Having reported on the T and B cells.
SARS-CoV-2 and Multiple Sclerosis: Not All Immune Depleting DMTs are Equal or Bad.Amor S, Baker D, Khoury SJ, Schmierer K, Giovanonni G.Ann Neurol. 2020 Jun;87(6):794-797
This time DrLove shows off her immunological knowledge to give some insight into how the innate (macrophages and neutrophils) etc. are involved in COVID-19.
Get a cup of Tea, and Relax and enjoy
These are the key elements that help us deal with SARS-CoV-2 and may in part explain that this virus has not been so dvastating to most people with MS on DMT.
Sandra Amor, Laura Fernandez Blanco, David Baker. Innate immunity during SARS-CoV-2: evasion strategies and activation trigger hypoxia and vascular damage. Authorea. August 04, 2020.
Innate immune sensing of viral molecular patterns is essential for development of antiviral responses. Like many viruses SARS CoV-2 has evolved strategies to circumvent innate immune detection including low CpG levels in the genome, glycosylation to shield essential elements including the receptor binding domain, RNA shielding and generation of viral proteins that actively impede anti-viral interferon responses. Together these strategies allow widespread infection and increased viral load. Despite the efforts of immune subversion SARS-CoV-2 infection does activate innate immune pathways inducing a robust type I/III interferon response, production of proinflammatory cytokines, and recruitment of neutrophils and myeloid cells. This may induce hyperinflammation or alternatively, effectively recruit adaptive immune responses that help clear the infection and prevent reinfection. The dysregulation of the renin-angiotensin system due to downregulation of angiotensin converting enzyme 2, the receptor for SARS-CoV-2, together with the activation of type I/III interferon response, and inflammasome response converge to promote free radical production and oxidative stress. This exacerbates tissue damage in the respiratory system but also leads to widespread activation of coagulation pathways leading to thrombosis. Here, we review the current knowledge of the role of the innate immune response following SARS-CoV-2 infection, much of which is based on the knowledge from SARS-CoV and other coronaviruses. Understanding how the virus subverts the initial immune response and how an aberrant innate immune response contributes to the respiratory and vascular damage in COVID-19 may help explain factors that contribute to the variety of clinical manifestations and outcome of SARS-CoV-2 infection.