- What is HIV/AIDS?
- What is HIV and AIDS?
- Transmission of HIV
- How HIV infects us: Mucous membranes, dendritic cells, and lymph nodes
- How HIV infects us: CD4 (T-helper) lymphocyte infection
- How HIV kills so many CD4 T cells
- Diagnosing HIV - Concepts and tests
- Treating HIV: Antiretroviral drugs
- HAART treatment for HIV - Who, what, why, when, and how
- Defining AIDS and AIDS defining illnesses
- Immune reconstitution inflammatory syndrome (IRIS) in AIDS
- Preventing an HIV infection
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- At1:02you say the cell doesn't necessarily have to start 'cranking out viral RNA' because it wants to 'lay low' and avoid the immune system. Does that mean that the HIV might wait until the immune system's busy fighting off a cold or flu or something before it decides to make its move with all that viral RNA?(4 votes)
- HIV has a reproductive phase called "window period" which mean after the virus enter the cell its do nothing to the cell. So the cell doesn't "feel" any damaged. But when the viral RNA activated to reproduction of the virus, the cell is damaged, and bam!, detected by Immune System. The windows period time is vary from weeks to month. Hope this help :)(3 votes)
- Why can't Equine Infectious Anemia can't be treated by anti-retroviral drus? EIA is also lentivirus, similar to hiv - long incubation period but diesease is really bad. Excuse me my grammar...(1 vote)
- 1. Unlike HIV, EIA is transmitted by mosquito, so other horses are at risk for a disease that causes abortion and permanent infection. Therefore euthanasia or quarantine is required. Quarantine is expensive. 2. The expense of research and of the medication would likely be quite high. It should also be pointed out this disease affects other horse owners, and the incidence is low, the USDA manages this problem and has no approved treatment available in the USA. 3. The expense of HIV treatment for an adult human is quite high, would it be 10 X more for a horse? In addition to daily pills, blood tests are required as they can potentially harm the patients liver. The real answer is that I am sorry if you have had to deal with this disease and make a very difficult decision. I am sorry. https://www.merckvetmanual.com/generalized-conditions/equine-infectious-anemia/overview-of-equine-infectious-anemia
- What happens if you catch HIV really early, before it has much of a chance to infect CD4 cells, and take ALL the medications at once? Would you be able to prevent ever getting a serious HIV infection?(3 votes)
- well, it would be hard to detect HIV before it infects most of your CD4 cells since it can take weeks or months before HIV is detectable and you start showing symptoms, and the willingness or ability of any given person to be tested is also a reason treatment can delay treatment. but if you did detect it soon enough, it is possible to suppress HIV to an "undetectable" level, but it is impossible to know for sure whether or not HIV will become resistant or if the medication is not particularly effective, etc. also, factors like age, adherence to medication, severity of the initial infection, and the type/brand of medications, random mutation, preexisting conditions, etc. can also affect any possible future infections. it is possible to avoid a serious HIV infection, but you can't ever know for sure. also, taking ALL medications at once would have very adverse side effects and quality of life would be terrible for the infected person.(1 vote)
- When will there be a cure for HIV? What will it be like?(1 vote)
- It's impossible to predict when a cure will be developed. HIV integrates itself into our own DNA and so it becomes part of the human genome. Therefore, to cure an infected person we would have to find a way of editing human genes in a living person or identifying and killing the latent cells.
My guess is that we would need some sort of genetic therapy that can recognise the viral sequence and either cut it out of the genome or tag the cell for destruction by the immune system. In combination with ARVs outlined in this video, that would potentially be a cure. In recent years technology such as CRISPR/Cas9 has opened up possibilities for gene editing that we hadn't imagined before, but it will be decades before we are using this sort of thing in our day to day lives.
A more effective approach is to focus on prevention of HIV transmission and the development of vaccines against HIV. If nobody catches the virus, it will eventually die out by itself without the need for a cure. This is also a huge challenge but is a more likely outcome than a complete cure. Sorry I can't give a better answer!(3 votes)
- At8:04, Integrase inhibitors block the Integrase enzyme from entering the cell nucleus, but what about Integrase strand transfer inhibitors? They stop the viral DNA strands from attaching themselves to the host cell chromosomal DNA, but whilst doing that don't they penetrate anyways into the cell nucleus?(1 vote)
- What does the GP in GP120 and GP41 stand for? What about the CD in CD4?(1 vote)
GP is for glycoprotein. 120 is for the molecular weight.
CD is for cluster differentiation, a naming protocol for surface antigens on white blood cells.
“The T-helper cell was originally known as leu-3 and T4 (after the OKT4monoclonal antibody that reacted with it) before being named CD4 in 1984.[1”
- How long do the CD4 T cells live for? Could the virus particles be killed off until the CD4 T cells have 'died'? Could the HIV infected CD4 T cells be destroyed in the body at the same time as the viral load is depleted? When the immune system is really low, could bone marrow be donated from a person with CCR5 Delta32 mutation so that the new CD4 T cells are immune to infection by the HIV virus?(1 vote)
- [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.