Complexity of immune responses in COVID-19. (June 2021)

• Record Type: Journal Article
• Authors: Mather, Michael William; Jardine, Laura; Talks, Ben; Gardner, Louis; Haniffa, Muzlifah
• Is Part Of: Seminars in immunology. Volume 55(2021)
• Publication Date: 2021-06
• Subjects: COVID-19 -- Immunity -- Immune system diseases -- COVID-19 vaccines -- Host microbial interactions; Immunology -- Periodicals; Allergy and Immunology -- Periodicals; Immunity -- Periodicals; Immunologie -- Périodiques; Electronic journals; 616.079
• DOI: 10.1016/j.smim.2021.101545
• Languages: English
• ISSNs: 1044-5323

Abstract

Highlights: Upper airway innate defenses are crucial for host protection. The release of pro-inflammatory cytokines influences host immune response. A sepsis-like immune dysfunction contributes to host tissue damage. Abstract: The global COVID-19 pandemic has caused substantial morbidity and mortality to humanity. Remarkable progress has been made in understanding both the innate and adaptive mechanisms involved in the host response to the causative SARS-CoV-2 virus, but much remains to be discovered. Robust upper airway defenses are critical in restricting SARS-CoV-2 replication and propagation. Further, the nasal abundance of viral uptake receptor, ACE2, and the host epithelial transcriptional landscape, are associated with differential disease outcomes across different patient cohorts. The adaptive host response to systemic COVID-19 is heterogeneous and complex. Blunted responses to interferon and robust cytokine generation are hallmarks of the disease, particularly at the advanced stages. Excessive immune cell influx into tissues can lead to substantial collateral damage to the host akin to sepsis. This review offers a contemporary summary of these mechanisms of disease and highlights potential avenues for diagnostic and therapeutic development. These include improved disease stratification, targeting effectors of immune-mediated tissue damage, and blunting of immune cell-mediated tissue damage.