A Brief Primer On Interferons And SARS-CoV-2
As the coronavirus disease (COVID-19) pandemic continues to affect millions worldwide, PBL aims to continue to provide support to researchers around the world.
Below you can find a collection of peer-reviewed articles utilizing some of PBL’s products in SARS-CoV-2-related research.
You can also find an article detailing the relationship between IFN and SARS-CoV-2.
Featured Peer-Reviewed Publications
- Liu W, et al. (2021) Activation of STING signaling pathway effectively blocks human coronavirus infection. American Society for Microbiology.
- Rebendenne A, et al. (2021) SARS-CoV-2 triggers an MDA-5-dependent interferon response which is unable to control replication in lung epithelial cells. American Society for Microbiology.
Cited Protein: Human IFN-Alpha Hybrid (Universal Type I IFN) (Cat. # 11200)
- Dorgham K, et al. (2021) Considering Personalized Interferon Beta Therapy for COVID-19. Antimicrobial Agents and Chemotherapy.
- Rao Y, et al. (2021) Targeting CTP Synthetase 1 to Restore Interferon Induction and Impede Nucleotide Synthesis in SARS-CoV-2 Infection. bioRxiv.
Cited ELISA: Mouse IFN-Beta ELISA (Cat. # 42400)
- Miner J, et al. (2020) HSV-1 and Zika Virus but Not SARS-CoV-2 Replicate in the Human Cornea and Are Restricted by Corneal Type III Interferon. Cell Reports.
Cited Protein: Mouse IL-28B/IFN Lambda 3 (Cat. # 12820-1)
- Combes A, et al. (2020) Global Absence and Targeting of Protective Immune States in Severe COVID-19. Nature.
Cited ELISA: Human IFN-Alpha All Subtype ELISA (Cat. # 41115-1)
Article – A Brief Primer on Interferons and SARS-CoV-2
The coronavirus disease 2019 (COVID-19) pandemic has affected millions worldwide since its emergence over a year ago. Similar to other coronaviruses, the causative agent of COVID-19, SARS-CoV-2, is highly transmissible and causes a broad spectrum of disease including mild to severe respiratory symptoms. In addition to significant mortality in high-risk populations, COVID-19 appears to cause long-lasting morbidity in an estimated 10% of all cases, irrespective of age or underlying health factors (long-COVID or chronic COVID syndrome)1. In a remarkably short time, more has been published regarding this disease than any other disease in modern history; however, much remains unknown. A large part of this effort has been focused on how dysregulated immune responses, and type I interferon (IFN) in particular, contribute to disease progression. Underscoring the role of the innate immune system, a recent search for predisposing genetic risk factors for severe disease revealed that human inborn errors of type I IFNs may underlie more than 12.5% of severe COVID-19 cases in men and 2.6% in women2.