COVID-19 and Autoimmunity
Are Severe Cases of COVID-19 Related to an Autoimmune Disease?
February 15, 2021
COVID-19, the disease caused by SARS-CoV-2, involves at least two distinct phases. The first phase is attributed to typical progress of respiratory disease by causing fever, cough, loss of taste/smell, and other symptoms typical of respiratory infections. The second phase, which occurs less frequently, is more serious and can include a great variety of multi-organ manifestations, including lung, heart, vasculature, and central nervous system. For more detail, please see the previous Perspective on COVID-19 Long Haulers (https://gvn.org/what-does-it-mean-to-be-a-covid-19-long-hauler/). It is important to note that the vast majority of infected people do not experience severe disease in the first place.
We will consider evidence that the latter stage of COVID-19 associates with autoimmunity. It should be pointed out that autoimmune phenomena falls into two categories: (1) the innate immune system activates adaptive B- or T-cell-mediated immune responses that lead to damaging inflammation (autoimmunity) and (2) the innate immune system causes inflammatory damage directly (autoinflammatory). In both cases, the innate immune system is intimately involved, and mostly, there is a spectrum of these patterns. It should also be noted that it can be difficult to clearly discriminate between functional and dysfunctional immune responses without an understanding of the specific correlates of protection. We will not consider situations in which autoimmunity exists prior to infection, as in the case of patients with pre-existing autoantibodies to type 1 interferons(1). Interestingly, some individuals have pre-existing stereotypic SARS-CoV-2 neutralizing antibodies, produced by naïve B cells, without any known case of viral exposure(2).
Autoimmune phenomena are likely an intimate aspect of the pathogenesis of COVID-19. Indeed, the use of corticosteroids has proven to be an effective treatment for latter stage of COVID-19. We need a significantly better understanding of the mechanisms by which SARS-CoV-2 influences innate immunity and type 1 interferon expression and activity to deal effectively with severe cases of COVID-19.