The IMEx coronavirus interactome: an evolving map of<i>Coronaviridae</i>–host molecular interactions

Perfetto, Livia; Pastrello, Chiara; del-Toro, Noemi; Duesbury, Margaret; Iannuccelli, Marta; Kotlyar, Max; Licata, Luana; Meldal, Birgit; Panneerselvam, Kalpana; Panni, Simona; Rahimzadeh, Negin; Ricard‐Blum, Sylvie; Salwiński, Łukasz; Shrivastava, Anjali; Cesareni, Gianni; Pellegrini, Matteo; Orchard, Sandra; Jurišica, Igor; Hermjakob, Henning; Porras, Pablo

doi:10.1093/database/baaa096

Cited by 37 publications

(26 citation statements)

References 31 publications

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“…Perfetto and colleagues (2020) [ 20 ]. A dataset of physical molecular interactions, manually extracted by IMEx Consortium curators from 86 publications, focused on proteins from SARS-CoV-2, SARS-CoV and other members of the Coronaviridae family, currently comprises over 2,200 binarized interactions.…”

Section: Methodsmentioning

confidence: 99%

RETRACTED: Rationale and Criteria for a COVID-19 Model Framework

Messina

Montaldo

Abbate

et al. 2021

Viruses

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Complex systems are inherently multilevel and multiscale systems. The infectious disease system is considered a complex system resulting from the interaction between three sub-systems (host, pathogen, and environment) organized into a hierarchical structure, ranging from the cellular to the macro-ecosystem level, with multiscales. Therefore, to describe infectious disease phenomena that change through time and space and at different scales, we built a model framework where infectious disease must be considered the set of biological responses of human hosts to pathogens, with biological pathways shared with other pathologies in an ecological interaction context. In this paper, we aimed to design a framework for building a disease model for COVID-19 based on current literature evidence. The model was set up by identifying the molecular pathophysiology related to the COVID-19 phenotypes, collecting the mechanistic knowledge scattered across scientific literature and bioinformatic databases, and integrating it using a logical/conceptual model systems biology. The model framework building process began from the results of a domain-based literature review regarding a multiomics approach to COVID-19. This evidence allowed us to define a framework of COVID-19 conceptual model and to report all concepts in a multilevel and multiscale structure. The same interdisciplinary working groups that carried out the scoping review were involved. The conclusive result is a conceptual method to design multiscale models of infectious diseases. The methodology, applied in this paper, is a set of partially ordered research and development activities that result in a COVID-19 multiscale model.

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Section: Methodsmentioning

confidence: 99%

RETRACTED: Rationale and Criteria for a COVID-19 Model Framework

Messina

Montaldo

Abbate

et al. 2021

Viruses

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“…PIK3C3 it was shown to be involved in the initial phase of the viral life cycle, such as endocytosis, fusion, translation, and replication [ 30 ], and use of PIK3C3 inhibitors have been shown to have antiviral effects [ 31 , 32 ]. We also applied the same approach to a larger list of SARS-CoV-2 interacting proteins (116), recently curated by the IMEx consortium [ 33 ]. This list, in addition to the results of the high throughput approaches, also includes results of low throughput experiments that have been supported by more than one report.…”

Section: Resultsmentioning

confidence: 99%

“…In addition to "stress granules" and "virus entry", this list was found to be significantly enriched in proteins that are functionally closer to innate response to dsRNA, fibrosis, and inflammation (Figure 4A). proteins (116), recently curated by the IMEx consortium [33]. This list, in addition to the results of the high throughput approaches, also includes results of low throughput experiments that have been supported by more than one report.…”

Section: Exploring the Function Of Sars-cov2 Interacting Proteinsmentioning

confidence: 99%

A Resource for the Network Representation of Cell Perturbations Caused by SARS-CoV-2 Infection

Perfetto

Micarelli

Iannuccelli

et al. 2021

Genes

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The coronavirus disease 2019 (COVID-19) pandemic has caused more than 2.3 million casualties worldwide and the lack of effective treatments is a major health concern. The development of targeted drugs is held back due to a limited understanding of the molecular mechanisms underlying the perturbation of cell physiology observed after viral infection. Recently, several approaches, aimed at identifying cellular proteins that may contribute to COVID-19 pathology, have been reported. Albeit valuable, this information offers limited mechanistic insight as these efforts have produced long lists of cellular proteins, the majority of which are not annotated to any cellular pathway. We have embarked in a project aimed at bridging this mechanistic gap by developing a new bioinformatic approach to estimate the functional distance between a subset of proteins and a list of pathways. A comprehensive literature search allowed us to annotate, in the SIGNOR 2.0 resource, causal information underlying the main molecular mechanisms through which severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and related coronaviruses affect the host–cell physiology. Next, we developed a new strategy that enabled us to link SARS-CoV-2 interacting proteins to cellular phenotypes via paths of causal relationships. Remarkably, the extensive information about inhibitors of signaling proteins annotated in SIGNOR 2.0 makes it possible to formulate new potential therapeutic strategies. The proposed approach, which is generally applicable, generated a literature-based causal network that can be used as a framework to formulate informed mechanistic hypotheses on COVID-19 etiology and pathology.

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“…Furthermore, a partial interactome of SARS-CoV-2 and host proteins was extracted from the Network Data Exchange (NDEx) public server ( ) [ 307 , 308 , 309 ] representing the IntAct/IMEx Coronavirus Dataset [ 310 ] to understand the point of interactions of SARS-CoV-2 proteins in the molecular machinery of mucociliary clearance ( Figure 4 b). The extracted viral–host protein interaction network was visualized in Cytoscape 3.7.2 (with CyNDEx-2 application) with the Compound Spring Embedder (CoSE) layout (the detailed methodology is present in the Supplementary Material, M&M S1 ).…”

Section: Coronavirus Disease Manifestation In the Respiratory Systmentioning

confidence: 99%

Mucociliary Respiratory Epithelium Integrity in Molecular Defense and Susceptibility to Pulmonary Viral Infections

Adivitiya

Kaushik

Chakraborty

et al. 2021

Biology

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Mucociliary defense, mediated by the ciliated and goblet cells, is fundamental to respiratory fitness. The concerted action of ciliary movement on the respiratory epithelial surface and the pathogen entrapment function of mucus help to maintain healthy airways. Consequently, genetic or acquired defects in lung defense elicit respiratory diseases and secondary microbial infections that inflict damage on pulmonary function and may even be fatal. Individuals living with chronic and acute respiratory diseases are more susceptible to develop severe coronavirus disease-19 (COVID-19) illness and hence should be proficiently managed. In light of the prevailing pandemic, we review the current understanding of the respiratory system and its molecular components with a major focus on the pathophysiology arising due to collapsed respiratory epithelium integrity such as abnormal ciliary movement, cilia loss and dysfunction, ciliated cell destruction, and changes in mucus rheology. The review includes protein interaction networks of coronavirus infection-manifested implications on the molecular machinery that regulates mucociliary clearance. We also provide an insight into the alteration of the transcriptional networks of genes in the nasopharynx associated with the mucociliary clearance apparatus in humans upon infection by severe acute respiratory syndrome coronavirus-2.

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The IMEx coronavirus interactome: an evolving map ofCoronaviridae–host molecular interactions

Cited by 37 publications

References 31 publications

RETRACTED: Rationale and Criteria for a COVID-19 Model Framework

RETRACTED: Rationale and Criteria for a COVID-19 Model Framework

A Resource for the Network Representation of Cell Perturbations Caused by SARS-CoV-2 Infection

Mucociliary Respiratory Epithelium Integrity in Molecular Defense and Susceptibility to Pulmonary Viral Infections

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