Biology: Discussion, Questions & Potential Solutions

[vox nihili]

I'll add that since the question refers to malfunctions in program cell death specifically, I would feel inclined to stay away from the action of cytotoxic t cells. Excessive apoptosis in these scenarios would be more so considered due to malfunctions in the immune system rather than malfunctions in the process of programed cell death itself. But that's just my opinion, and I can't speak on behalf of vcaa.

I'm not sure I agree. If the immune system is involved in cell death, then a malfunction in the immune system that causes a change in cell death is by definition also a malfunction in cell death.
Anyway, neither here nor there. VCAA could argue either way to be honest.

[Erutepa]

I'm not sure I agree. If the immune system is involved in cell death, then a malfunction in the immune system that causes a change in cell death is by definition also a malfunction in cell death.
Anyway, neither here nor there. VCAA could argue either way to be honest.

I suppose it just depends on whether you consider the source of the signalling to be part of apoptosis/programmed cell death. I will be interested to see what vcaa end up saying.

[jainamhs]

I'm not sure I agree. If the immune system is involved in cell death, then a malfunction in the immune system that causes a change in cell death is by definition also a malfunction in cell death.
Anyway, neither here nor there. VCAA could argue either way to be honest.

My rationale during the exam was that a malfunction in a specific cell (say, one somatic cell) that lead it to over-produce caspases would only lead to the death of that one cell - in short, I saw no malfunction in the apoptotic mechanisms of a cell that would lead to other cells also dying that seemed reasonable.

Hence, I made the argument that a specific mutant T-helper cell detects many similar cells as foreign and activated cytotoxic T and NK cells to kill this mass cluster of tissue.

[vox nihili]

My rationale during the exam was that a malfunction in a specific cell (say, one somatic cell) that lead it to over-produce caspases would only lead to the death of that one cell - in short, I saw no malfunction in the apoptotic mechanisms of a cell that would lead to other cells also dying that seemed reasonable.

Hence, I made the argument that a specific mutant T-helper cell detects many similar cells as foreign and activated cytotoxic T and NK cells to kill this mass cluster of tissue.

Your rationale for the first bit is close but a little flawed, but that's neither here nor there because you didn't talk about that in the question (it would have been the reasoning in your head). The short and sweet is that a cell can still have a flaw that lowers the threashold for apoptosis, which means that the cells can still propagate viable tissues before the apoptosis kicks in.

If you went to that level of detail in your explanation, you might have got the marks for it. It's certainly a bioplausible argument, and indeed a very intelligent one. I'd be disappointed if VCAA didn't award marks for your answer; it's very sensible.

[jainamhs]

The short and sweet is that a cell can still have a flaw that lowers the threashold for apoptosis, which means that the cells can still propagate viable tissues before the apoptosis kicks in.

Thanks for the feedback, but could you briefly explain this? I'm still having trouble understanding why the circumstances of one cell could affect another or many others.

[vox nihili]

Thanks for the feedback, but could you briefly explain this? I'm still having trouble understanding why the circumstances of one cell could affect another or many others.

If the mutation is germ line, then all cells have it.

Any cell will undergo apoptosis if provoked. Some cells more readily than others (think of a gut cell versus a neuron, the latter being highly resistant to apoptosis). What the mutation in all the cells might do is lower the threshold for apoptosis. Where a cell would need x amount of stress normally to undergo apoptosis, it might only need a lesser amount in the context of the mutation. Therefore you can still propagate entire tissues, but when a low level stressor occurs, rather than the tissues resisting it, they apoptose.

[jainamhs]

If the mutation is germ line, then all cells have it.

Any cell will undergo apoptosis if provoked. Some cells more readily than others (think of a gut cell versus a neuron, the latter being highly resistant to apoptosis). What the mutation in all the cells might do is lower the threshold for apoptosis. Where a cell would need x amount of stress normally to undergo apoptosis, it might only need a lesser amount in the context of the mutation. Therefore you can still propagate entire tissues, but when a low level stressor occurs, rather than the tissues resisting it, they apoptose.

Ah I get it...

So basically the original cell experiences a mutation that lowers it's stress threshold, and hence all daughter cells also inherit this.

That makes sense, thanks vox nihili!

[vox nihili]

Ah I get it...

So basically the original cell experiences a mutation that lowers it's stress threshold, and hence all daughter cells also inherit this.

That makes sense, thanks vox nihili!

That's right! To be clear this is some fairly complex reasoning that, whilst not necessarily beyond a VCE student, would be fairly impressive. I'm sure there are simpler answers out there too

[PopcornTime]

For the question about two pieces of evidence to justify two organisms are different species could you do:

- comparative anatomy + explanation
- if the two organisms were brought together and could not produce fertile offspring, then they are separate separate species

[Erutepa]

For the question about two pieces of evidence to justify two organisms are different species could you do:

- comparative anatomy + explanation
- if the two organisms were brought together and could not produce fertile offspring, then they are separate separate species

I would agree with this response. I think you will get the full marks.

[jainamhs]

Also, though it seems most correct, why does the introduction of antiviral drugs cause a reduction in death rates despite people living with HIV increasing? Shouldn't the HIV infection proportion decrease too?

[Sine]

Also, though it seems most correct, why does the introduction of antiviral drugs cause a reduction in death rates despite people living with HIV increasing? Shouldn't the HIV infection proportion decrease too?

The antiviral drugs basically helps those with HIV to continue living - it doesn't remove the infection thus it increases the life span of those with HIV and decreases the death rates of HIV.

The treatment of HIV is not a cure so this means people who would've previously died with HIV would now continue living thus increasing the amount of people living with HIV.

Hope this helps

[jainamhs]

The antiviral drugs basically helps those with HIV to continue living - it doesn't remove the infection thus it increases the life span of those with HIV and decreases the death rates of HIV.

The treatment of HIV is not a cure so this means people who would've previously died with HIV would now continue living thus increasing the amount of people living with HIV.

Hope this helps

Awesome that makes sense... cheers!

[jainamhs]

And also, what would have been an appropriate answer to the questions asking why the tubes were kept in the dark (or their purpose)? I wrote something along the lines of a control and to see how reduced absorption of light impacts on pH colour as an explanation to the results in the main experimental groups, but really not sure.

Thanks in advance! 😊

[Erutepa]

Also, though it seems most correct, why does the introduction of antiviral drugs cause a reduction in death rates despite people living with HIV increasing? Shouldn't the HIV infection proportion decrease too?

The thing with HIV is that it is a bit sneaky and hides latent/dormant within T helper cells. In this dormancy, antiviral drugs are ineffective. However, HIV will spontaneously reactivate/break dormancy and will start replicating again and be present in the blood. This replicating virus can then be targeted by the antiviral drugs, lowering the number of replicating virus to negligible numbers. As such, the individual can suppress the HIV infection, but will not completely overcome it as there will always be this latent virus hiding in the T helper cells. This also means that as soon as one stops antiviral medication, the presence of replicating virus will rapidly increase and cause problems.

And also, what would have been an appropriate answer to the questions asking why the tubes were kept in the dark (or their purpose)? I wrote something along the lines of a control and to see how reduced absorption of light impacts on pH colour as an explanation to the results in the main experimental groups, but really not sure.

Thanks in advance! 😊

I think I say something like:
To act as a control where the colour change can be compared to that of the algae in the presence of light in order to determine if the colour change is a result of photosynthesis since in the absence of light no photosynthesis will occur.