Supplementary Table 5. Current studies investigating COVID-19/ other coronavirus strains and JAK inhibitors.

Study Ref	Title	Authors	Country of study	Year	Summary of results
[57]	Baricitinib as potential treatment for 2019-nCoV acute respiratory disease	Richardson et al	England	2020	ACE2 is a cell-surface protein on lung cells in corona viral infected patients AAK1 receptor promoted endocytosis involved in ACE2 The study suggests the use of Baricitinib to inhibit AAK1 in patients with 2019-nCoV acute respiratory disease, to reduce both the viral entry and the inflammation in patients, using endpoints such as the MuLBSTA score, an early warning model for predicting mortality in viral pneumonia [58].
[59]	The Coronavirus Transmissible Gastroenteritis Virus Evades the Type I Interferon Response through IRE1α-Mediated Manipulation of the MicroRNA miR-30a-5p/SOCS1/3 Axis	Ma et al	China	2018	JAK-signal transducer and activator of transcription (STAT), the suppressor of cytokine signaling protein 1 (SOCS1), and SOCS3. IFN-I are major antiviral molecules, and coronaviruses have evolved diverse strategies to counter the IFN-I response during infection. This study uses endoplasmic reticulum stress and IFN-I production after infection with transmissible gastroenteritis virus (TGEV) to understand how coronavirus-elicited ER stress is actively involved in viral replication and manipulates the host IFN-I response. Increased SOCS1 or SOCS3 expression impaired the IFN-I antiviral response, promoting TGEV replication. IRE1α is an endoplasmic reticulum stress sensor, which led to the increased expression of negative regulators of JAK-STAT SOCS1 and SOCS3. Therefore, IRE1α may be a novel target against coronavirus infection.
[60]	Targeting Coronaviral Replication and Cellular JAK2 Mediated Dominant NF-kappaB Activation for Comprehensive and Ultimate Inhibition of Coronaviral Activity	Yang et al	Taiwan	2017	Tylophorine-based compounds exert broad spectral, potent inhibition of coronaviruses. NF-κB activation is a common pro-inflammatory response of host cells to viral infection. The combination treatment, wherein a tylophorine compound targets TGEV and a JAK2 inhibitor blocks the alternative dominant NF-κB activation mediated by JAK2, is more effective and comprehensive than either one alone and constitutes a feasible approach for the treatment of SARS-CoV or MERS-CoV
[61]	Severe Acute Respiratory Syndrome Coronavirus Evades Antiviral Signaling: Role of nsp1 and Rational Design of an Attenuated Strain	Wathelet et al	USA	2007	Expression of non-structural protein 1 (nsp1) significantly inhibited the activation of SARS-Cov signaling pathways. However, the study results show that SARS-CoV nsp1 does not inhibit JAK phosphorylation.