the cell is surviving
relative to its environment. So it has become one with the cell. And unfortunately once that
cell is overly stressed, it’s time for the virus to escape and reproduce and move on to another cell that’ll be able to house
it and help it grow.

10 Replies to “Pathophysiology of herpes | Infectious diseases | NCLEX-RN | Khan Academy”

  1. I love these videos, but will say this one is one of the worst. It isn't until around 5 minutes & 30 seconds in that you start talking about Herpes specifically. If I wanted a video about viral affects on the the cell cycle, I'll click on a video about that – this video should be shortened up to 3 minutes & just focused on painting a picture of herpes.

  2. This channel is so underrated. I'm a medical student and your videos make concepts so much easier to I understand. Thank you!

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