The 2019-novel coronavirus is the main reason for disaster in the recent century.1 The innate immune system is the first line of antiviral defense. The host response and clearance of viral infections significantly rely on type I interferon (T1IFN) expression. It is guessed that SARS-CoV-2, similar to other coronaviruses, compromises the early defense against the virus because of delayed-T1IFN production and neutralizing T1IFN signaling through inhibition of STAT family transcription factor phosphorylation. Suppression of these innate immune mechanisms in infected cells permits coronaviruses without an impressive antiviral response to be proliferated. Also, an early burst of T1IFN leads to conservation against viral infections.2 In this case, it has been demonstrated that the interferons type I and III are the essential components in defense against viruses. Shreds of evidence indicate that SARS-CoV-2 is sensitive to pretreatment with IFN-I/III in vitro. As a viral pathogenic mechanism, CoVs are using different tools for inhibition of induction and signaling of IFN-I.3 Interleukin-29 (IL-29) (interferon-λ1) is a newly discovered member of type III interferon.4 It is mostly produced by maturing dendritic cells and macrophages and involved in many immunological responses and indicates antiviral activity similar to T1IFNs.5 Pegylated form of IFN-λ1 decreased the disease severity and transmission of SARS-CoV-2 in preclinical investigations on different animal models.6 Due to limited research attending the role of IL-29 in COVID-19, it remains undecided whether IL-29 can affect the prognosis of COVID-19 or not. So, in the current study, we aimed to investigate whether IL-29 has a protective role in patients with COVID-19, and decreased levels of this cytokine could predict the severe condition in this disease or not
