Year: 2026
Type: article
Abstract: Introduction The mammalian protein suppressor of cytokine signaling 1 (SOCS1), can inhibit the activity of Janus Kinase 2 (Jak2), serving to critically limit the magnitude and duration of inflammatory processes and prevent autoimmunity. SOCS1 can be hijacked by viruses, such as SARS-CoV-2, and cancers to prevent Jak2-mediated detection and elimination. Notably, a peptide corresponding to the activation loop of JAK2, pJAK2(1001—1013), has been shown to act as a decoy for SOCS1 binding and suppresses SOCS1 activity. However, the ability of the SOCS1 antagonist, pJAK2(1001—1013), to restore cellular immune responses and enhance viability in response to SARS-CoV-2 infection remains unclear. Methods To evaluate this, we assessed viability (crystal violet), viral replication (confocal microscopy), and gene expression (qPCR) of baby hamster kidney (BHK) cells expressing the human ACE-2 receptor with a laboratory safe SARS-CoV-2 pseudo virus with and without pJAK2 treatment. Results Based on our findings, the SOCS1 antagonist peptide decreased cell death caused by SARS-CoV-2 infection. Treatment with pJAK2 also reduced viral replication compared to cells without treatment. Preliminary findings indicate that pJAK2 can significantly enhance gene expression of proinflammatory cytokines such as IL-1, IL-6, and TNFï•¡. Conclusion These results suggest that the antagonist peptide has potential as a therapeutic agent against SARS-CoV-2 infection, or cancers, by enhancing cell viability and boosting immune responses through activation of the JAK/STAT signaling pathway. Future research will investigate the effects of pJAK2 on viral entry and replication using flow cytometry. Funding Source University of Florida Topic Categories Vaccines and Immunotherapy (VAC)
Source: The Journal of Immunology
Institution: University of Florida
Language: English
Subfield: Oncology
Field: Medicine
Domain: Health Sciences
Open Access status: bronze
OpenAlex ID: W7171555321
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