Severe acute respiratory syndrome (SARS) coronavirus 2 (SARS-CoV-2) emerged and spread rapidly worldwide leading to the coronavirus disease 2019 (COVID-19) pandemic. While symptoms vary widely throughout the population there is growing evidence that the innate immune response plays a crucial role in determining the severity of COVID-19(1, 2). Innate immunity utilizes pattern recognition receptors to recognize pathogen-associated molecular proteins (PAMPs) of the invading viruses, which results in the activation of signaling cascades and production of inflammatory cytokines; for example, type I IFN. Proper activation of the innate immune system functions as the first line of defense for host cells and can lead to suppression of viral replication. Interestingly, several key innate immunity signaling cascades utilize post-translational modifications as regulatory mechanisms and are often hijacked by viruses to evade immune detection(3). We will discuss how SARS-CoV-2 specifically evades innate immunity through manipulation of these key signaling cascades through dysregulation of ubiquitination...
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