Understanding Cell Recognition and Immunity

Hi everyone, welcome back to my channel. Today I'm going to take you through the cell recognition and immune system section for AQA A Level Biology which is part of the Cells Unit. Also I'll be going through a few exam style questions and their mark schemes and as always I'll be putting timestamps in the comments section so you can skip to the relevant sections that you want to revise from as this is a quite a long topic and there is a lot to learn. So let's get started. So each type of cell, whether it's a normal, what we call a self cell, which is a cell from your own body or a foreign cell, for example, a pathogen, has specific molecules on its surface that identify it, which are often proteins. This enables the identification of pathogens, abnormal body cells, toxins. and cells from other organisms of the same species. So these molecules allow the identification of foreign cells as the structure of the molecules are different to cell cells or cells from your own body. Now the main molecules that identify pathogens are called antigens. The definition of an antigen is foreign proteins present on the cell surface membrane that stimulate an immune response. The key term here is, just get my pen out, foreign. So this is an example of a, well it's kind of like a simplified pathogen that I've drawn here, and the antigens which I have denoted through kind of like purple triangles. So these allow the identification that this is a pathogen. Now a clever tactic that pathogens such as bacteria and viruses use to survive is that the antigens mutate so the DNA or RNA sequence of the antigens change. So for example mutations can take place in these antigens which changes their tertiary structure so they can look different. This can have implications, for example, the immune system will not be able to detect the newly mutated antigens, so it won't be able to kill the pathogen. This is what we call antigenic variability. Now this is one of the reasons why flu vaccinations have to be updated every year, as the flu virus undergoes antigenic variability to aid its survival. Now, you need to know about three kinds of immune responses called phagocytosis, cell-mediated response and humoral response. First, we're going to talk about phagocytosis. So here I've drawn a simplified version of a white blood cell called a phagocyte. Phagocytosis is basically the engulfment of a pathogen by a phagocyte, which I've drawn here. Engulfment basically means the pathogen is eaten. but don't write the word eaten in the exam, write the word engulfment. So the first step is the phagocyte is attracted to the pathogen by chemical attractants and binds to the pathogen via molecules on its surface called receptors. So it moves towards the pathogen which I've drawn a red circle to represent. So the next step in phagocytosis is the pathogen is engulfed by the phagocyte by a process called endocytosis. So you have the pathogen being engulfed here. And this means when the pathogen is engulfed into the phagocyte, a phagosome is formed, which is a vesicle containing their pathogen. So here we have the phagosome here. So the next step is lysosomes which as you can recall from my structure of eukaryotic and prokaryotic cells videos is an organelle that breaks down unwanted materials in the cell. The lysosomes fuse with the pathogen and lysosomes break down pathogen into soluble materials. Lysosomes are proteolytic enzymes that are present in the lysosomes. So you've got your phagocyte here and your phagosome. And here we have your lysosome with these black dots inside which are your lysosomes. So the lysosome fuses with the phagosome and the pathogen is broken down into soluble materials which are used by the phagocyte for various processes. But what is crucial is that the antigens on the pathogen are then presented on the surface of the phagocyte. So the phagocyte becomes what we call an antigen presenting cell. This antigen presenting cell is crucial in the cell mediated response. So there are two kind of what we call lymphocytes that you need to know about. Lymphocytes are types of white blood cells. So there are two types, B cells and T cells. B cells mature in the bone marrow and are involved in the humeral response, but T cells mature in the thymus gland involved in cell mediated response. The way you remember this is that B for bone marrow and T for thymus gland. It's pretty easy to remember, don't get them mixed up. So now we're going to talk about the cell mediated response. So you have your antigen presenting cell here as a result of phagocytosis of a pathogen. Now here you have your T cell. T cells have molecules on their surface called receptors just like the phagocyte does. What the receptor does is it binds to the antigens. This then stimulates the rapid differentiation of the T cells, which is clones of T cells. This can then differentiate into helper T cells, which are involved in the human response, cytotoxic T cells, which produce a protein called perforin, which makes holes in the cell membrane of pathogens. This allows substances to enter the pathogen and therefore cause cell death. Or these clones of T cells can stimulate phagocytosis. So now we're going to talk about antibodies which you have probably heard of before. Antigens are not antigens antibodies are involved in the human response. The definition of an antibody is a protein that has binding sites complementary to antigens and destroy the pathogen. So here we have the structure of an antibody, this kind of Y shape here. Now antibodies have four polypeptide chains so we can conclude that antibodies are a quaternary structure. So it has four polypeptide chains, two light chains and two heavy chains. The light chains are this shorter chain here and the heavy chains are this kind of long bit here. Now the chains are linked by disulfide bonds which we said in my protein and enzymes video hold the tertiary structure together. Now antibodies have a constant region denoted by the blue parts here. A constant region is called the constant region because it is present in all antibodies but the purple bit here represents the variable region. This is important as this makes antibodies specific to the particular antigen for the particular pathogen so it can be killed. So now we're going to talk about the humoral response. The first step in the humoral response is that helper T cells, which is what we mentioned earlier, stimulate B cells so they attach to B cells. This stimulates the B cells to rapidly divide by mitosis to form clones of plasma cells. This process is called clonal selection. This term here is key as the examiners like it when you use this term. So here we have a B cell which rapidly divides into clones of plasma cells so they are genetically identical. Now it is the plasma cells that produce the antibodies. These antibodies have a specific shape or a specific tertiary structure to antigens so they attach to the antigen and destroy the pathogen. So here you can see the plasma cells producing antigen antibodies which then attach to the antigens on the antigen presenting cell or the pathogen and destroy it. So how do the antibodies actually destroy the pathogens? They do this by the process of agglutination. Agglutination is when the antibodies that have bound to the antigens forming an antibody antigen complex all stick together. Now, the advantage of this sticking together or agglutination is the fact that the pathogen can then be easily digested by phagocytosis as larger clumps will be easily detected by the phagocyte. Now the first contact with the pathogen is called a primary response and the second contact with the pathogen is called a secondary response. The secondary response is present because once the antibodies have destroyed the pathogen, memory B cells are formed. These memory B cells remember how to produce the antibodies that can kill that particular pathogen. So as you can see from this graph, initial exposure, which is when you are first infected with the pathogen, the concentration of antibodies increases as the B cells try to fight the pathogen off. The concentration of antibodies then decreases as the pathogen is killed. Then upon reinfection, so when the pathogen enters the body for the second time, This is called secondary exposure and their memory B cells rapidly produce their antibodies and produce more of them so that they can kill the pathogen before it causes infection and causes symptoms. So as you can see the concentration of antibody increases much more rapidly than the primary immune response as the antibodies are produced more rapidly and at a higher intensity. This provides a basis for the process of vaccination. In a vaccine you have a dead or inactive pathogen or particular parts of the pathogen, for example just the membrane with the antigens on. A vaccine initiates a primary response leading to the formation of memory B cells as we have mentioned. So this means that upon reinfection, secondary response is stimulated so antibodies are produced at a higher rate so that the pathogen is killed before it can cause infection or symptoms. The main purpose of vaccination is to provide what we call herd immunity. Herd immunity works by immunising the majority of the population. If the majority of the population are vaccinated, This means that an unvaccinated person is less likely to come into contact with an infected person. Now there are ethical issues associated with vaccines, as you have probably seen in the news a lot recently, if you are watching this during the coronavirus pandemic. So the first issue is should vaccinations be compulsory? So should people be vaccinated against their will for the good of the population? Also, who should vaccinations be tested on? Should they be tested on sick people, young people, old people? It's a question that is hard to answer. Also, are they 100% effective in the long term? This is especially true for relatively newly introduced vaccinations, for example the HPV vaccination in girls, as you have not seen the long-term effects, so you can't conclude that they are 100% effective. So now I'm going to talk about a concept called active and passive immunity. Active immunity is immunity that results from antibody production by the immune system in response to the presence of an antigen, e.g. through vaccination. So active immunity is when immunity is acquired through your own body. Passive immunity is immunity that results from the introduction of antibodies from another person or an animal, for example antivenom or the process of breastfeeding. Now there are two subtypes of passive immunity, artificial passive immunity and natural passive immunity. Antivenom will be would be an example of artificial passive immunity and breastfeeding would be an example of natural passive immunity as the antibodies are passed on via breastfeeding are produced naturally by the mother. So now I'm going to talk about another crucial topic monoclonal antibodies. A monoclonal antibody is a type of antibody that is isolated from a single clone of B cells. So monoclonal antibodies will be of the same type, so will attach to the same pathogen and kill it. The main use of monoclonal antibodies is drug targeting. So in the process of drug targeting using monoclonal antibodies, a drug is attached to the monoclonal antibody. Now the specificity of these antibodies means that the drug can be targeted specifically to the target of the drug, for example a tumour. However, an ethical issue associated with monoclonal antibodies is the fact that mice are used to produce them, which obviously brings up animal rights issues. Now another use of these antibodies is the detection of diseases. This is through the ELISA test or the enzyme linked immunosorbent assay. This is used in the detection of antigens so it can detect if a person has a particular disease. So the first step in the ELISA test is the antigen of interest or the antibody is immobilized it doesn't matter which way around you do it. So the antigen that you want to detect is immobilized. The next step is monoclonal antibodies are added and they bind to their appropriate antigen if it is present because you do not know that yet. May I just add here that the antigen of interest is immobilised through a patient's blood sample. The apparatus that you immobilise the antigens and the antibodies is washed. The reason that you do this is to remove unbound antigens that could obscure your results. The next step is more monoclonal antibodies added or what we call secondary antibodies. These are different as they are linked to colour changing enzymes and they bind to the antigens. So as you can see by the diagram here the secondary antibodies with the enzyme length detection molecule bind to the antigen as well as the first set of antibodies that you added in. The apparatus is then washed again to remove the antibodies that are unbound which would obscure your results again. So the final step and the proof of the test is that the complementary substrates to the enzyme's active site is added. If the substrate has bound This triggers a colour change upon the binding, therefore showing the presence of the antigen. So if the colour change is seen, that means that the antigen is present. This has implications as it can allow treatment of harmful diseases. So the last part of this section that you need to know about is HIV structure and replication. So here I have drawn a simplified version of the HIV virus. So it has many components. The first thing is these kind of spikes that poke around the edge. These are called glycoproteins. Sometimes they're called spike proteins or sometimes they're called attachment proteins. The main role of these glycoproteins is that they attach to the receptors on the host cell which is the cell that they infect, which allows the genetic material to be injected into the host cell. The next part is the capsid. The capsid is kind of like a protein coat which houses the genetic material and reverse transcriptase enzymes. So we have here these squiggly lines which represent the genetic material. The genetic material in HIV is RNA, it's not DNA. These yellow circles here represent reverse transcriptases. which are enzymes which convert RNA to DNA or more specifically cDNA. The importance of this will become clearer next. So we're going to talk about HIV replication now. So here is a nice diagram that I found from the internet. So the first step is HIV glycoproteins attached to CD4 receptors on helper T cells. So they can't attach to any other receptors or any other cells. They can only attach to what we call CD4 receptors on helper T cells, which, as we mentioned earlier, are involved in the humoral response. This allows the RNA and the enzymes, so reverse transcriptases, to enter the host T cell. What happens next is the reverse transcriptases convert the viral RNA to cDNA. This allows the cDNA to move into the nucleus of the T cell, where it's transcribed and translated using host machinery. So the... transcription and translation machinery of the T cell to produce viral proteins that make new viruses or virions. So this is a very unique survival strategy in viruses. They hijack the protein production machinery of the host cell to make copies of itself. The next step is that the new virus particles or the virions break off the T cell membrane and can go on to replicate in even more cells. So you probably have heard of the link between HIV and AIDS or acquired immunodeficiency syndrome. So how does HIV cause AIDS? So as I said HIV viruses infect helper T cells. When the newly replicated HIV viruses break off from the T cell membrane the helper T cell dies. This means that there are less helper T cells, so there is a decreased stimulation of B cells, so there is less human response, so there is a decreased immunity. This can leave the patient vulnerable to minor infections and the most simplest of infections, for example, the common cold, can be deadly. So they are vulnerable to infections that are fatal. Now there are many treatments for HIV, but the most common treatment is the targeting of the reverse transcriptase enzyme. If the reverse transcriptase enzyme is blocked, this means that the genetic material, which is RNA in the virus, cannot be converted into cDNA. So the genetic material cannot move into the nucleus, so can't be replicated in the host cell, so the virus won't survive. So this is the last piece of content. Antibiotics are not used to treat viruses because they are completely ineffective. This is because antibiotics kill bacteria. Bacteria have a very different method of infecting the host. This includes producing toxins. Also, viruses and bacteria replicate in different ways and have different structures. So a drug that targets bacteria. will be completely ineffective against the viruses as they have different structures and replicate in different ways. So that is it for the content and now I will get on to some exam style questions. Let's get my highlighter. So here is a question which is quite a simple one. Give two ways in which pathogens can cause disease. Now the trick here is it is not asking you how the pathogen infects you, it is asking how pathogens can cause disease. So here I've put releases toxins which is often the case in bacteria and kills host cells as we exemplified by the fact that HIV kills the T cells. So if you look at the mark scheme releases toxins which we wrote or kills cells or tissues. Now here it says accept any reference to cell or tissue damage. so you don't have to write it kills them you can just write it damages the cells. However it says ignore infecting or invading cells as the question doesn't ask how the pathogen infects the body, the question asks how the infection causes disease. So that is two marks there. Let's look at this next question which is a quite a complicated looking graph. So it says suggests two reasons why the percentage of infants vaccinated decreased between 1973 and 1975. So if we look at the graph here, so we look at 1973 which is around here and 1975 which is here. Now for this graph there are two lines, one is the number of cases of whooping cough reported and the other one which is the dotted line is a percentage of infants vaccinated against whooping cough. As this question asks us about the percentage of infants we need to look at the dotted line here. So the percentage of infants vaccinated rapidly decreases between 1973 and 1975. Now as this is a suggest question it often doesn't require knowledge from the specification, it requires your own ideas. So this is what I've suggested, not enough vaccine was available, so this can be a result of over demand of the vaccine, so not enough is available for everyone. Also there were decreased cases of whooping cough so people couldn't see the reason for vaccination. So let's look at the mark scheme. Any two from decreased link to fewer cases of whooping cough which I've written, risk of fear of side effects which is becoming more common nowadays. or insufficient vaccine available or too expensive to produce or distribute. Now I didn't write insufficient I just wrote not enough vaccine is available this is okay to write as the word insufficient isn't in bold or it isn't underlined. Now here it says too expensive unqualified is insufficient for the mark so if you just put that you can't get the mark. Now it says too max here This means that you can't get three marks if you write all three of these points, you can only get a maximum of two. Let's look at the next question, part of the question even. So between 1980 and 1990 there were three peaks in the number of reported cases of whooping cough. After 1981 the number of cases of whooping cough in each peak decreased. Use the information in the graph to suggest why. I have written the rate of vaccination increases. As you can see after 1981 from the dotted line the percentage of infants vaccinated increases rapidly so the rate of vaccination increased. This means that more people are immune so there will obviously be less cases of whooping cough. So if we look at the mark scheme the vaccination rate increases which we wrote. So there are fewer people to spread the disease or whooping cough or more people are immune and fewer are susceptible. You can put any of those to get the mark. Here it says a greater herd effect. When the mark scheme says neutral it means that the examiner doesn't really want you to write that but it means that you can get the mark. So you can mention herd immunity in there and it says here a loud description of immune but reject resistant as that is not proper terminology and as it says reject if you write resistant in your answer you don't get any marks on the question no matter if you put the first marking point correct so that's two marks there so let's see the next part of the question the percentage of the population vaccinated does not need to be 100% to be effective in preventing the spread of pooping cough suggest why Now as again this is a suggest question so often requires your own ideas instead of knowledge from the specification. Now you're probably thinking this is to do with herd immunity which is correct so you need to explain the concept of herd immunity in your answer. So I have written the majority of the population are immune so the unvaccinated people are less likely to come into contact with an infected person. and that is two marks so I've written two points here so the majority are immune so they're less likely to come into contact with an infected person two points so let's look at the mark scheme more people are immune or fewer people carry the pathogen so I've got that mark there now here it says if neither point one or two awarded so if you didn't put any of these answers but you mentioned the term herd immunity you can get a mark. Here it says unvaccinated does not mean infected but it says do not accept disease for the pathogen as the disease is the result of the infection of the pathogen. So if you look at the second marking point so susceptible or unvaccinated people are less likely to contact infected people so that's two marks there. So let's move on to the next question. Now I think I remember actually doing this question as part of my revision for A-Levels and I remember absolutely hating it and always getting it wrong so that is why I am taking you through it now. So let's read it. Malaria is a disease caused by parasites belonging to the genus Plasmodium. Two species that cause malaria are Plasmodium falciparum and Plasmodium vivax. So we can highlight those. A test strip that uses monoclonal antibodies can be used to determine whether a person is infected by Plasmodium. It can also be used to find which species of Plasmodium they are infected by. A sample of a person's blood is mixed with a solution containing an antibody A that binds to a protein found in both species of Plasmodium. This antibody has a coloured dye attached. A test strip is then put into the mixture. The mixture moves up the test strip by capillary action to an absorbent pad. Three other antibodies B, C and D are attached to the test strip. the position of these antibodies and what they bind to is shown in figure one. We explain why antibody A attaches only to the protein found in species of Plasmodium. Now this question is asking you about antibody action so you need to explain how antibodies are specific and why they are specific as this is an explained question. So this is what I've written. Antibody A has a specific tertiary structure that is complementary to the protein's binding site. So let's look at the mark scheme. Antibody has a tertiary structure, or more specifically a specific tertiary structure, that is complementary to the binding site and the protein. So we wrote both of those points so we've got two marks. Let's look at the next section. Antibody B is important if this test shows a person is not infected with Plasmodium. Explain why antibody B is important. So if we go back, antibody B binds to antibody A. Now the purpose of this is to prevent false negatives, which means the test shows that you are negative for the disease even though you actually are infected. This is as antibody A hasn't bound to any Plasmodium protein. So let's look at the mark scheme. So it prevents some false negative results since it shows antibody A has moved up the strip or has not bound to plasmodium protein. I think this is, yes this is the last question. So one of these test strips was used to test a sample from a person thought to be infected with plasmodium. Figure two shows the result. What can you conclude from this result? explain how you reached your conclusion. So for simplicity we can write here, forget my pen, this band here as you can remember, just change the colour of my pen, represents A and B as antibody A and antibody B are present. This band has C and this band has D. Now as you can see the colour dye is shown for the bands with A and B and C. So we can conclude that the person is infected with Plasmodium Vivax as antibody C only binds to Plasmodium Vivax proteins. So I've written the person is infected with Plasmodium Vivax because where antibody C is, which is this band here, the dye is coloured which only binds to Plasmodium Vivax proteins proving that the person is infected with this. So this kind of links into the ELISA test and monoclonal antibodies. So let's look at the mark scheme. So the person is infected with Plasmodium which we have basically written or you can write has malaria. It doesn't matter which one you put you still get the mark. The second marking point is that you need to be specific so infected with Plasmodium vivax. So we have kind of written these first two marking points in the same sentence. So there is coloured dye where antibody C is present, so we wrote that. That only binds to proteins from vivax or no reaction with antibody for falciparum, as the band for antibody D which binds to plasmodium falciparum has not been coloured. So it says here, person is infected with p-vivax or plasmodium vivax is two marks. So if you write these in the same sentence you can still get two marks. Right, so that is it. That is all I want to say. Please comment below if you have any questions at all about this video or about A-level biology in any context and I'll see you in the next video.

So let's get started. So each type of cell, whether it's a normal, what we call a self cell, which is a cell from your own body or a foreign cell, for example, a pathogen, has specific molecules on its surface that identify it, which are often proteins. This enables the identification of pathogens, abnormal body cells, toxins.

and cells from other organisms of the same species. So these molecules allow the identification of foreign cells as the structure of the molecules are different to cell cells or cells from your own body. Now the main molecules that identify pathogens are called antigens.

The definition of an antigen is foreign proteins present on the cell surface membrane that stimulate an immune response. The key term here is, just get my pen out, foreign. So this is an example of a, well it's kind of like a simplified pathogen that I've drawn here, and the antigens which I have denoted through kind of like purple triangles.

So these allow the identification that this is a pathogen. Now a clever tactic that pathogens such as bacteria and viruses use to survive is that the antigens mutate so the DNA or RNA sequence of the antigens change. So for example mutations can take place in these antigens which changes their tertiary structure so they can look different. This can have implications, for example, the immune system will not be able to detect the newly mutated antigens, so it won't be able to kill the pathogen. This is what we call antigenic variability.

Now this is one of the reasons why flu vaccinations have to be updated every year, as the flu virus undergoes antigenic variability to aid its survival. Now, you need to know about three kinds of immune responses called phagocytosis, cell-mediated response and humoral response. First, we're going to talk about phagocytosis.

So here I've drawn a simplified version of a white blood cell called a phagocyte. Phagocytosis is basically the engulfment of a pathogen by a phagocyte, which I've drawn here. Engulfment basically means the pathogen is eaten. but don't write the word eaten in the exam, write the word engulfment. So the first step is the phagocyte is attracted to the pathogen by chemical attractants and binds to the pathogen via molecules on its surface called receptors.

So it moves towards the pathogen which I've drawn a red circle to represent. So the next step in phagocytosis is the pathogen is engulfed by the phagocyte by a process called endocytosis. So you have the pathogen being engulfed here. And this means when the pathogen is engulfed into the phagocyte, a phagosome is formed, which is a vesicle containing their pathogen.

So here we have the phagosome here. So the next step is lysosomes which as you can recall from my structure of eukaryotic and prokaryotic cells videos is an organelle that breaks down unwanted materials in the cell. The lysosomes fuse with the pathogen and lysosomes break down pathogen into soluble materials.

Lysosomes are proteolytic enzymes that are present in the lysosomes. So you've got your phagocyte here and your phagosome. And here we have your lysosome with these black dots inside which are your lysosomes. So the lysosome fuses with the phagosome and the pathogen is broken down into soluble materials which are used by the phagocyte for various processes.

But what is crucial is that the antigens on the pathogen are then presented on the surface of the phagocyte. So the phagocyte becomes what we call an antigen presenting cell. This antigen presenting cell is crucial in the cell mediated response. So there are two kind of what we call lymphocytes that you need to know about. Lymphocytes are types of white blood cells.

So there are two types, B cells and T cells. B cells mature in the bone marrow and are involved in the humeral response, but T cells mature in the thymus gland involved in cell mediated response. The way you remember this is that B for bone marrow and T for thymus gland.

It's pretty easy to remember, don't get them mixed up. So now we're going to talk about the cell mediated response. So you have your antigen presenting cell here as a result of phagocytosis of a pathogen. Now here you have your T cell.

T cells have molecules on their surface called receptors just like the phagocyte does. What the receptor does is it binds to the antigens. This then stimulates the rapid differentiation of the T cells, which is clones of T cells. This can then differentiate into helper T cells, which are involved in the human response, cytotoxic T cells, which produce a protein called perforin, which makes holes in the cell membrane of pathogens. This allows substances to enter the pathogen and therefore cause cell death.

Or these clones of T cells can stimulate phagocytosis. So now we're going to talk about antibodies which you have probably heard of before. Antigens are not antigens antibodies are involved in the human response. The definition of an antibody is a protein that has binding sites complementary to antigens and destroy the pathogen.

So here we have the structure of an antibody, this kind of Y shape here. Now antibodies have four polypeptide chains so we can conclude that antibodies are a quaternary structure. So it has four polypeptide chains, two light chains and two heavy chains.

The light chains are this shorter chain here and the heavy chains are this kind of long bit here. Now the chains are linked by disulfide bonds which we said in my protein and enzymes video hold the tertiary structure together. Now antibodies have a constant region denoted by the blue parts here. A constant region is called the constant region because it is present in all antibodies but the purple bit here represents the variable region.

This is important as this makes antibodies specific to the particular antigen for the particular pathogen so it can be killed. So now we're going to talk about the humoral response. The first step in the humoral response is that helper T cells, which is what we mentioned earlier, stimulate B cells so they attach to B cells.

This stimulates the B cells to rapidly divide by mitosis to form clones of plasma cells. This process is called clonal selection. This term here is key as the examiners like it when you use this term.

So here we have a B cell which rapidly divides into clones of plasma cells so they are genetically identical. Now it is the plasma cells that produce the antibodies. These antibodies have a specific shape or a specific tertiary structure to antigens so they attach to the antigen and destroy the pathogen. So here you can see the plasma cells producing antigen antibodies which then attach to the antigens on the antigen presenting cell or the pathogen and destroy it.

So how do the antibodies actually destroy the pathogens? They do this by the process of agglutination. Agglutination is when the antibodies that have bound to the antigens forming an antibody antigen complex all stick together.

Now, the advantage of this sticking together or agglutination is the fact that the pathogen can then be easily digested by phagocytosis as larger clumps will be easily detected by the phagocyte. Now the first contact with the pathogen is called a primary response and the second contact with the pathogen is called a secondary response. The secondary response is present because once the antibodies have destroyed the pathogen, memory B cells are formed. These memory B cells remember how to produce the antibodies that can kill that particular pathogen. So as you can see from this graph, initial exposure, which is when you are first infected with the pathogen, the concentration of antibodies increases as the B cells try to fight the pathogen off.

The concentration of antibodies then decreases as the pathogen is killed. Then upon reinfection, so when the pathogen enters the body for the second time, This is called secondary exposure and their memory B cells rapidly produce their antibodies and produce more of them so that they can kill the pathogen before it causes infection and causes symptoms. So as you can see the concentration of antibody increases much more rapidly than the primary immune response as the antibodies are produced more rapidly and at a higher intensity.

This provides a basis for the process of vaccination. In a vaccine you have a dead or inactive pathogen or particular parts of the pathogen, for example just the membrane with the antigens on. A vaccine initiates a primary response leading to the formation of memory B cells as we have mentioned. So this means that upon reinfection, secondary response is stimulated so antibodies are produced at a higher rate so that the pathogen is killed before it can cause infection or symptoms. The main purpose of vaccination is to provide what we call herd immunity.

Herd immunity works by immunising the majority of the population. If the majority of the population are vaccinated, This means that an unvaccinated person is less likely to come into contact with an infected person. Now there are ethical issues associated with vaccines, as you have probably seen in the news a lot recently, if you are watching this during the coronavirus pandemic. So the first issue is should vaccinations be compulsory? So should people be vaccinated against their will for the good of the population?

Also, who should vaccinations be tested on? Should they be tested on sick people, young people, old people? It's a question that is hard to answer.

Also, are they 100% effective in the long term? This is especially true for relatively newly introduced vaccinations, for example the HPV vaccination in girls, as you have not seen the long-term effects, so you can't conclude that they are 100% effective. So now I'm going to talk about a concept called active and passive immunity.

Active immunity is immunity that results from antibody production by the immune system in response to the presence of an antigen, e.g. through vaccination. So active immunity is when immunity is acquired through your own body. Passive immunity is immunity that results from the introduction of antibodies from another person or an animal, for example antivenom or the process of breastfeeding.

Now there are two subtypes of passive immunity, artificial passive immunity and natural passive immunity. Antivenom will be would be an example of artificial passive immunity and breastfeeding would be an example of natural passive immunity as the antibodies are passed on via breastfeeding are produced naturally by the mother. So now I'm going to talk about another crucial topic monoclonal antibodies.

A monoclonal antibody is a type of antibody that is isolated from a single clone of B cells. So monoclonal antibodies will be of the same type, so will attach to the same pathogen and kill it. The main use of monoclonal antibodies is drug targeting.

So in the process of drug targeting using monoclonal antibodies, a drug is attached to the monoclonal antibody. Now the specificity of these antibodies means that the drug can be targeted specifically to the target of the drug, for example a tumour. However, an ethical issue associated with monoclonal antibodies is the fact that mice are used to produce them, which obviously brings up animal rights issues.

Now another use of these antibodies is the detection of diseases. This is through the ELISA test or the enzyme linked immunosorbent assay. This is used in the detection of antigens so it can detect if a person has a particular disease.

So the first step in the ELISA test is the antigen of interest or the antibody is immobilized it doesn't matter which way around you do it. So the antigen that you want to detect is immobilized. The next step is monoclonal antibodies are added and they bind to their appropriate antigen if it is present because you do not know that yet.

May I just add here that the antigen of interest is immobilised through a patient's blood sample. The apparatus that you immobilise the antigens and the antibodies is washed. The reason that you do this is to remove unbound antigens that could obscure your results. The next step is more monoclonal antibodies added or what we call secondary antibodies. These are different as they are linked to colour changing enzymes and they bind to the antigens.

So as you can see by the diagram here the secondary antibodies with the enzyme length detection molecule bind to the antigen as well as the first set of antibodies that you added in. The apparatus is then washed again to remove the antibodies that are unbound which would obscure your results again. So the final step and the proof of the test is that the complementary substrates to the enzyme's active site is added.

If the substrate has bound This triggers a colour change upon the binding, therefore showing the presence of the antigen. So if the colour change is seen, that means that the antigen is present. This has implications as it can allow treatment of harmful diseases.

So the last part of this section that you need to know about is HIV structure and replication. So here I have drawn a simplified version of the HIV virus. So it has many components. The first thing is these kind of spikes that poke around the edge. These are called glycoproteins.

Sometimes they're called spike proteins or sometimes they're called attachment proteins. The main role of these glycoproteins is that they attach to the receptors on the host cell which is the cell that they infect, which allows the genetic material to be injected into the host cell. The next part is the capsid. The capsid is kind of like a protein coat which houses the genetic material and reverse transcriptase enzymes. So we have here these squiggly lines which represent the genetic material.

The genetic material in HIV is RNA, it's not DNA. These yellow circles here represent reverse transcriptases. which are enzymes which convert RNA to DNA or more specifically cDNA. The importance of this will become clearer next.

So we're going to talk about HIV replication now. So here is a nice diagram that I found from the internet. So the first step is HIV glycoproteins attached to CD4 receptors on helper T cells. So they can't attach to any other receptors or any other cells.

They can only attach to what we call CD4 receptors on helper T cells, which, as we mentioned earlier, are involved in the humoral response. This allows the RNA and the enzymes, so reverse transcriptases, to enter the host T cell. What happens next is the reverse transcriptases convert the viral RNA to cDNA. This allows the cDNA to move into the nucleus of the T cell, where it's transcribed and translated using host machinery. So the...

transcription and translation machinery of the T cell to produce viral proteins that make new viruses or virions. So this is a very unique survival strategy in viruses. They hijack the protein production machinery of the host cell to make copies of itself. The next step is that the new virus particles or the virions break off the T cell membrane and can go on to replicate in even more cells.

So you probably have heard of the link between HIV and AIDS or acquired immunodeficiency syndrome. So how does HIV cause AIDS? So as I said HIV viruses infect helper T cells. When the newly replicated HIV viruses break off from the T cell membrane the helper T cell dies.

This means that there are less helper T cells, so there is a decreased stimulation of B cells, so there is less human response, so there is a decreased immunity. This can leave the patient vulnerable to minor infections and the most simplest of infections, for example, the common cold, can be deadly. So they are vulnerable to infections that are fatal. Now there are many treatments for HIV, but the most common treatment is the targeting of the reverse transcriptase enzyme. If the reverse transcriptase enzyme is blocked, this means that the genetic material, which is RNA in the virus, cannot be converted into cDNA.

So the genetic material cannot move into the nucleus, so can't be replicated in the host cell, so the virus won't survive. So this is the last piece of content. Antibiotics are not used to treat viruses because they are completely ineffective. This is because antibiotics kill bacteria. Bacteria have a very different method of infecting the host.

This includes producing toxins. Also, viruses and bacteria replicate in different ways and have different structures. So a drug that targets bacteria. will be completely ineffective against the viruses as they have different structures and replicate in different ways. So that is it for the content and now I will get on to some exam style questions.

Let's get my highlighter. So here is a question which is quite a simple one. Give two ways in which pathogens can cause disease. Now the trick here is it is not asking you how the pathogen infects you, it is asking how pathogens can cause disease. So here I've put releases toxins which is often the case in bacteria and kills host cells as we exemplified by the fact that HIV kills the T cells.

So if you look at the mark scheme releases toxins which we wrote or kills cells or tissues. Now here it says accept any reference to cell or tissue damage. so you don't have to write it kills them you can just write it damages the cells. However it says ignore infecting or invading cells as the question doesn't ask how the pathogen infects the body, the question asks how the infection causes disease.

So that is two marks there. Let's look at this next question which is a quite a complicated looking graph. So it says suggests two reasons why the percentage of infants vaccinated decreased between 1973 and 1975. So if we look at the graph here, so we look at 1973 which is around here and 1975 which is here.

Now for this graph there are two lines, one is the number of cases of whooping cough reported and the other one which is the dotted line is a percentage of infants vaccinated against whooping cough. As this question asks us about the percentage of infants we need to look at the dotted line here. So the percentage of infants vaccinated rapidly decreases between 1973 and 1975. Now as this is a suggest question it often doesn't require knowledge from the specification, it requires your own ideas.

So this is what I've suggested, not enough vaccine was available, so this can be a result of over demand of the vaccine, so not enough is available for everyone. Also there were decreased cases of whooping cough so people couldn't see the reason for vaccination. So let's look at the mark scheme.

Any two from decreased link to fewer cases of whooping cough which I've written, risk of fear of side effects which is becoming more common nowadays. or insufficient vaccine available or too expensive to produce or distribute. Now I didn't write insufficient I just wrote not enough vaccine is available this is okay to write as the word insufficient isn't in bold or it isn't underlined.

Now here it says too expensive unqualified is insufficient for the mark so if you just put that you can't get the mark. Now it says too max here This means that you can't get three marks if you write all three of these points, you can only get a maximum of two. Let's look at the next question, part of the question even. So between 1980 and 1990 there were three peaks in the number of reported cases of whooping cough. After 1981 the number of cases of whooping cough in each peak decreased.

Use the information in the graph to suggest why. I have written the rate of vaccination increases. As you can see after 1981 from the dotted line the percentage of infants vaccinated increases rapidly so the rate of vaccination increased.

This means that more people are immune so there will obviously be less cases of whooping cough. So if we look at the mark scheme the vaccination rate increases which we wrote. So there are fewer people to spread the disease or whooping cough or more people are immune and fewer are susceptible.

You can put any of those to get the mark. Here it says a greater herd effect. When the mark scheme says neutral it means that the examiner doesn't really want you to write that but it means that you can get the mark. So you can mention herd immunity in there and it says here a loud description of immune but reject resistant as that is not proper terminology and as it says reject if you write resistant in your answer you don't get any marks on the question no matter if you put the first marking point correct so that's two marks there so let's see the next part of the question the percentage of the population vaccinated does not need to be 100% to be effective in preventing the spread of pooping cough suggest why Now as again this is a suggest question so often requires your own ideas instead of knowledge from the specification. Now you're probably thinking this is to do with herd immunity which is correct so you need to explain the concept of herd immunity in your answer.

So I have written the majority of the population are immune so the unvaccinated people are less likely to come into contact with an infected person. and that is two marks so I've written two points here so the majority are immune so they're less likely to come into contact with an infected person two points so let's look at the mark scheme more people are immune or fewer people carry the pathogen so I've got that mark there now here it says if neither point one or two awarded so if you didn't put any of these answers but you mentioned the term herd immunity you can get a mark. Here it says unvaccinated does not mean infected but it says do not accept disease for the pathogen as the disease is the result of the infection of the pathogen. So if you look at the second marking point so susceptible or unvaccinated people are less likely to contact infected people so that's two marks there. So let's move on to the next question.

Now I think I remember actually doing this question as part of my revision for A-Levels and I remember absolutely hating it and always getting it wrong so that is why I am taking you through it now. So let's read it. Malaria is a disease caused by parasites belonging to the genus Plasmodium. Two species that cause malaria are Plasmodium falciparum and Plasmodium vivax.

So we can highlight those. A test strip that uses monoclonal antibodies can be used to determine whether a person is infected by Plasmodium. It can also be used to find which species of Plasmodium they are infected by.

A sample of a person's blood is mixed with a solution containing an antibody A that binds to a protein found in both species of Plasmodium. This antibody has a coloured dye attached. A test strip is then put into the mixture.

The mixture moves up the test strip by capillary action to an absorbent pad. Three other antibodies B, C and D are attached to the test strip. the position of these antibodies and what they bind to is shown in figure one.

We explain why antibody A attaches only to the protein found in species of Plasmodium. Now this question is asking you about antibody action so you need to explain how antibodies are specific and why they are specific as this is an explained question. So this is what I've written. Antibody A has a specific tertiary structure that is complementary to the protein's binding site.

So let's look at the mark scheme. Antibody has a tertiary structure, or more specifically a specific tertiary structure, that is complementary to the binding site and the protein. So we wrote both of those points so we've got two marks.

Let's look at the next section. Antibody B is important if this test shows a person is not infected with Plasmodium. Explain why antibody B is important. So if we go back, antibody B binds to antibody A.

Now the purpose of this is to prevent false negatives, which means the test shows that you are negative for the disease even though you actually are infected. This is as antibody A hasn't bound to any Plasmodium protein. So let's look at the mark scheme.

So it prevents some false negative results since it shows antibody A has moved up the strip or has not bound to plasmodium protein. I think this is, yes this is the last question. So one of these test strips was used to test a sample from a person thought to be infected with plasmodium.

Figure two shows the result. What can you conclude from this result? explain how you reached your conclusion.

So for simplicity we can write here, forget my pen, this band here as you can remember, just change the colour of my pen, represents A and B as antibody A and antibody B are present. This band has C and this band has D. Now as you can see the colour dye is shown for the bands with A and B and C.

So we can conclude that the person is infected with Plasmodium Vivax as antibody C only binds to Plasmodium Vivax proteins. So I've written the person is infected with Plasmodium Vivax because where antibody C is, which is this band here, the dye is coloured which only binds to Plasmodium Vivax proteins proving that the person is infected with this. So this kind of links into the ELISA test and monoclonal antibodies.

So let's look at the mark scheme. So the person is infected with Plasmodium which we have basically written or you can write has malaria. It doesn't matter which one you put you still get the mark. The second marking point is that you need to be specific so infected with Plasmodium vivax. So we have kind of written these first two marking points in the same sentence.

So there is coloured dye where antibody C is present, so we wrote that. That only binds to proteins from vivax or no reaction with antibody for falciparum, as the band for antibody D which binds to plasmodium falciparum has not been coloured. So it says here, person is infected with p-vivax or plasmodium vivax is two marks.

So if you write these in the same sentence you can still get two marks. Right, so that is it. That is all I want to say.

Please comment below if you have any questions at all about this video or about A-level biology in any context and I'll see you in the next video.

Transcript for:Understanding Cell Recognition and Immunity

Transcript for:
Understanding Cell Recognition and Immunity