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Piloerection (e.g., goosebumps) is an essential thermoregulatory and social signaling mechanism in non‐human animals. Although humans also experience piloerection—often being perceived as an indicator of profound emotional experiences—its comparatively less effective role in thermoregulation and communication might influence our capacity to monitor its occurrence. We present three studies (total N = 617) demonstrating participants' general inability to detect their own piloerection events and their lack of awareness that piloerection occurs with a similar frequency on multiple anatomical locations. Self‐reported goosebumps were more frequent than observed piloerection. However, only 31.8% of self‐reports coincided with observable piloerection, a bias unrelated to piloerection intensity, anatomical location, heart‐rate variability, or interoceptive awareness. We also discovered a self‐report bias for the forearm, contradicting the observation that piloerection occurs with equal frequency on multiple anatomical locations. Finally, there was low correspondence between self‐reports of being "emotionally moved" and observed piloerection. These counterintuitive findings not only highlight a disconnect between an obvious physiological response and our capacity for self‐monitoring, but they underscore a fascinating divergence between human and non‐human species. Although piloerection is vital in non‐human organisms, the connection between piloerection and psychological experience in humans may be less significant than previously assumed, possibly due to its diminished evolutionary relevance. This research reveals a striking dissociation between an obvious physiological response—piloerection—and human capacity for self‐perception. Although this highlights the limitations of relying on self‐report measures, it also underscores an important divergence between humans and non‐human species. We propose that the relation between piloerection and psychological experience in humans is less pronounced than in other species, potentially due to its diminished role in human evolution. [ABSTRACT FROM AUTHOR]

Severe COVID-19 is characterized by persistent lung inflammation, inflammatory cytokine production, viral RNA, and sustained interferon (IFN) response all of which are recapitulated and required for pathology in the SARS-CoV-2 infected MISTRG6-hACE2 humanized mouse model of COVID-19 with a human immune system 1-20 . Blocking either viral replication with Remdesivir 21-23 or the downstream IFN stimulated cascade with anti-IFNAR2 in vivo in the chronic stages of disease attenuated the overactive immune-inflammatory response, especially inflammatory macrophages. Here, we show SARS-CoV-2 infection and replication in lung-resident human macrophages is a critical driver of disease. In response to infection mediated by CD16 and ACE2 receptors, human macrophages activate inflammasomes, release IL-1 and IL-18 and undergo pyroptosis thereby contributing to the hyperinflammatory state of the lungs. Inflammasome activation and its accompanying inflammatory response is necessary for lung inflammation, as inhibition of the NLRP3 inflammasome pathway reverses chronic lung pathology. Remarkably, this same blockade of inflammasome activation leads to the release of infectious virus by the infected macrophages. Thus, inflammasomes oppose host infection by SARS-CoV-2 by production of inflammatory cytokines and suicide by pyroptosis to prevent a productive viral cycle.