Plagiarising *Borrowing SnekiSnek's idea to jump on this opportunity and kickstart a new thread for VCE Physics, I'll start one for Biology! 
(everyone can join in obviously 
)
First question!
"Responses of the Adaptive Humoral Immunity can be classified as either primary or secondary responses. Secondary responses are typically stronger, faster-acting and longer-lasting than their corresponding primary response. Explain why."
Moskva
The body already contains Memory B cells from your previous infection, thus recognising the pathogen's antigen and starts creating IgG antibodies. This happens at a faster rate than the first exposure as the body develops memory B cells for the pathogen during the primary immune response.
Interesting answer! You did made some good key points, such as mentioning Memory B cells arising from the primary response. However note that you repeated some information in your answer:
"The body already contains Memory B cells from your previous infection..."
"...as the body develops memory B cells for the pathogen during the primary immune response."
It won't make you lose marks but it will waste writing space and time in tests.
Also you specified IgG antibodies? To be honest I am not sure myself whether this is the only isotype of antibodies produced by Plasma cells differentiated from Memory B cells, but I would assume that isn't the case. So again, best off not mentioning it as it could invalidate your answer.
Hi, how do we determine if a pathogen is intracellular or extracellular and therefore if its humoral or cell mediated
how are T helper cells activated?
are they activated by cytokines
Thanks
hi_hi
Hey!
To be honest I am not too sure on many of the questions (you kinda forget about this stuff after a year haha), but one question I still remember really well is:
"What is a new advancement in science within the last 50 years? And what is its significance?"
I think it was a pretty good question, as it demonstrated scientific interests of the applying-students at a personal level; and whether they actually care about science or not. I think I said something about the Human Genome Project.
Hope this helps 
Hello!
Unfortunately, there isn't a be-all-end-all method for determining whether a pathogen is intracellular or extracellular, but this isn't usually important, and if it is it will probably be given information [in a question]. However, if needed, you can always use logic. For example, helminths can't be intracellular as they are simply too massive.
All pathogens (with the exception of prions) are subject to Adaptive Humoral Immunity responses, but only intracellular pathogens will be subject to (Adaptive) Cell-Mediated Immunity responses. This makes sense, as all pathogens will have to be outside of a host cell eventually -- even viruses need to leave their host cells to infect new ones --, but only those that infect cells can be eliminated by apoptosis of their host cells.
Helper T cells are activated when their receptors bind to ligands (MHC class II) on activated Antigen Presenting Cells (e.g. Dendritic Cell). Cytokines, such as Interleukins, are involved, but this cannot occur independent of APC binding -- in other words the binding of the Naive Helper T cell and APC is the first and crucial step.
ohhh okay thank you very much. Also, I know the second line of defence is non specific, but do interferons also release cytokines when infected with bacteria or just when infected with viruses. Also, I'm just trying to understand how the 2nd line and 3rd line work together if that makes sense. If anyone recommends any youtube videos on this please link to me.
Moskva
also you said that "All pathogens (with the exception of prions) are subject to Adaptive Humoral Immunity response", does this mean virus included as well, as I thought they typically followed cell mediated. If a virus has infected cell it is ...
chemistry1111
I remember having this exact same question last year lmao.
In reality - I think it's both. An antibody could bind to the capsid (protein coat) of the virus, or even the antigens it leaves on the membrane of the infected cell. But I think, for VCE anyway, it's best to pretend that this doesn't happen.
So if they ask a question about a virus, don't go talking about the humoral immune response.
UNLESS they are referencing an anti-body level graph for vaccinations. (Primary exposure, secondary expose, etc...)
Maybe someone else can give a more definite answer, but my suggestion would just be to work out the vibe of the question, and go from there...
Good luck with your year! 
chemistry1111
"Interferons are a group of signalling proteins made and released by host cells in response to the presence of several viruses. " - Wikipedia
They are sought of like a 'help me' flag. They aren't specific to the virus (hence not part of the adaptive immune response) - and they aren't a type of cell. Rather, they are a protein (like cytokines).
"It is now known that type I IFNs are cytokines produced in response to viral, bacterial, and fungal pathogens, as well as parasites." - Source
I presume it's all types of pathogens - but for written responses, probably just mention for viruses.
Yes, antibodies (Adaptive Humoral Response) are incredibly diverse in their functions. They can even target toxins.
In the case of viruses, they can bind to their receptors and prevent them from infecting cells; this is referred to as neutralisation.
Source: Jacaranda Nature of Biology VCE
EDIT: I realised that this could be a bit confusing. So for clarity; just because a pathogen can be targeted by Adaptive Humoral Immunity, it does not mean it cannot also be targeted by (Adaptive) Cell-Mediated Immunity. Viruses are good examples of this, they can be targeted by both.
Does anyone know the answer to this:
What is the immune response in a person receiving their first vaccination? Use the following terms in your response:-plasma cells, memory cells, B cells, antibodies, cytokines
Thanks !
Does anyone know if the cell-mediated response has to occur before the humoral response in order to have T helper cell? Cause I have a question that asks if HIV stimulates a cell-mediated or humoral response and i am unsure.
Upon first vaccination, the humoral immune response is activated where the attenuated pathogen interacts with the b cell that has matching antibodies. The b cell engulfs the pathogen by phagocytosis and presents the antigens on the MHC II markers on the cell's surface. The Th cell binds to the complementary antigen on the MHC II marker and secretes cytokines, that stimulate the B cell to undergo clonal expansion and produce B plasma cell and B memory cells
Hi everyone,
Is anyone able to explain briefly what the difference in function is between the 5' methyl G cap and 3' poly A tail added during RNA processing, as I thought they both functioned to stabilise the mRNA strand but when I came across it in an exam paper it said that the methyl cap protects against attacks from enzymes (which I don't quite understand).
Thanks!
When the mRNA travels into the cytoplasm, a class of enzymes that break down RNA (conveniently called RNases) will be like "you've came to the wrong 'hood" and attempt to degrade the mRNA strand. Even in the absence of cytoplasmic RNases, mRNA isn't very stable on its own without modifications and can react with other chemicals in the cytosol. That's why you need the 7-methylguanosine cap to prevent premature degradation of the mRNA before it's translated
Does anyone know if the cell-mediated response has to occur before the humoral response in order to have T helper cell? Cause I have a question that asks if HIV stimulates a cell-mediated or humoral response and i am unsure.
I can't remember exactly, but here's my understanding:
My guess would be that it stimulates the cell-mediated response (it being a virus and all).... but I'm not 100% sure... Maybe someone else can help
