Taking Charge of Your Health

– [Voiceover] So let’s actually
start this treatment video with just a quick refresher
on how an HIV particle actually takes over one
of your CD4 T-cells. So here you can see HIV meeting up with one of your CD4 T-cells, right? And then these proteins that
are on both of them, they sort of start to shake hands,
I guess you could call it. And you know, because of
this little handshake that they have going on, this secret handshake, the HIV fuses with the CD4 cell, right? And it kind of injects
its genetic material and its enzymes into your cell. So the single-stranded RNA,
that it brought with it, gets reverse-transcribed,
and it eventually gets made into double-stranded DNA. And then this double-stranded
DNA gets taken into our nucleus, and
then gets spliced into our DNA by this integrase enzyme here. Then our cell starts to
crank out viral RNA, right? All sorts of viral RNA, I mean,
it actually doesn’t have to, sometimes it kinda lays low
and doesn’t do anything, because it wants to
avoid our immune system. But in this case it starts to crank out all sorts of viral RNA,
so some of it’s the RNA genome of the HIV, and some of it’s viral MRNA, which then
goes on to get translated into a viral polyprotein,
and then it gets cleaved up by protease, HIV
protease, and then it gets packaged into these sort
of new, shiny HIV particles that are now mature and really infectious. So now that we’ve done that refresher, let’s sort of just talk about
the possible treatments, and where along this pathway
we can use our treatments. So the key treatment for
people with HIV infections is antiretroviral medication, or ARVs. And you know, these aren’t cures for HIV, but they’re really really important for a few different reasons. So for one they can
stop people from getting really really sick with their HIV. They can reduce the amount
of HIV in someone’s body to levels that are pretty
undetectable on lab tests. And you know I guess
kind of related to that, they therefore make it a lot less likely for someone to pass on
the virus to someone else, because of these really low levels. So I guess the overall
idea, the big idea behind ARV treatment is to keep the
viral levels really really low. And you know I should have
probably mentioned this a bit earlier, but the reason it
doesn’t cure an HIV infection, is because there’s this pool,
there’s this big pool of infected CD4 cells that get established really early on in an infection,
and they sort of lay low. Essentially what I showed you earlier. So this pool of low-lying
CD4 cells I guess, infected CD4 cells, they avoid both detection by our immune
systems, so we can’t pick them out and sort of deal with them, and they avoid the effects of
these antiretroviral drugs. And then at any given
time, they might sort of spontaneously activate
and start producing new HIV infectious particles. But let’s talk about the
antiretroviral medication, so there’s about six main
groups, six main types that we use to prevent
HIV from working properly, and they all kinda work in
slightly different ways, they all have their own sort of flair. So a typical treatment regimen, right, that involves taking
at least two of these, but preferably three of
these different types of medications at the same time. And you know, we don’t
just do that arbitrarily. The reason we do this is
because it’s been found that taking just one kind of
drug gives the virus the opportunity, the chance to
become resistant to that drug, and that’s obviously not very good, but it turns out that giving
a few different kinds, two or three all at once,
makes it really really tough for HIV to get
resistant to any of them. Because essentially the HIV dies before it has a chance to mutate
and become resistant. So because of this, before
you’re actually started on any of these antiretrovirals,
you’ll probably have some testing done to
see maybe which types of medications you’re already resistant to. So let’s work on our list
now, so two drugs that we can have as part of our treatment,
they start right at the very beginning here, so we’ve
got fusion inhibitors, right, and they bind to this Gp120 protein, or the Gp41 of the virus. And they prevent HIV from binding to, and entering our CD4 cells,
so they work by sticking to certain proteins that HIV
kinda needs to enter our cell. And they stop this fusion
step from happening. And we also have CCR5 antagonists, which bind to the CCR5 protein here that sits beside the CD4 protein. So remember in most
cases this CCR5 is also necessary for HIV entry. So now all of the sudden,
this HIV’s gonna have a really really hard
time entering our cells. It’s kind of like gumming up a lock on, say your car door or something like that, so you just can’t really
get the key in anymore, and you’re kinda locked out. And you know you got tons of CCR5 proteins all over your CD4 cell
and there’s obviously tons of Gp41 proteins on HIV particles, but the idea is that you take
the right dose of the drug, so that you end up with enough little bits to gum up the majority of these proteins. So let’s actually keep our
list up here up-to-date. So fusion inhibitors are a type, and CCR5 antagonists, they’re another type of antiretroviral. But you know, let’s say
some HIV does get through, does fuse, or maybe you’re
just not on one of these fusion inhibitors, where’s
the next place in this sort of pathway that we can block off HIV? Well, remember this step here
is reverse transcriptase, that enzyme, jumping onto the viral RNA once it gets into our cell,
and then it starts to make single-stranded DNA out of it, right? Well, we actually have
another two types of drugs that work at this stage,
so one is called a nucleoside reverse transcriptase
inhibitor, an NRTI. So just think about what’s
happening here, all right? So reverse transcriptase
is using viral RNA, right? This really nice cobalty-blue strand, as a template to create viral
single-stranded DNA, right? This lighter blue one. So to actually put together
this new single-stranded viral DNA, reverse
transcriptase has to kind of fish around in the area
and grab onto some of our nucleosides that are floating around. And then it attaches them
together, right, like end-to-end, to build a strand of DNA. Remember, nucleotides and nucleosides are the building blocks for our DNA. So what we’ve come up with,
right, what this NRTI does, is it’s essentially a decoy
nucleoside, so it looks just like one of our normal nucleosides. But geniously, it’s
missing a key component, which makes it impossible for
HIV’s reverse transcriptase to attach another nucleoside to its end. And if it can’t do that, then this DNA just can’t be built, right? It stops being created because it can’t be elongated anymore, right? The next piece can’t sort of
be tagged on, attached on. So those are NRTIs, but
you know another way this reverse transcriptase step can
be interfered with, is just by gumming up the reverse
transcriptase enzyme itself. You know, think about how
Spiderman catches Doc Ock or the Hobgoblin, he kind of gums
them up with his web blaster. And you know it’s a similar
thing that goes on here, obviously, unfortunately minus Spiderman. So these drugs that gum up
reverse transcriptase are called non-nucleoside reverse
transcriptase inhibitors, NNRTIs. Because they do inhibit
reverse transcriptase, just not by anything
to do with nucleosides. They actually work on the enzyme itself. But let’s say that HIV mutates, again, as it often does, and then these drugs
just don’t work anymore. What’s the next sort of step? What’s the next stage we
can interfere with it at? Well remember here right,
this viral integrase enzyme, it kinda grabs a hold of
this double-stranded viral DNA here, and then it tries
to bring it into the nucleus to integrate it into our DNA. Well, we have integrase
inhibitors that stop this little viral enzyme here from
doing what it wants to do, so our drug essentially
grabs onto the integrase, and just hangs on really really tight, so then integrase can’t bring any viral DNA into our nucleus, right? Which means ultimately it doesn’t end up integrating the viral DNA into our DNA. And you know this step
is really really good, this is an extra-important step here, because it’s been shown
that viral DNA integrating into our DNA is a major
major trigger for our cell to undergo apoptosis, or self-destruction. So you know, just as a general
rule, the less viral DNA that actually does this integration step, the fewer CD4 cells that we end up losing. So now let’s add that to our
list, integrase inhibitors. Now let’s say you’re not
taking an integrase inhibitor? What’s the next and sort of
last step we’ll talk about where you can interfere with HIV? Well, remember that after integration, our RNA polymerase is
gonna come along, right? And it’s gonna transcribe
this bit of DNA here, including the viral DNA, unfortunately, and turn it into viral RNA and viral MRNA. And then this MRNA is gonna
sort of hop into a ribosome, and get translated into
a viral polyprotein. And that’ll get cleaved
up by viral protease, so that a really infectious working viral particle gets produced, right? Well, not if we can help it,
so our last drug that we’ll talk about is called a protease inhibitor. And you know there’s actually
a few different kinds of these too, but the one
I’ll mention actually binds to the active site, the
site that does all the work on this protease enzyme here,
the sort of Pacman mouth part. And again, it sort of gums it
up, it stops it from working so it can’t then go on to cleave up to this viral polyprotein. So that’s good, that’s
great, now this little baby virion here won’t go on to get
mature, or become infectious. So you can see that by
using some of these drugs, in combination, we can
really really minimize how much HIV can replicate
within our bodies, right? Because we can stop it from
getting into our CD4 cells which it kinda needs to replicate. And as you saw, we can stop it at a few other places as well. So ultimately, you just end up with a way lower viral load in your bloodstream.

69 thoughts on “Treating HIV: Antiretroviral drugs | Infectious diseases | NCLEX-RN | Khan Academy

  1. Very nice video, the only miss conception in the video is the amount of Gp120/41 trimer on the virus surface. Is been shown that compared to other viruses HIV has a very low amount of envelope proteins, around 15-20 per virus. This fact really makes hard to antibodies to recognize the virus and trigger immune response. More info here

  2. I love Khan Academy (all the way from South Africa)
    #thanks to the Health and Medicine content specialists at Khan Academy.

  3. You mentioned that 1-3 anti-retroviral drugs should be used to prevent developing resistance, can you use all types of drugs available to further minimise resistance developing?

  4. hiv is nothing but a scam a multibilion scam just like cancer don't let these scientists.and doctors fool y'all HIV was created was created in a laboratory for population control. Search Dr Sebi he's the real deal.

  5. Can I ask you a question maybe you wont know? Here in Britain and Europe we have free National Health Systems, where HIV homosexual get drugs to prevent it becoming AIDS, thus draining our economy tremendously, and the NHS is in crisis. But in the USA you have no NHS, so…… as HIV drugs are so expensive, how do the huge number of homosexual men infected with HIV pay for the drugs? Any idea?

  6. Zero respect for these losers they want to cover everything and sorry but you can't Khan academy, teaching math and medicine, you are joke

  7. Good of pharmacology and what it wants people to know. None of these videos show the immune system and its contribution. It is as though natural killer cell isn't there, macrophages, (phagocytes) B cell. Lol we are not Fools at all. Those are artificial target points so is their chemical structure. Nature did not introduce those target points. When the virus escapes the antibodies and phagocytes it must now become a CD8 territory. The virus must be left alone to enter the cell as in a boosted immune system therapy then when the cell is infected it will cut off the virus particle display it on its outer body so CD8 can kill it. Not to be pursued in buts and pieces of its life cycle. We need to boost the immune system so we also increase antibodies and phagocytes so we may prevent the virus from entering the cell.

    But those that escape the antibodies we will boost, they should be left to enter the cell not caught at fusion, reverse transcript, integrase or budding. Why haven't the pharmaceutical also inhibited the CXCR4? It is also a binding site.

    If pomegranate juice can inhibit both sites (CCR5 and CXCR4) , why did they not copy chemical structure as they do with many other drugs? Lol eih God how has this possibly happened? Idolization and an illusion that Ph.D is wisdom and power. The target points are corrupt so is their chemical structure. One can never get off ARV it is a chase going nowhere. Factories need to be shut down. ARV does not come close to a cure. Cures are being looked for through the lens of ARV that if possibly something can be done whilst ARV suppresses viral loads. This approach is unproductive.

  8. Recently I read that it is possible to catch HIV from a healthy person. And, they say, there are several ways.
    The first is when a person has already contracted, but the body has not yet realized that the viruses are sitting in it. And even tests show that a person is healthy – HIV is negative.
    The second way is through blood transfusion. Blood is frozen for six months, type during this time you can accurately find out if the donor is infected or not – and HIV, it turns out, can wake up even after a year (some hundredths of a percent, of course).
    Still, they say, there is a third option …

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  10. Lord when you walked this earth , you healed the sick, gave blind sight, raised the dead. You are the same, then,yesterday, today and forever. Please lord do good to your people who are suffering from this disease, especially the ones I know. Amen.

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  15. Technically we do have the cure. Why can all this drugs be combined into a virus or capsomere What is called and inject the body with that as a vaccine.

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  25. This is one of the best videos ive come across showing how HIV invades and takes over a cell but also the different medications and how each one works! Excellent stuff! One question though…. once a CD4 cell is infected does it forever remain infected or does the HIV inside the cell die after a period? Also i've heard that HIV floating around your blood only lives around 36 hours.. is that also true?

  26. This is great! I watched most of the videos about HIV and you explained it brilliantly!
    Thank you so much and I am really glad I descovered this!!!!!!

  27. Im in nursing school and this is not NCLEX level. We don't study any specific proteins, that is MCAT level. Why can't someone do an NCLEX level HIV video?

  28. Brilliant presentation. I can't think of more logical and simplified way to explain the drugs used in HIV.

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