"Lachak" and the Normalization of Nonbelonging: Skilled Migration, Symbolic Capital, and Settlement in Canada.

Since December 2019, millions of individuals worldwide have been affected by Coronavirus Disease 2019 (COVID‐19) (Liu et al. ). The International Committee on Taxonomy of Viruses designated the causative agent as Severe Acute Respiratory Syndrome Coronavirus 2 (SARS‐CoV‐2), which shares approximately 88% sequence identity with bat‐derived SARS‐related coronaviruses but exhibits lower homology with the original SARS‐CoV strain (ICTV ). Clinically, COVID‐19 commonly presents with fever, cough, myalgia and rhinorrhea and may progress to headache, dyspnoea, viral pneumonia and respiratory failure in severe cases (Li et al. ). Radiological findings frequently include alveolar infiltrates, fibrotic streaks, pleural effusion and hypoxemia (Zhou et al. ). These clinical manifestations are closely linked to a dysregulated immune response known as the ‘cytokine storm’, characterized by excessive production of pro‐inflammatory cytokines following viral entry (Velavan and Meyer ). Elevated levels of interleukin‐6 (IL‐6), interleukin‐1β (IL‐1β) and tumour necrosis factor‐α (TNF‐α) promote immune cell infiltration, tissue injury and acute lung damage (Xie et al. ). Pain, particularly myalgia and arthralgia, is frequently reported in patients with COVID‐19 and represents a major contributor to early functional impairment (Lovell et al. ). Pro‐inflammatory cytokines play a pivotal role in pain modulation at both peripheral and central levels. Peripherally, cytokines stimulate macrophages and monocytes to release prostaglandin E, which sensitizes nociceptors and facilitates nociceptive transmission to the central nervous system (Jang et al. ). Centrally, cytokines activate spinal microglial cells, leading to the release of neuromodulators and inflammatory mediators that amplify nociceptive signalling (Song et al. ).