Alright, this is the chapter 12 video. We're going to cover viruses, viroids, and prions. These are acellular infectious particles.
Many infections of humans, animals, plants, and even bacteria are caused by acellular, noncellular particles, such as viruses, viroids, and prions. Looking at the characteristics of viruses, they are much smaller than bacteria. We usually measure them in nanometers. The influenza virus might be around 150 nanometers.
There are even viruses smaller, such as rhinovirus, which is maybe 50 nanometers in diameter, where bacteria are 1 to 5 micrometers, which is about 1,000 to 5,000 nanometers. The viruses are much too small to be seen with our normal light microscopes that we use in the lab. electron microscopes would be needed to actually view them.
These acellular infectious agents have either DNA or RNA. They do not contain both. So this is actually a non-living characteristic. They have the DNA or RNA and they use that as their genetic material or genome. They cause many infections in humans, animals, and plants and even bacteria.
And they cause many of the diseases that affect humans in our industrialized world. So examples, the common cold, influenza, herpes, SARS, polio, HIV. And just a reminder, these viral infections are not treated with antibiotics.
There are antiviral medications used for certain scenarios when somebody has HIV or hepatitis, for example. Influenza, there's Tamiflu, which isn't often prescribed. because it is expensive and it doesn't usually, isn't usually needed. So looking at the size of a red blood cell compared to a bacteria, bacteria much smaller than red blood cell, and then the bacteria much larger than the viruses.
So a bacterial ribosome might be 25 nanometers, here the poliovirus is around 30 nanometers. So very, very tiny infectious agents. Some more characteristics of viruses, they don't carry out any metabolic pathway outside of a cell. So they have an extracellular state that we'll go over here in a second. But outside of the body, outside of the host, they do not metabolize or reproduce on their own.
Therefore, they do not grow or respond to the environment like other cells do. So they cannot reproduce independently. They recruit or hijack the cell's metabolic pathways in order to reproduce.
Like I said, they have an extracellular state and an intracellular state. Looking at the extracellular state of a naked virus, what they have is a protein coat or capsid which surrounds a nucleic acid. The capsid is made up of individual subunits called capsomeres.
The extracellular state of an envelope virus, they have a phospholipid envelope which surrounds the capsid. The capsid... The envelope also has protein spikes that I'll show you here in just a moment.
So the outermost layer provides protection and recognition sites for host cells. Naked viruses are more resistant to chemical disinfectants than enveloped viruses. The intracellular state, once the virus enters into the cell, the capsid is removed, and the virus exists only as the nucleic acid, the DNA or RNA.
Genome so looking at the naked virus anatomy here. We have the capsid which is protein and then the individual subunits here the little circles are capsule mirrors, which are the protein subunits and Inside of that capsid is the nucleic acid or the viral genome. So this capsid is what's going to provide the protection and recognition For host cells.
So what they do is they interact with host cell receptors In a lock and key theory, if they have the correct proteins interacting with one of your host receptors, they can enter. Envelope virus anatomy, here we have the phospholipid envelope. So this is a bilayer, phospholipid bilayer.
Protein spikes, and these spike proteins are what's going to interact with the host cell receptor in, again, that lock and key theory. So if there is a circular shaped host receptor, these can attach to that and gain entry. So this envelope surrounds the capsid, and again there's the capsomere proteins, and then there's the nucleic acid inside the capsid.
If we disrupt this outer layer, either the envelope or in the naked virus, the capsid, we interfere with the recognition and attachment. process and we can deactivate the virus. So one way we differentiate viruses is by whether or not they're naked or enveloped. Kind of like gram-positive versus gram-negative in bacteria. There is no gram-positive or gram-negative viruses.
I'm just using that as a comparison. But we can also differentiate viruses from one another based on their genetic material. So the viral genome may be DNA or RNA like I mentioned, but they never contain both. And the diversity of the genome can be either double-stranded DNA, single-stranded DNA, double-stranded RNA, or single-stranded RNA. And the way, basically the shape in which we see the DNA or RNA can be either linear or segmented, can be single and circular, just depends on the virus.
Influenza virus contains eight. linear segments of single-stranded RNA, for example. Cells, on the other hand, always have double-stranded DNA.
Single-stranded DNA and double-stranded RNA are almost non-existent in cells. So this is another difference between cells and viruses. We can also differentiate viruses based on their host. So basically, if you are a cell, you can be infected by a virus. Bacteria, fungi...
Animal plant cells can be infected by viruses. And most viruses infect only one particular type of a host cell. So they're species specific.
So for example, a dog virus does not infect a human, for example. They may be so specific they infect only a particular kind of cell in a host. So an example would be HIV attacking T lymphocytes in human, but they don't infect other.
the types of cells inside the human. Generalists infect many kinds of cells in different hosts. So there's cross-species barriers, and a good example would be rabies. So that rabies virus can infect humans, it can infect dogs, skunks, raccoons, bats, things like that.
Here's some examples of some viruses. Here's Tobacco Mosaic Virus infecting the leaf of a tobacco plant. You see the little pock marks on the leaf indicating where the virus is infecting.
Here is a Bacteriophage infecting a bacterial cell. So Bacteriodophage in pink, bacterial cell in this bluish gray. And the HIV virus here highlighted in blue attaching to a human T lymphocyte.
The host specificity is due to the viral surface proteins which have a precise affinity or attraction to complementary proteins on the host cell membranes. So those host cell receptors interacting with the viral surface proteins in a lock-in key theory. I'll show you a quick video here showing the entry mechanisms and how they interact based on the type of virus.
So here we have an envelope virus, and this is the host cell here, and these red proteins will be the receptors. There are two mechanisms by which enveloped viruses enter host cells. In one of the mechanisms, the virion attaches to host cell receptors by specific proteins on its surface, called spikes.
The envelope of the virus fuses with the plasma membrane of the host. and the nucleocapsid is released directly in. So one of the viral entry mechanisms for an enveloped virus is fusion with the host cell membrane.
So you see that the viral spikes are now part of the host cell membrane, and that allows the capsid to gain entry into the cell. The cytoplasm. The nucleic acid then separates from the protein coat. In the second mechanism, the enveloped virus adsorbs to the host cell by specific proteins on its surface, and the virion is taken in by endocytosis.
In this process, the host cell plasma membrane surrounds the whole virion and forms a vesicle. So endocytosis is the second mechanism which enveloped viruses enter. And here you see that vesicle formed around the entire structure of that virus.
The envelope of the virion then fuses with the plasma membrane of the vesicle, and the nucleocapsid is released into the host cytoplasm. The capsid protein is then removed, releasing the nucleic acid of the virus. So the whole goal is to get that capsid into the cell.
Once the capsid is into the cell, that capsid is degraded, and the virus exists again only as the nucleic acid. A naked virion also enters by endocytosis. Since the virus has no envelope, it cannot fuse with the plasma membrane. After being engulfed, the viral nucleic acid is released from the endocytic vesicle.
The nucleic acid then separates from the capsid. Since the naked virus has no envelope, the only way those enter is through endocytosis. Again, here's just an image showing you the entry mechanism for the naked virus.
This looks like it's actually an injection type of an entry mechanism, but for our class, we are considering naked viruses only entering through endocytosis, where the vesicle forms around it. Here's an envelope virus where we're showing the fusion, and then an envelope virus showing the... endocytosis of that virus.
Looking at the animal virus replication process, first we have to have recognition and attachment, so the capsid or the envelope proteins recognizing the host cell receptors as we just saw in the video. Entry mechanism, fusion, or endocytosis, and then we get synthesis. Synthesis is when the DNA is replicated or the RNA is replicated inside of the cell and the viral proteins are produced during the synthesis step as well. So you're making all the parts for the virus during the synthesis step and this synthesis is done by the host cell enzymes. The polymerases and the ribosomes are doing all the work for the virus.
Once we have all the parts they're assembled and then release. Depending on the type of virus, the release mechanism is different. Envelope viruses may cause persistent infections, and they release from the cell by what's called budding.
They can also release through exocytosis. Naked viruses are released by exocytosis, or lysis, of the cell. This image shows the process of budding.
Here we have the viral capsid produced inside the cell, and basically it's pushing against the cell membrane of the actual animal virus. So the cell membrane becomes the actual envelope of that virus. So it's a phospholipid bilayer.
These protein spikes would have been produced inside the cell and transported to the cell membrane and stuck protruding out from the actual cell membrane. So we have this slow release of the virus through this budding process. Now we're going to look at bacteriophage replication and bacteriophages are viruses that infect only bacteria. So these would attach using their little tail fibers here or little spikes in a specific manner to a bacterial cell. Here they have the capsid which encloses the surrounds the nucleic acid and we study bacteriophages because they're very simple to do and their replication process is very similar to animal viruses.
So there's two cycles for bacteriophage replication. There's lytic cycle which results in lysis of the cell and death of that host cell and then there's lysogenic that we'll talk about here in a moment. So looking at the basic stages of lytic replication cycle We have recognition and attachment. Entry is actually through an injection process where the bacteriophage shoots the nucleic acid into the cell by attaching these little pins to the cell membrane. So we have entry through an injection, and I believe in the book I have these steps switched.
Step three would actually be synthesis. including the synthesis of viral enzymes, and those enzymes are used to degrade the chromosome of the bacteria. So we need to switch these two steps.
So synthesis of viral enzymes, viral proteins, and things like that, and the viral enzymes are what are going to degrade the chromosome of the bacteria. Next we have assembly and then release through lysis. So here's an image showing the basic steps here.
We have attachment, recognition attachment, entry into the cell. The, again, the chromosome is going to be degraded. Again, switching these steps because what we need to have is we need to have viral encoded enzymes to actually break up the chromosome. Synthesis making the new viral parts, assembling. those and then release through the viral or the lysis of that bacterial cell.
The lysogenic cycle or lysogeny is a modified replication cycle, or modified lytic cycle I should say. And this what happens is we have the infected host will actually grow so the bacteria grow and reproduce normally for many generations before they actually lyse. So we have an inactivated bacteriophage that's called a prophage that's actually inserted into the chromosome of the bacteria. So the bacteria is replicating along with the prophage for many generations.
Induction occurs and the prophage is actually cut out from the host chromosome and activates and enters into the lytic cycle. So induction is caused by DNA damaging events such as chemicals, UV light, x-rays can cause induction which is basically activation of virus. It may be suboptimal conditions as well that the bacteria is experiencing that activates the virus. After induction the lytic cycle will occur. So here is another image.
This is the lytic cycle over here that we just talked about. But with the lysogenic cycle, we have a attachment entry. We're going to go over here to the right. Here the viral DNA is actually inserted into the chromosome. Okay, so you see the viral DNA here in this bluish color and then the purplish color is the bacterial chromosome.
So the prophage is inserted. And here we have normal replication of the bacteria. So many generations. We've got billions of cells now with the bacterial chromosome and the prophage being replicated.
We get replication, further divisions, and then that process of induction occurs, where it's a DNA damaging event where that virus is cut out, and we enter into a synthesis step, assembly, and then release. Now if you remember transduction from chapter 9, transduction is the process of the transfer of bacterial DNA to another bacteria using the virus, a bacteriophage. So this is just a simplified little image here.
Here we have the bacteriophage, viral genome in red. It's going to be injected into the bacteria here, and the virus will... begin that process of replication and degrading this chromosome, the bacterial chromosome in purple.
So the bacteriophage assembles and what happens is little bits and pieces of the bacterial chromosome can be inserted into the actual bacteriophage. So now the virus contains bacterial DNA instead of the viral DNA in red. So when the virus lices the cell here, this virus will infect a new cell and it will insert a piece of bacterial DNA rather than the viral DNA. So this is a completely random process, but with the numbers of bacteria and the numbers of viruses you can have in an environment, this does happen.
Viruses also play a role in human cancers. Viruses have been shown to cause about 20 to 25 percent of human cancers. So some specific viruses known would be Kapsozi's sarcoma with HIV patients, cervical cancer caused by the HPV virus. So the big question regarding viruses is are they alive? If you talk to me, I consider them non-living, but they do have lifelike characteristics.
Living characteristics are that they can reproduce, but only in a living cell. And they can mutate, since they are being replicated, and that DNA or RNA is going to be replicated as well. Non-living characteristics are, well, they're not cells.
There's no cytoplasm or organelles. They do not carry out metabolize on their own. And they only have DNA or RNA, but they do not have both. The next acellular infectious particle would be byroids.
Viroids are extremely small circular pieces of RNA that are only known to be infectious in plants. It's possible that there are viroids that infect humans, but we just don't know. But these are only RNA.
There is no capsid. There is no envelope that surrounds the RNA. So it's similar to an RNA virus. They lack the capsid. So they're significant because since they do infect...
plants, well one of the plants that can be infected are potato plants. So here this is a normal healthy potato here and these potatoes here were infected by viroid disease and causes a reduced storage of the starch in the actual potato. So they're still edible but the farmer experiences a reduced yield. Prions are the last acellular infectious agent, and these are protein only, infectious protein.
They cause what are called spongiform encephalopathies, so mad cow disease, scrapie, Kuru, Creutzfeldt-Jakob syndrome, chronic wasting disease in deer, and only protein. And these proteins are resistant to proteases, which is an enzyme that breaks down protein. UV light, heat, and disinfectants.
So they can only be destroyed by incineration or autoclaving in sodium hydroxide. So these are referred to as the most resistant form of microbe. Protein only, no nucleic acid.
What they do is they cause these fatal neurological degenerative diseases resulting in a loss of brain matter. So the spondyloform encephalopathy here we have a cross-section of a brain, we have these large vesicles or vacuoles that are formed here causing the spongy appearance. This is a deer infected with chronic wasting disease, and if they do not succumb to a predator or get hit by a car or get shot by a hunter, they would eventually starve to death. These diseases are 100% fatal. There is no cure for prion diseases.
What they do, they kind of act like an enzyme. So the cellulose, all mammals have this protein called PRP protein, and the normal structure has these alpha helices. The prion PRP has these, what are referred to as beta pleated sheets, so it's a different, it's a change in the shape of the protein basically. This information isn't.
important for the exam as far as knowing alpha helices and beta pleated sheets, but it is a change in the protein structure. So the prion PRP turns the normal PRP into the prion PRP. Very slowly, the changes occur, resulting in the vacuoles in the brain. So this concludes the chapter 12 video, viruses, viroids, and prions.