1. The spleen is a lymph node containing cytotoxic T cells and phagocytes.
-when it infects the cell, the malaria antigen is expressed on the surface of the red blood cell
- by anchoring the cell to vessel walls, it prevents circulation of the cell into the lymph node, hence preventing Cytotoxic T cells detecting the foreign antigen on the surface
- Therefore the red blood cell will not be destroyed and plasmodium can continue to grow within the cell
2.
- PfEMp1 protein anchors the cell; hence is essential for the survival of plasmodium
- Because the protein is vital for the survival of the species, it cannot afford to have any mutations that will lead to a non-functional protein
- therefore there exists 60 genes to ensure that sufficient, functional PfEMp1 proteins are produced
3.
- a lot, 60 or more genes
- plasmepsin is a vital enzyme for the survival of plasmodium, as it allows the proteins to be secreted
- the correct production of this enzyme is equally important to the anchoring protein because it allows secretion of the protein
Even though its already been answered pretty well i think
1
-There are an abundance of lymph nodes in the spleen which contain numerous T and B lymphocytes as well as other leukocytes which aim to destroy the pathogenic protozoa
-Once it has infected a red blood cell, Plasmodium anchors the cell to the vessel walls in order to prevent it from circulating with the blood to lymph nodes such as the spleen-where the protozoa would be susceptible
2 (was gonna talk about mutations but someone beat me to it so not sure if this is right)
-The PfEMP1 protein is one of great significance for the survival of Plasmodium
-This protein likely acts by attaching to a specific receptor on the red blood cell which then activates a signal transduction pathway
-In order to ensure specificity to a wide arrange of red blood cells on different species able to be infected by Plasmodium, different genes allow the construction of PfEMP1 with a slightly different conformational shapes
-The 60 genes coding for slightly different shapes of PfEMP1 could also be a way for the Plasmodium to get around vaccines which allow for the recipient to have T and B memory cells for a specific form of the protein
3 (0 clue)
This could be either very little due to Plsmepsin only having to work inside the cell and thus not having to have a variety of forms
Or the same number as PfEMP1 (60) or more as it would have to work with the proteins and thus would need to have a wide variety of specific shapes in order to work with a specific protein
1) The spleen is a component of the immune system and contains many white blood cells that would likely detect an infected red blood cell, initiating an immune response against plasmodium. Plasmodium developed the mechanism to reduce the risk of being detected by the hosts immune system.
2) The PfEMP1 is placed on the red blood cells surface, where it is prone to detection by the white blood cells which will initiate an immune response against this specific antigen. By having many different genes, with only one activated per red blood cell, the PfEMP1 antigens will be differently shaped depending on the gene activated, making it harder for the immune system to completely detect and eradicate the plasmodium.
3) 60. One for each of the different PfEMP1 genes, as enzymes are specific to their substrate. The 60 different genes for PfEMP1, each will be a different shape, therefore there will need to be 60 enzymes, one to match each different PfEMP1.
Here's my best guess 
1. -The spleen is a primary lymphoid organ, having an important role in the regulation of erythrocytes and immunity.
-If the red blood cell containing the parasite was able to reach the spleen, it may be recognised as abnormal due to non self protein presented on MHC I markers, and thus potentially be destroyed, including the plasmodium inside.
-Therefore, by developing an anchoring mechanism, P.falciparum is able to avoid the risks associated with entering the spleen and instead grow in a more stable environment, upon the vessel wall.
2. -The immune systems primary method of dealing with parasites such as P.falciparum once inside the body is via a specific immune response.
-Specific immune responses act upon the principle that a particular pathogen will be able to be recognised by a particular antigen it displays.
-By containing 60 genes for the PfEMP1 gene, it allows the parasite to have at least 60 different variants of the PfEMP1 at it's disposal, allowing it to cycle through them, making it increasingly difficult for the specific immune system to identify which RBCs are affected due to the wide variety of antigens that may be displayed upon different infected RBCs surface's.
3. -It is likely that there is more than 60 genes for plasmepsin.
-PfEMP1 is only one of potentially many proteins that P.falciparum exports
-Each enzyme is specific to a certain substrate, and thus there must be a large variety of enzymes to be able to export a large variety of proteins
-Therefore, it is probable that there are 60 different genes coding for Plasmepsin for the PfEMP1 protein alone, with many other potential Plasmepsin genes coding for other exported proteins.
Thanks so much for doing these questions by the way, I've found them super helpful and I really appreciate it
Sorry about the tiny hiatus!
Here are some comments on your answers:
1. All answers were pretty well spot on, certainly for VCE-level knowledge too.
What I expected you to know for question 1 is that the spleen is chock-a-block with lymphoid tissue and therefore there are lots of immune cells there. By anchoring the infected RBC to the wall, they can't be passaged to the spleen for detection and destruction by the immune system.
Some bonus beyond-VCE knowledge: the spleen is responsible for destroying defective RBCs...so if you're a RBC with a parasite in it, you're defective and will be destroyed by the spleen. This is actually the major reason to avoid going to the spleen but it's not knowledge you'd be expected to have, of course
Vaike: don't forget that RBCs don't have MHC class I molecules on them! They're the only say (in VCEland) that doesn't express MHC class I!
2. read sweetcheeks' answer to this, it's spot-on. Vaike's answer is also spot-on if you want more detail.
Gogo14: an interesting idea and not an unreasonable one. There's really no point though having multiples of the one protein as a mechanism to avoid mutation; natural selection does that for you (high selective pressure, so parasites with mutation in PfEMP1 die...)
AhNeon: very close, but the signal transduction is irrelevant. You were given the function of PfEMP1 in the stem
3. AhNeon got the closest for this one.
I did like everyone's thinking of this and I perhaps should have given you more information. Way beyond VCE, of course, but Plasmepsin recognises a small stretch of amino acids, in a huge number of proteins. When it binds to these amino acids, it will cut the protein there, which allows it to be recognised by a transporter and, thus, moved out of the parasite cell. So in actual fact, no matter the type of PfEMP1 you have, the small section that plasmepsin will recognise is exactly the same on each of the proteins; therefore, one plasmepsin can cleave all 60 different PfEMP1 forms.
I'd almost be inclined to give the rest of you marks, because you have thought about this issue really well, particularly in the context of VCE.
Here's the reasoning I wanted you to think of though:
-PfEMP1 is expressed on the surface of infected RBCs and is therefore exposed to the immune system
-PfEMP1 acts as an antigen to induce a specific immune response to
Plasmodium-once a PfEMP1 form is identified by the immune system, the immune system will effectively clear
Plasmodium-in order to avoid the immune system,
Plasmodium will produce a different PfEMP1 from one of the ~60 other genes
-there are 60 genes so as to avoid the immune system
so,
-plasmepsin is found inside the
Plasmodium cell
-it is therefore not exposed to the immune system
-there is thus no benefit in having more than one gene coding for plasmepsin
Just a little tidbit, this stuff about PfEMP1 and plasmepsin (including the means of protein export in
Plasmodium) are all really critical discoveries, as they could provide a way to create drugs (by rational drug design btw) to deal with malaria. Given more than half a million people die each year of malaria, and more than 200 million get the disease every single year, this is obviously huge stuff.
Interestingly, these discoveries were made in Melbourne #straya
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