IFNA1 and COVID-19: Mechanistically, it is currently unclear if the general IFN system deficiency caused by presence of anti-IFN autoantibodies is sufficient to trigger herpesvirus reactivations directly (and thus contribute to disease severity in affected COVID-19 patients) or whether herpesvirus reactivations are an epiphenomenon of severe inflammatory disease caused by uncontrolled SARS-CoV-2 replication in these patients, perhaps who are then also more likely to be treated with steroids that can increase herpesvirus reactivations [33].