Tropenpinguin t1_issvs1d wrote
You're more likely to catch another. You're immune system and overall body is stressed and needs time to recover. That's why it's important to rest and avoid strenuous activities like training. If you start to early to hard it can even lead to heart muscle inflammation.
You are more protected from the same strain of cold for some time.
CrateDane t1_isu6m6d wrote
That is generally not correct. The first infection will cause release of PAMP and DAMPs which trigger an induced innate immune response, which will tend to limit the second infection. For example, interleukin 12 will activate natural killer cells, to better kill virus-infected cells. The response also acts on fat and muscle to mobilize nutrients for use (eg. to sustain the required energy for a higher body temperature - which is incidentally another response that limits the growth of some pathogens).
NatAttack3000 t1_isv6o3h wrote
That inflammation doesn't make us super immune for a time, otherwise we would be inflamed all the time. Inflammation comes at a cost - causes cell death, uses up energy. When you have an acute infection, you can deplete things like DCs and other phagocytes briefly and become somewhat immunosuppressed until they recover - this explains the very real phenomenon of secondary infections (eg. Bacterial pneumonia at the tail and of a bad influence infection). So in real terms most people ARE at higher risk of infection following an initial infection, particularly if the infection was severe
CrateDane t1_iswoeir wrote
> When you have an acute infection, you can deplete things like DCs and other phagocytes briefly
That is not really true, GM-CSF for example actually causes proliferation so you have more phagocytic cells available.
It's true that it isn't super-immunity though, and secondary infections can happen in some cases. But generally, an acute infection that the immune system can handle is something that will briefly boost your resistance to other infections. Especially infections of the same type and even more so in the same area - see eg. viral interference.
NatAttack3000 t1_iswpok1 wrote
It does, but GM-CSF is released to create more phagocytic cells because they are being depleted by the infection - DCs definitely die off due to increased apoptosis in sepsis (this contributes to post sepsis immunosuppression) and in severe infections like severe influenza. I suppose this is far more relevant for something relatively severe, with heavy symptoms that you take days to fight. An acute infection with little symptoms is not likely to do this, but I'm still dubious about saying you have more effective innate immunity during an acute infection given how common confections are too... Active inflammation also inhibits other immune functions like for formation of germinal centres, some t cell functions etc, so having extra neutrophils might help with some aspects but not others.
An example is BCG vaccination (a live vaccine) induces emergency granulopoiesis which confers short term protection against bacterial sepsis, so an infectious 'nudge' like thia to the immune system can help it in the short term but you don't want to whack it with a baseball bat (eg. Severe influenza).
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