Systemic lupus erythematosus and varicella-like rash following COVID-19 in a previously healthy patient.

We have read the recent article by Slimani et al. entitled “Systemic lupus erythematosus and varicella like rash following COVID‐19 in a previously healthy patient." They have described a healthy 23‐year‐old patient who presented, coincidently with COVID‐19, a systemic lupus erythematosus (SLE). They concluded that the SLE disease was triggered by COVID‐19. They have written in the discussion section that viruses, including parvovirus B19, Epstein–Barr virus, cytomegalovirus, herpes virus‐6, HTLV‐1, hepatitis A and C virus, and rubella virus are linked to SLE and maybe have a possible role in the pathogenesis of the disease. Available data indicate that viral‐induced autoimmunity can be activated through multiple mechanisms, mainly via molecular mimicry. Other mechanisms include epitope spreading, bystander activation, and immortalization of infected B cells. Recent studies have shown that acute viral infections such as parvovirus B19 and EBV can mimic lupus, trigger lupus, or trigger SLE Flares. Slimani et al. should have evaluated the patient for other viral infections, especially EBV. Therefore, they cannot conclude that COVID‐19 alone has definitely triggered SLE. If they had evaluated the presence of infection with the noted viruses at least by enzyme‐linked immunosorbent assay and had obtained negative results, they could strongly link the SARS‐CoV‐2 to SLE. To date, several reports of SLE with COVID‐19 have been published, but none of them tested the patient for other acute or chronic viral infections associated with SLE. , , , A severe immune activation in patients with COVID‐19 results in an acute respiratory distress syndrome, and a cytokine storm. New coronavirus increases interferon‐γ, tumor necrosis factor‐α, macrophage inflammatory protein‐1α, IL‐2, IL‐6, IL‐7, IL‐10, in patients, that show a form of secondary hemophagocytic lymphohistiocytosis or macrophage activation syndrome (sHLH/MAS). Previous studies reported HLH in the background of SLE. Acute infection with coronavirus may produce autoantibodies, such as anti‐CCP antibodies and antinuclear antibodies. Future reports can support or refute this hypothesis.

CONFLICT OF INTERESTS

The authors declare that there are no conflict of interests.