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Several mechanisms have been proposed to help explain this complex process, including (i) the persistence of HIV viral reservoirs, (ii) the dysregulation of intestinal mucosa and microbial translocation, (iii) the depletion of regulatory T (Treg) cells, and (iv) co-infection with other viruses [13]

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In contrast, acute inflammation induces neuronal plasticity of both synaptic transmission and intrinsic excitability, leading to sickness-like behavior over a relatively short time span, indicating neural receptors against innate immunity and their distinct responses