Today is Monday, October 21st. This is Lecture 15, Part 1 on Viruses. For your attendance, access code is 414. Word of the day is phage. Make sure you do this quickly.
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I'll give you a couple more minutes because we did start late because of the latecomers. But hopefully most people had a chance to submit it. There's a couple people on the chat. Just hold on for a sec, please.
Okay, so if you were not able to do your attendance, I gave you a couple more minutes to do it, but I am going to shut it off in a couple minutes so that we can finish. All right, please write it down if you haven't already. Okay, let's move on. So for your homework, remember assignment seven was due last Friday. I'm going to update Canvas this week.
So if you have not submitted that, or if you submitted it late, you know, please let me know, but we're going to update Canvas this week. Then there's really only two assignments for unit three. We have one homework assignment on chapter 13, which is viruses.
That's what we're covering this week. And then a couple weeks later, we have assignment nine on chapter 15, which is microbial pathogenesis. These next chapters of, you know, unit three and unit four are quite dense.
You know, I'll say each of these chapters could easily be a class taught throughout an entire semester. So really try to hone in, you know, on the information that we discussed during class and on the PowerPoint. I will make the study guide available to you.
Try not to get lost, you know, on the internet looking at a bunch of different resources and videos because, again, this subject matter is very complex and I want you to just focus on what you need to know for this class so you can do well. All right, and then here's our Unit 3 schedule. Here we are on the top for viruses.
We'll do viruses again on Wednesday. Then the following week we have the human microbiome, disease and epidemiology. and then mechanisms of pathogenicity after that. And then you'll notice we have two review sessions on the following week.
Again, that's because there's a lot of information for these chapters, so I want to make sure you have plenty of time to practice and study so you can do well on Unit 3. There have not been that many people that have taken Exam 2. I know it's a busy time of the semester, but please don't wait until the last minute. Again, it is a little bit harder than our first exam, so give yourself enough time to study and take that without feeling pressured. All right, so for our learning objectives, we're going to talk about virology. So there's many different types of viruses. There's bacteriophages, which is a prokaryotic virus.
There's animal viruses. There are envelope versus non-envelope viruses. When we talk about bacteriophages, there's two different cycles. And then importantly, when you are multiplying or replicating, you know, our viral DNA, it can be, you know, enveloped or non-enveloped, positive or single-stranded. It can be made of DNA or RNA.
We're going to talk about that. So this is quite complex, 13-10. And just make sure that you are studying by and by because it's too much to kind of cram at the end before the exam.
All right, so remember with the stars, it doesn't mean that if it's not starred, it's not on the exam, but the stars do mean that it's a critical piece of information that you'll probably be studied, questioned on, and you just need to make sure to study that slide specifically. So again, viruses. What is a virus? There's a lot of debate about whether viruses are alive or not.
Depending on your source, when you look online, you'll see different perspectives. but they are obligatory intracellular parasites, which means that a virus must have another host in order to replicate. Oh, I'm looking at the chat.
Someone said we don't have class on November 11th because it's a holiday. I will double check that. If it's a university holiday, then you're correct. We won't have class. We'll just make up that day, but I'll get back to you on that.
Okay, so then again, our viruses, they can contain either DNA or RNA. When we were talking about biology thus far, and we're talking about genetic information, we were mostly talking about, you know, DNA being what the genome is made of. But our viruses can be made of DNA or RNA.
Viruses do not have ribosomes. So that means they do not have any ATP generating mechanism. Again, this is why they must infect another host cell in order to replicate. All viruses have a protein coat. And then some RNA viruses can contain a small number of enzymes within a capsid.
Okay, but not all of them. So the vital pieces of information that every virus has, they have either DNA or RNA, and they have a protein coat. Again, no ribosomes, no ATP generating mechanism. That's why they have to infect another host cell in order to replicate itself. Okay.
Some viruses could be enclosed by an envelope. Not all of them, but some can be. There's some viruses that have spikes, which are glycoproteins. We all live through the pandemic, so we know what spiked viruses are. Coronavirus was an example of that.
And then most viruses infect only specific types of cells in one host. So example, again, using COVID, they specifically infected a particular type of lung cell with the ACE2 receptor. And most viruses, they infect a particular cell type or tissue type.
The host range is determined by specific host attachment sites and cellular factors. Again, my example of COVID, it was the ACE2 receptor in the lungs. that the spike protein attached to in order to infect those cells. Later on in part two, I believe we do have a little bit of information about COVID, just so you can understand kind of the pandemic that we went through from a biologist perspective.
Okay, when it comes to virus sizes, they are diverse in size, but they're very, very small. So they're in the nanometer type size. And to put it into perspective, this big rod at the bottom, this is an E. coli bacterium as compared to poliovirus. Look how small this is as compared to the bacterium.
And then that's very, very small as compared to a human red blood cell right here on the right. So we're dealing with viruses very, very, very small. That's why it was kind of ironic during the pandemic.
You really needed those. you know, specific type of viral protector mask in order to prevent you from getting COVID from transmission, you know, from breathing on someone. But any type of mask is better than no mask.
All right, the virion structure. So the virion structure is the actual like virus itself and how it's made and put together. So again, it will have some form of nucleic acid.
It can be DNA or RNA, and it can be single-stranded or double-stranded. Again, this is different from humans because we have double-stranded DNA. Some viruses, for example, could be RNA, or they could be single-stranded, they could be double-stranded. Because a virus could be, you know, DNA or RNA, Specifically with RNA, you have to consider whether it's the positive strand or the negative strand.
And we'll talk about that and give you more clarification when we talk about replication. Then there's the capsid, which is the protein. It's kind of like the protein coat that covers the virus. And it's made of capsomeres. Some viruses could have an envelope, which would be made of lipids.
And then some viruses can also have spikes, which are made of glycoproteins. But again, the basic structure, all viruses have some type of nucleic acid and a capsid to protect the virus. All right, just looking at the morphology, just showing the different shapes. So here's an example of, you know, a polyhedral virus.
This is mastodonovirus right here. So it's an icosahedral shape. It means it has 20 sides.
And so the nucleic acid is, you know, on the inside, and then the capsid is the protein coat to cover it. You have to have some type of protection over the nucleic acid so that you don't have degradation. All right, a different example right here, this is influenza.
And so here on the inside, we have the nucleic acid, and then it's covered by the capsomere. And then this particular virus has both an envelope and spikes. So the yellow is showing us the envelope that's made up of lipids. And then the spikes are the green made of glycoproteins.
All right. And then here we have, again, this is a helical virus, Ebola as an example. They can be of many different diverse shapes. So the nucleic acid. right here is in the middle and then we have the protein cover the capsid made up these capsomers nice just showing you diversity all right and then some complex viruses right here so this is a bacteriophage a bacteriophage is a prokaryotic virus which would mean a virus that invades or infects prokaryotic cells As opposed to animal viruses, that's what we're used to.
Like, for example, coronavirus would be an animal virus. Ebola would be an animal virus. Animal viruses are viruses that infect different types of animals or eukaryotic cells. All right.
So here we are right here on part A. This is a diagram and a micrograph of a T-even bacteriophage. It's just how we can categorize and label different bacteriophages. Again, they're made of DNA. You have the capsid head right here.
You have the sheath. There's the pen and then the tail fibers. So what happens, it kind of looks like a spaceship.
So it'll kind of land on a particular host cell. And then it uses the pen to inject the DNA into, or the nucleic acid into the particular host cell. All right. And then here's a different example of an orthopox virus right here.
It's, you know, variola. It's a member of the pox, you know, viral family, just to show you the different complexities. All right. So this was part of your learning objectives.
And you do have a question on how you can culture different viruses. All right. So viruses, again, they must be grown in living cells.
Remember that. We have to have a living cell in order to grow virus because viruses do not have their own ATP generating machinery. So they have to hijack that of the host that they've infected.
All right. So this is kind of different than what we're used to seeing if we're trying to grow up a bacteria, for example. So our bacteriophages, they form plaques on a lot of bacteria.
So what happens is we have a different agriplate of bacterium of whatever species, and then we can put the bacteriophage on the particular culture. And the area where we see where it's clear, those are called plaques. And within those plaques, that's the area in which we were able to grow our particular bacteriophage because the virus actually killed those host cells. So that's why it appears clear right here because those cells are dead, but they have the viral genome within it that we can collect to study. All right.
Then animal viruses, they may be grown in living cells or in embryonated eggs or in cell cultures. Think about like a continuous cell line when it comes to animal viruses. All right.
So make sure. that you're able to remember this because you do have a question on how to culture bacteriophages or animal viruses. Either way, viruses have to be grown in living cells. And then the cells that they infect, it depends on the virus, you know, because oftentimes it's specific.
A virus will infect specific cell types. All right, so how do we identify our viruses? There's three different kind of ways of analysis.
We have cytopathic effects. That's the structural changes in host cells that are caused by viral invasion. So example right here, if we're looking at part A, which this is mouse titu culture cells.
So part A would be an unaffected, you know, healthy cells. And then B would be infected with VSV virus. So we can see there's a completely different form an appearance of the tissue when it's been affected by the virus.
Then there's also serological tests. So we can detect antibodies against a virus in a patient. So for example, you know, talking about the pandemic COVID, you know, one of the ways in which you can assess if you have that particular virus is by testing your body for antibodies against the virus. And You can see if you have a certain number of antibodies against the virus, then you know your body is fighting an active infection. You can also use antibodies to identify viruses and neutralization tests, such as viral hemagglutination and the Western block.
So again, it's just testing the different antibodies to see what particular virus is there. So you would use the antibodies right here in this particular test to see if it binds with... any of the viruses that you are trying to detect and then you could identify the virus that way. Then there's also nucleic acids in which you can sequence the nucleic acid through PCR and you can determine the genome and by the genome you can determine the viral type.
I have something in the chat. Okay. All right, and so this is important.
You do have a question on this, and then there's a couple diagrams coming up a little bit on the next slides. So bacteriophages, they can exist, you know, in two types. So you can have two types of phage, either a virulent phage or a temperate phage.
There's two possible types of cycles that exist for bacteriophage, the lytic cycle and the lysogenic cycle. All right, so for the lytic cycle, The phage causes lysis and death of the host cell, and it's the only cycle in a virulent phage. The lysogenic cycle, that's when the prophage DNA is incorporated into the host DNA, and the temperate phage, it can do both cycles.
Again, so the virulent phage, the lytic cycle is the only cycle for a virulent phage. A temperate phage can either undergo the lytic cycle or the lysogenic cycle. And how does the temperate phage do that?
By inserting this prophage DNA into the host DNA. It's kind of a way of the virus hiding, you know, within the genome of the host. All right. So let's take a look at this. So this is the lytic cycle of a T-even bacteriophage.
T-even, we're talking about the numbers T2, T4. They're just categories of our bacteriophage. And again, our lytic cycle is a virulent phage. Virulent meaning it's always going to cause some type of damage or pathology in the host because it's going to cause the host cell to lyse or rupture and die, right?
So what ends up happening, part one, we have attachment where the phage is going to attach to the host cell. And as you can see above right here, that's kind of where the spaceship kind of lands. We have part two, which is penetration. So the phage penetrates the host cell and it injects its DNA.
That's what kind of the purple being inserted is. That's the DNA. Part three would be the biosynthesis.
That's when the phage DNA, it directs synthesis of the viral components by the host cell. So again, right here, the phage DNA, it's going to... then cause more replication of that particular fade so that it can multiply itself.
That's kind of the purpose of why viruses will infect host cells so they can replicate as well. All right, then maturation. The viral components, they're assembled into virions. Again, a virion is the completed structure.
And then release is when the host cell lysis and the new virions are released and they can go on to infect other cells. All right, so make sure you remember the steps, kind of the order. When it comes to viral replication, it's pretty much, I'll say for a lot of different viruses, it's similar, you know, and just slight different changes.
that differentiate them? Let's look at the chat. Good question. So let me go back one slide.
So the question that I received in the chat is, is there a type of phage that can only exist in a lysogenic cycle? The answer to that is no, because we have two different types of phages. We have the virulent phage, which only has the lytic.
And then the temperate phage can do both of these cycles. In the next coming slides, I think it's the slide right after this, we're going to go over a temperate phage and their cycles, and it might make a little bit more sense. So I'm going to use this.
Yeah, here's our life cycle. So I'll explain that question while I'm going over this. So again, there's two types of phages. The first slide we went over, this is a virulent phage, and it's always going to lyse the host cell. That's why it's a virulent phage.
It will always cause damage and pathology. A temperate phage, though, can exist two different ways. So a temperate phage will start at the top. So the phage will attach to the host cell and injects its DNA. This purple is the bacterial chromosome.
And then for number two, the phage DNA, it circularizes and it enters either the lytic cycle or the lysogenic cycle. So just to recap, with the lytic cycle, the new phage DNA and proteins, they're synthesized into virions. Then the cell lyses releasing those phage virions and it can infect another host cell.
But what happens if we enter the lysogenic cycle? And some students ask, you know, what causes it? There's many different things that can cause it. It could just be from, you know, the regular replication of the cells. It could be environmental, but you can just kind of think of it as chance for right now as to how it enters either cycle.
Okay. So in the lysogenic cycle, what happens is the prophage kind of hides within the host DNA. So make sure you highlight prophage right here in your notes so that you remember what that is.
So the phage bacterium DNA will hide within the bacterium DNA. Right here, the phage DNA, it integrates within the bacterial chromosome by recombination, becoming a prophage. Then the lysogenic bacterium, it reproduces normally.
So you can see with the replication, it's also replicating the phage DNA. Then after many different cell divisions, what happens is the prophage can end up exiting the chromosome, and then it has the potential to enter the lytic cycle. So depending on the type of virus that we're looking at, some enter the lysogenic cycle, you know, more often than others. And some, you know, there's different pros and cons, you know, for why a phage would be lytic or lysogenic or excuse me, temperate.
But you can think of just the differences as far as being able to, you know, infect the host overall. you have more, you know, divisions, more copy of the actual DNA that could potentially be released when you do, when you have a temperate phage. Just think about all of the different prophage that could exist in all of the different bacterium.
And then if they switch to lytic at the same time, you'd have a whole bunch of virions being released simultaneously. All right. So just remember the steps, you know, in the different cycles. Now we're going to talk about animal viruses. So animal viruses, again, this is what we're more familiar with.
And they infect animal cells or eukaryotic cells. So make sure you remember, it says multiplication. It's, you know, the same thing as replication in many different ways.
We say multiplication because it has to multiply within a host cell. You know, remember, it's going to hijack the machinery of the host cell in order to replicate. So our steps, it's similar to prophage.
So our bacteriophage, so we have attachment. That's when the virus attaches to the cell membrane. Penetration, either by endocytosis or fusion.
We're going to talk about the difference between the two. Endocytosis or fusion has to do with whether it has an envelope or not. Uncoating by the viral or the host enzymes. Again, you have to uncoat, take off that protein coat to see the nucleic acid. Biosynthesis would be the production of the nucleic acid and the proteins.
And then maturation would be the nucleic acid and the capsid proteins that assemble. And then they would be released either by budding or rupture. And again, this depends on whether it's enveloped or non-enveloped.
If it's an envelope virus, it's going to release by budding because it's going to take some of the cell membrane from the host cell with it in order to be the envelope of the new virus. If the virus does not have an envelope, then the cell membrane is going to rupture so that the completed virions could be released without. the envelope protein the envelope coating i mean because it's made of lipids all right so here's a difference right here so we're looking at the entry of viruses into host cells right here so this would be the virus then you have the attachment spikes and then what happens is the plasma membrane of the host cell right here when the virus enters it's going to kind of enter through and take some of that plasma membrane with it.
All right. So here's an example of like at the bottom of the herpes virion by fusion, similar concept. All right. So let's make sure.
Does that make sense? So one of them has an envelope. One of them does not.
All right, and then here's a different kind of cartoon version of showing you in a different way. So this is the budding of an envelope virus. So we have the viral capsid, the host cell plasma membrane, and then the viral proteins.
Again, they're within the host cell because the virus has taken over the host to produce, you know, its nucleic acid and its proteins versus that of the actual host itself. Then when we need an envelope, the virus it's going to release by budding. So it's going to push some of that plasma membrane out with it to become the envelope.
All right, and here's a different example just showing us with a TEM microscope. So this is showing us the lentivirus and how it releases by budding. It literally takes some of that plasma membrane with it. Okay, and then how do we replicate a DNA-containing animal virus?
All right, so again, this is just the cartoon version. It's very similar to the first slide that we talked about with the steps. So right here, this is just an example of a Pepova virus.
It's a typical DNA-containing virus that attacks animal cells. All right, so step one is attachment. That's when the virion attaches to the host cell. Step two is entry and encoding. meaning the virion, it enters the cell and its DNA is uncoded.
And we can see the viral DNA and then the capsid proteins again from the virus. Number three, a portion of the viral DNA, it's transcribed producing mRNA that encodes for early viral proteins. So again, what happens now, the nucleic acid, the viral DNA, it's taken over the host.
And from that, viral DNA, it's able to make our mRNA from the virus so that from that mRNA, we can translate that into our early viral proteins. Then step four, we have biosynthesis. That's when the viral DNA is replicated and then some of the viral proteins are made. Step five is late translation.
So that's when the capsid proteins are synthesized. So again, we're just making everything for the virus right here. Then number six is maturation.
That's when the virions mature. And then number seven is the release. That's when the virions become released.
All right, so make sure you remember the steps. I have something in the chat. So someone asked, is budding the same thing as budding from our last unit?
And I believe you're talking about budding from the yeast as far as how it replicates. So it's a similar concept, but this is kind of a different form of budding from the sense that it's going to take, the virus will take some of the cellular membrane with it. So that that cellular membrane can become the envelope of the virus. So budding only exists for envelope viruses. Hopefully that's clear.
All right. So the central dogma, remember, normally DNA gets transcribed into RNA, which gets translated into proteins. The issue, if we have RNA viruses, it contradicts the central dogma of how we replicate and how things are made.
Okay. So this is a very... important figure. I'm going to spend some time on this. You have a couple questions on this, and this can be difficult for some students to understand.
The way to study this, take a look at the different colors right here. So what's in red would be if you have a negative-stranded, you know, RNA-based virus. What would be in blue is if you have, actually, sorry.
This is the positive sense at the top. Yeah, I said that wrong. The red is if you have a positive single-stranded RNA, so meaning that the sense strand right here is the genome.
What's in blue, part B, would be a negative single-stranded RNA. That's the antisense strand. And then what's in yellow right here, part C, is if you have double-stranded RNA, meaning that the genome is both the positive and the negative strand of RNA.
All right, so everything is the same as far as replication is concerned from what we've already discussed. But when we get to part three and four, that's when things are different of how these viruses go about it. All right, to make sure that you understand the terminology, again, the positive or the sent strand, it has the same sequence as mRNA, which is being transcribed using the negative strand as a template. All right, so just reminding us right here, if this were to be DNA, so the sense strand is what is 5'to 3', the antisense or the template strand is 3'to 5', that's backwards. All right, so when you are transcribing your mRNA, remember that the sense strand, it has the same sequence as the mRNA, and the antisense strand is used as a template to make the mRNA.
When we're looking at how to read this chart, this is our key kind of at the bottom left. So what's in dark green or teal, depending on your colors on your computer, that's the viral genome, meaning the genome of that particular virus. So again, when we're talking about RNA-based viruses, they can be positive-stranded or negative-stranded if they're single-stranded, and they can be double-stranded. All right, to take our key a bit further.
The light green is the positive or the sense strand of the viral genome. And then what's in kind of an outlined green is the negative or anti-sense strand of the viral genome. All right, so let's go through this.
Part A, if we're looking at a positive single-stranded RNA viral genome, an example of that is the picornaviridae. All right, so what ends up happening right here, the negative strand transcribed from the positive strand viral genome. So immediately after we have the insertion or the penetration of the viral genome, then the negative strand becomes transcribed from the viral genome. Then from that negative strand, which again is the template, then our mRNA is transcribed from the negative strand. From that mRNA, we can then translate our proteins right here.
And then we would have more of the positive strand, you know, that would then go on, you know, to be matured together. And then you would have the complete virion formed and then the release. So what we're going over right here, it's only the differences.
After we get to how the virus is replicated, how the proteins are made, everything else becomes the same as far as the steps. We have the maturation and the release. Part B, what happens if we have a negative single-stranded RNA genome?
The rhabdoviridae is an example of that. So what happens is the positive strand, the mRNA, must first be transcribed from the negative viral genome before the proteins can be synthesized. So that's the first part as far as Part B. Again, if it's negative-stranded, Then the first step is then to transcribe the positive stranded mRNA.
before you can make the proteins. You also have additional negative strands that can be transcribed from the mRNA. Why?
Because the original genome of the virus is negative stranded and if we're trying to replicate the virus we're going to need more of those negative strands. All right so then we have from the positive you know mRNA that we made then we can translate our capsid proteins The negative strands are incorporated into the capsid. Then you have the maturation of the virion and then the release.
So notice right here, there is kind of less of a step for part A right here, because again, the viral genome, it's going to be the same as like the mRNA. So we're able to kind of do things a lot quicker. with part A if the genome is a positive, you know, sense RNA strand.
All right. And then for part C right here, suppose we have a double-stranded RNA virus. So that means the genome is both the positive strand and the negative strand.
All right. So what happens is the, it's kind of a combination of part A and B. So the mRNA, it's produced inside the capsid. and then it's released into the cytoplasm of the host.
So then the RNA polymerase, it initiates production of the negative strands. Then the mRNA and the negative strands, they form the new double-stranded RNA that gets incorporated as the new viral genome. And then again, the capsoproteins and the RNA-dependent RNA polymerase are used to make these proteins.
All right, so when we're talking about DNA replication, we had DNA polymerase. Here specifically, we're talking about RNA polymerase. All right, so hopefully this makes sense. We're going to go over this again many different times. This is just the first time going over it.
I know it can be quite overwhelming, but again, we'll have many opportunities to review this. All right, so here's just another way of taking a look at things to hopefully make it easier to grasp. So we're talking about the positive-stranded RNA viruses right now.
Again, when it's positive single-stranded RNA, the genome itself can serve as mRNA, meaning that we can start making proteins immediately. So let's go at the top. If you're interested in reading about this, which you don't have to, but there is the link to the actual paper at the top left.
So part one, you have the ribosome assembly and the translation of some or all the viral proteins from the genomic RNA. Key among this is the RNA-dependent RNA polymerase. That's what this stands for. So what happens is the RNA-dependent RNA polymerase is what will then help to translate and make those proteins.
Okay, then the RNA, dependent RNA polymerase, it synthesizes a copy of the genome right here. And then make sure that was clear. Again, this little hamburger type shape at part one, this is the ribosome.
Here's your key at the bottom. Just make sure you can understand the different figures. All right, because I saw a question in the chat.
So I'm going to repeat myself just to make sure that's clear. So remember that when you're dealing with positive single-stranded RNA viruses, the genome can serve as the mRNA. All right, so immediately we can start translating our proteins. So again, this is the ribosome assembly.
These are ribosomes right here. And we can translate our viral proteins. So that's what's happening immediately from the genome. Then afterwards, the RNA-dependent RNA polymerase.
It's going to synthesize a complementary copy of the genome. Complementary be kind of like the opposite copy. So because this is positive stranded, we're going to make the negative stranded RNA.
Why do we do that? Because we want to be able to use that as a template to make more of our positive stranded RNA as the genome. And then part four is when our viral mRNAs, they become translated. And then the viral genome is packaged.
So again, here's the translation of our viral proteins. And then you would have the, you know, maturation, the packaging, and the release. Something in the chat.
Someone said the audio cut out, but I think I'm still here. That may have been just an individual thing, but you can always go back and look at the recording. All right.
And then what happens when we have the negative stranded? RNA. Some people call this ambisense. For this class, we're just going to say negative single-stranded RNA right here. So again, make sure you understand the key.
So step one is the viral ribonucleotide protein right here. It consists of the genomic RNA, which is in green, and then the associated viral proteins right here in purple and blue. And then RNA-dependent RNA polymerase, it's a component of the viral ribonuclear protein particles. So then what happens as early after infection, the viral mRNAs in red, they're synthesized. Again, from this negative-stranded genome, we can make many different mRNAs from it, which would be the positive strand or the opposite.
Then those viral mRNAs, they're translated, meaning we make the proteins for the virus. Then the concentration of the viral proteins, it increases, leading to a switch from transcription, which would be mRNA synthesis, to our genome replication. All right, it's basically after we've made enough proteins, then we're going to switch to make more of the genome replication. Because this is negative stranded, again, we want to make sure that we are creating more negative stranded RNAs, which is going to be the genome that will mature and be packaged together to make the complete virion and then released. All right, so these last three slides, they've been kind of saying the same thing in a different way.
Don't get overwhelmed. Just some people learn differently than others, different styles. So you can pick the style that's best for you as far as learning. But remember that this particular figure, I want you to focus on this because this is what your questions will kind of be based on. And it's a good summary versus these two papers.
You know, it's more so as far as explanation of the different genomes and to give you a different, more focused way of looking at that figure. All right. And then the multiplication and inheritance of retroviridae. I think is that our last? Yeah, so this is our last slide for today.
And so this is important. Make sure you listen up so we can finish up quickly. All right, so retroviridae.
These are important because they have reverse transcriptase right here. So right here, the retrovirus right here, it enters by fusion between attachment spikes and the host cell receptors. Then you have the encoding.
which releases two viral RNA genomes and the viral enzymes reverse transcriptase, integrase, and protease. What's special about retroviridae is the viral genome can be inserted into the host genome. And so again, these are RNA-based viruses, so they're able to break the central dogma to make DNA from reverse transcriptase that can be integrated into the host chromosome.
That's what happens in part three. So here's our viral DNA right here. The reverse transcriptase, it copies the viral RNA to produce double-stranded DNA. Again, reverse transcriptase is what does that. When that DNA is integrated into the host chromosome, it's called a provirus.
This is similar to the prophage that was inserted into the bacterias plasmid. The provirus is inserted into... the host's DNA, the host chromosome. So part four, the new viral DNA, it's transported into the host cell's nucleus where it's integrated into a host cell chromosome as a provirus by the viral integrase.
The provirus may be replicated when the host cell replicates. So again, this is a way in which the virus is able to kind of hide within the host chromosome. The advantage to this for the virus is it's a way of hiding specifically from the immune system of the host so that it can't be killed and destroyed before it replicates and builds itself up. Then part five, we have transcription of the provirus.
It may also recur, producing RNA for new retrovirus genomes, and RNA that encodes the retrovirus capsid, enzymes, and envelope proteins. All right, so again, because it's integrated into the host chromosome, it can produce viral RNA, which then will produce viral proteins in identical strands of RNA right here. Then we have the viral proteins. They're processed by the viral protease.
And then some of the viral proteins are moved to the host plasma membrane. The mature retrovirus, it leaves the host cell, acquiring an envelope and attachment spikes as it buds. Again, that's because of the viral proteins that were put into the cell membrane so that when it leaves through budding, those proteins can become the spikes. And then that mature virus can then go on and infect other cells. So make sure you study this.
The retroviridae is who has the provirus, meaning that has the ability to break the central dogma in which the RNA can then produce double-stranded DNA by the viral enzyme reverse transcriptase. Integrase is what will allow the viral DNA to integrate into the host chromosome and it becomes a provirus at that point. Then the protease is what allows the viral proteins to be translated.
Okay, so hopefully that makes sense to you all. We're going to continue part two on Wednesday and I will stay a few minutes for office hours. Great job today.