Corpus overview


MeSH Disease

HGNC Genes

SARS-CoV-2 proteins

ProteinS (2)

ProteinE (1)


SARS-CoV-2 Proteins
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    The Host Interactome of Spike Expands the Tropism of SARS-CoV-2 MESHD

    Authors: Tom Casimir Bamberger; Sandra Pankow; Salvador Martinez-Bartolome; Jolene Diedrich; Robin Park; John Robert Yates III

    doi:10.1101/2021.02.16.431318 Date: 2021-02-16 Source: bioRxiv

    The SARS-CoV-2 virus causes severe acute respiratory syndrome MESHD ( COVID-19 MESHD) and has rapidly created a global pandemic. Patients that survive may face a slow recovery with long lasting side effects that can afflict different organs. SARS-CoV-2 primarily infects epithelial airway cells that express the host entry receptor Angiotensin Converting Enzyme 2 HGNC ( ACE2 HGNC) which binds to spike protein PROTEIN trimers on the surface of SARS-CoV-2 virions. However, SARS-CoV-2 can spread to other tissues even though they are negative for ACE2 HGNC. To gain insight into the molecular constituents that might influence SARS-CoV-2 tropism MESHD, we determined which additional host factors engage with the viral spike protein PROTEIN in disease-relevant human bronchial epithelial cells (16HBEo-). We found that spike recruited the extracellular proteins laminin and thrombospondin and was retained in the endoplasmatic reticulum (ER) by the proteins DJB11 and FBX2 HGNC which support re-folding or degradation of nascent proteins in the ER. Because emerging mutations of the spike protein PROTEIN potentially impact the virus tropism, we compared the interactome of D614 spike with that of the rapidly spreading G614 mutated spike. More D614 than G614 spike associated with the proteins UGGT1 HGNC, calnexin HGNC, HSP7A and GRP78 HGNC/ BiP HGNC which ensure glycosylation and folding of proteins in the ER. In contrast to G614 spike, D614 spike was endoproteolytically cleaved, and the N-terminal S1 domain was degraded in the ER even though C-terminal S2-only proteoforms remained present. D614 spike also bound more laminin than G614 spike, which suggested that extracellular laminins may function as co-factors for an alternative, S2-only dependent virus entry. Because the host interactome determines whether an infection is productive, we developed a novel proteome-based cell type set enrichment analysis (pCtSEA). With pCtSEA we determined that the host interactome of the spike protein PROTEIN may extend the tropism of SARS-CoV-2 beyond mucous epithelia to several different cell types, including macrophages and epithelial cells in the nephron. An S2-only dependent, alternative infection of additional cell types with SARS-CoV-2 may impact vaccination strategies and may provide a molecular explanation for a severe or prolonged progression of disease in select COVID-19 MESHD patients.

    A proteomic model of SARS-COV2 infection by comparing the interactomes of BRD4 HGNC with BET HGNC-inhibition and SARS-COV2 viral proteins – implications for re-purposing approved drugs or ubiquitin-mediated degradation of select candidates

    Authors: GIRISH NALLUR

    doi:10.21203/ Date: 2020-04-22 Source: ResearchSquare

    The novel coronavirus SARS-CoV-2, the causative agent of COVID-19 MESHD respiratory disease MESHD, has infected 2,029,930 people worldwide and caused 136,320 deaths. Consequently, the hunt for drugs showing efficacy against this deadly disease, or vaccines for prevention, are being intensely investigated. Unfortunately, there is a scarcity of research data on the molecular mechanisms of SARS-CoV-2 infection MESHD for quickly finding effective therapies, or repurposing existing drugs approved by the US FDA. This report models existing knowledge of SARS-COV2 viral proteins and the cellular proteins they interact with by comparisons with BRD4 HGNC interacting proteins identified from B cells, with or without BET HGNC inhibition. The E protein PROTEIN of SARS-COV2 interacts with BRD4 HGNC, and the Spike (S) protein PROTEIN with CANX HGNC. Extensive similarities were observed with published cellular interactants of 13 SARS-COV2 proteins resulting in 47 BRD4 HGNC-interacting protein candidates, with or without BET HGNC inhibition. 61 cellular protein targets and 132 FDA approved drugs which use these proteins as targets are proposed, which can be investigated for efficacy against SARS-COV2 infections MESHD. The implications to SARS-COV2 disease MESHD diagnosis, therapy and vaccine creation are discussed.

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MeSH Disease
HGNC Genes
SARS-CoV-2 Proteins

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