Abstract
Like other RNA viruses, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) replicates in host cells, continuously modulating the molecular environment. It encodes 28 multifunctional proteins that induce an imbalance in the metabolic and proteostatic homeostasis in infected cells. Recently, proteomic approaches have allowed the evaluation of the impact of SARS-CoV-2 infection in human cells. Here, we discuss the current use of proteomics in three major application areas: (i) virus-protein interactomics, (ii) differential proteotyping to map the virus-induced changes in different cell types, and (iii) diagnostic methods for coronavirus infectious disease 2019 (COVID-19). Since the nasal cavity is one of the entry sites for SARS-CoV-2, we will also discuss the potential application of olfactory proteomics to provide novel insights into the olfactory dysfunction triggered by SARS-CoV-2 in patients with COVID-19.
Highlights
Since the outbreak of the pandemic in Wuhan (China) in December 2019, coronavirus infectious disease 2019 (COVID-19) has spread globally, causing a crisis in our healthcare systems and in the world economy (Dong et al, 2020; Wu et al, 2020c; Zhou et al, 2020)
The application of proteomic workflows may be highly beneficial to increase our understanding of the pathogenesis of COVID-19, to identify potential therapeutic targets, and even to develop fast and effective diagnostic tests (Struwe et al, 2020; Whetton et al, 2020). In this mini-review, we focus on different proteomic methodologies currently used to decipher novel severe acute respiratory syndrome (SARS)-CoV-2 targets and potential COVID-19 biomarkers (Table 1)
Together with alterations in the thrombotic and metabolic pathways, the mammalian target of rapamycin/hypoxia-inducible factor 1 (HIF-1) signaling route was proposed as a potential therapeutic target against SARS-CoV-2 infection (Appelberg et al, 2020)
Summary
Since the outbreak of the pandemic in Wuhan (China) in December 2019, coronavirus infectious disease 2019 (COVID-19) has spread globally, causing a crisis in our healthcare systems and in the world economy (Dong et al, 2020; Wu et al, 2020c; Zhou et al, 2020). Interactions between human inflammatory and innate immune key players, such as NF-κB repressing factor [NKRF; a repressor of interleukin (IL)-8 and IL-6 production], C1QBP (involved in complement C1 activation), and a great variety of viral non-structural proteins (nsp9, nsp10, etc.), have been described by Liang et al (2020) using AP-LC/MS analysis, explaining the high inflammatory response of patients with COVID-19 (Tay et al, 2020).
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