La fiebre bifasica que no siempre es un patron que se presente, se da por dos episodios viremicos en los que interviene la respuesta inmune, la primera viremia esta asociada a la primoinfección, mientras que la segunda a los virus que se forman dentro del organismo hospedero
I'm a dengue and Immuno-Oncology researcher, and I think the first febrile period is due to innate activation: IL-1B, TNFa, IL-8, etc. Then, the innate signatures drop and the there is a lull before the adaptive T cells come out secreting IL-2 family cytokines, which induce high TNFa from macs downstream. That is what we saw with our timed ELISA assays on dengue infection of human PBMC. This second phase is the most dangerous phase in dengue, and the point where close watch on fluid management and hemodynamics is critical
Hi
I'm not a clinician, but I've studied dengue for 30+ years. It appears that the saddleback fever pattern results from the activation of the innate system through TLR ligation and activation in skin fibroblasts and monocyte/macs/DC cells. This results in an early rise in pro-inflammatory cytokines such as IL-1B, IL-12p70, TNFa, etc. These are released by monocyte/macs and DC and activate NK cells of the innate system to mount a "holding" response to check the virus while the adaptive T cell response is mobilizing in the secondary lymphatics. After 48 hours, this response tapers off, and there is a dip in fever symptoms. Then, the massive CD4 and CD8 CTL response comes out of the SLO to clear the infection. The rise in IFN-gamma and IL-2 to mobilize the CTL response has the downstream effect of re-activation of monoctye/macs to increase TNFa, which acts as a pyrogen. This phase is the most dangerous, and can lead to plasma leakage and shock if not managed correctly. After virus clearance, the majority of CTL effectors die by apoptosis, and you see the rise in IL-4 and IL-10, which put the brakes on the immune response, and also promote CTL memory by inducing switch to fatty acid from glycolysis set up by IL-7 and IL-15.
Bruce
why if it's so, the saddle back is not present in almost bacterial\viral infections? I refer to the innate and later acquired immunity response.
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