To the Editor—The correspondence by Cimolai suggests that the activation of nonspecific polyclonal B cells could be responsible for the presence of autoantibodies after severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. Viral infections induce transient autoimmune responses with low titers of autoantibodies. However, progression of this immune state to an established autoimmune disease with production of organ- or tissue-specific autoantibodies has been described in multiple infections [1]. Some viral infections have been shown to trigger autoimmunity due to mechanisms such as epitope spreading, bystander activation, molecular mimicry, and cryptic epitopes [1]. SARS-CoV-2 shares characteristics of other viruses associated with the development of autoimmunity; these include the following: The effect of autoantibodies may partly explain the phenomenon of PCS, in which individuals experience persistent symptoms weeks or months after infection. Evidence indicates that latent autoimmunity may precede the appearance of autoimmune disease several years before...