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Nano‐therapeutic strategies to target coronavirus

ABSTRACT: Abstract The coronaviruses have caused severe acute respiratory syndrome (SARS), the Middle East respiratory syndrome (MERS), and the more recent coronavirus pneumonia (COVID‐19). The global COVID‐19 pandemic requires urgent action to develop anti‐virals, new therapeutics, and vaccines. In this review, we discuss potential therapeutics including human recombinant ACE2 soluble, inflammatory cytokine inhibitors, and direct anti‐viral agents such as remdesivir and favipiravir, to limit their fatality. We also discuss the structure of the SARS‐CoV‐2, which is crucial to the timely development of therapeutics, and previous attempts to generate vaccines against SARS‐CoV and MERS‐CoV. Finally, we provide an overview of the role of nanotechnology in the development of therapeutics as well as in the diagnosis of the infection. This information is key for computational modeling and nanomedicine‐based new therapeutics by counteracting the variable proteins in the virus. Further, we also try to effectively share the latest information about many different aspects of COVID‐19 vaccine developments and possible management to further scientific endeavors. The role of nanotechnology in the detection and the therapeutics of the COVID‐19. The image was created with biorender.com.

SUBMITTER: Rauf M

PROVIDER: S-EPMC8250313 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:The interferon (IFN)-stimulated gene product 15 (ISG15) represents an ubiquitin-like protein (Ubl), which in a process termed ISGylation can be covalently linked to target substrates via a cascade of E1, E2, and E3 enzymes. Furthermore, ISG15 exerts functions in its free form both, as an intracellular and as a secreted protein. In agreement with its role as a type I IFN effector, most functions of ISG15 and ISGylation are linked to the anti-pathogenic response. However, also key roles in other cellular processes such as protein translation, cytoskeleton dynamics, exosome secretion, autophagy or genome stability and cancer were described. Ubiquitin-specific protease 18 (USP18) constitutes the major ISG15 specific protease which counteracts ISG15 conjugation. Remarkably, USP18 also functions as a critical negative regulator of the IFN response irrespective of its enzymatic activity. Concordantly, lack of USP18 function causes fatal interferonopathies in humans and mice. The negative regulatory function of USP18 in IFN signaling is regulated by various protein-protein interactions and its stability is controlled via proteasomal degradation. The broad repertoire of physiological functions and regulation of ISG15 and USP18 offers a variety of potential intervention strategies which might be of therapeutic use. Due to the high mutation rates of pathogens which are often species specific and constantly give rise to a variety of immune evasion mechanisms, immune effector systems are under constant evolutionarily pressure. Therefore, it is not surprising that considerable differences in ISG15 with respect to function and sequence exist even among closely related species. Hence, it is essential to thoroughly evaluate the translational potential of results obtained in model organisms especially for therapeutic strategies. This review covers existing and conceptual assay systems to target and identify modulators of ISG15, ISGylation, USP18 function, and protein-protein interactions within this context. Strategies comprise mouse models for translational perspectives, cell-based and biochemical assays as well as chemical probes.

Project description:BackgroundPancreatic ductal adenocarcinoma (PDAC) remains a major challenge in cancer medicine and is characterized by a 5-year survival rate of <10%. Compelling evidence suggests that the devastating disease outcome of PDAC patients is linked to a high degree of intra- and interindividual tumor heterogeneity, which is predominantly installed at the level of gene transcription. The cellular and molecular complexities of the disease explain the poor efficacy of "one-size-fits-all" therapeutic approaches in PDAC treatment and strongly argue for pursuing tailored therapeutic strategies to tackle PDAC. In a highly dynamic manner, a network of transcription factors and epigenetic regulatory proteins temporally and spatially control the diverse transcriptomic states determining PDAC heterogeneity. Given the reversibility of epigenetic processes, pharmacological intervention with key epigenetic drivers of PDAC heterogeneity appeals as a promising concept to shift the transcriptomic phenotype of PDAC toward a less aggressive and more chemosensible state.SummaryIn this review, we discuss the chances and pitfalls of epigenetic treatment strategies in overcoming and shifting molecular and cellular PDAC heterogeneities in order to combat PDAC. To this end, we utilized the keywords "pancreatic cancer," "heterogeneity," and "epigenetics" to search for relevant articles on the database PubMed and selected interventional studies enrolling PDAC patients as displayed in clinicaltrails.gov to generate a synopsis of clinical trials involving epigenetic targeting.Key messagesTargeting epigenetic regulators in PDAC represents a promising concept to reprogram molecular and cellular tumor heterogeneities in the pancreas and hence to modulate the PDAC phenotype in favor of a less aggressive and more therapy susceptible disease course. However, we just start to understand the complex interactions of epigenetic regulators in controlling PDAC plasticity, and a clinical breakthrough utilizing epigenetic targeting in PDAC patients has not been achieved yet. Nevertheless, increasing translational efforts which consider the pleiotropic effects of targeting epigenetic regulation in different cellular compartments of the tumor and that focus on the utility and sequence of combinatory treatment approaches might pave the way toward novel epigenetic treatment strategies in PDAC therapy.

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Nano‐therapeutic strategies to target coronavirus

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