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HGNC Genes

SARS-CoV-2 proteins

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    Targeting Scavenger Receptor Type B-1 ( SR-B1 HGNC) and Cholesterol Inhibits Entry of SARS-CoV-2 Pseudovirus in Cell Culture

    Authors: Stephen E Henrich; Kaylin M McMahon; Nicole Palacio; Pankaj Bhalla; Pablo Penaloza-MacMaster; Colby Shad Thaxton; Komal Arora; Margo A Brinton; Mukesh Kumar; Adolfo Garcia-Sastre; Robert M Krug; Gaetano T. Montelione

    doi:10.1101/2020.12.14.420133 Date: 2020-12-14 Source: bioRxiv

    The novel human coronavirus, severe acute respiratory syndrome coronavirus 2 MESHD (SARS-CoV-2), emerged in Wuhan, China in late 2019 and has now caused a global pandemic. The disease caused by SARS-CoV-2 is known as COVID-19 MESHD. To date, few treatments for COVID-19 MESHD have proven effective, and the current standard of care is primarily supportive. As a result, novel therapeutic strategies are in high demand. Viral entry into target cells is frequently sensitive to cell membrane lipid composition and membrane organization. Evidence suggests that cell entry of SARS-CoV-2 is most efficient when the target cell plasma membrane is replete with cholesterol; and recent data implicate cholesterol flux through the high-affinity receptor for cholesterol-rich high-density lipoprotein (HDL), called scavenger receptor type B-1 ( SR-B1 HGNC), as critical for SARS-CoV-2 entry MESHD. Here, we demonstrate that a cholesterol-poor synthetic biologic high-density lipoprotein (HDL NP) targets SR-B1 HGNC and inhibits cell entry of a SARS-CoV-2 spike PROTEIN protein pseudovirus. Human cells expressing SR-B1 HGNC are susceptible to SARS-CoV-2 infection MESHD, and viral entry can be inhibited by 50-80% using HDL NPs in an SR-B1 HGNC-dependent manner. These results indicate that HDL NP targeting of SR-B1 HGNC is a powerful potential therapy to combat COVID-19 MESHD and other viral diseases.

    SARS-CoV-2 manipulates the SR-B1 HGNC-mediated HDL uptake pathway for its entry

    Authors: Congwen Wei; Luming Wan; Qiulin Yan; Xiaolin Wang; Jun Zhang; Yanhong Zhang; Jin Sun; Xiaopan Yang; Jing Gong; Chen Fan; Xiaoli Yang; Yufei Wang; Xuejun Wang; Jianmin Li; Huan Yang; Huilong Li; Zhe Zhang; Rong Wang; Peng Du; Yulong Zong; Feng Yin; Wanchuan Zhang; Yumeng Peng; Haotian Lin; Rui Zhang; Wei Chen; Qi Gao; Yuan Cao; Hui Zhong

    doi:10.1101/2020.08.13.248872 Date: 2020-08-14 Source: bioRxiv

    The recently emerged pathogenic severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has spread rapidly, leading to a global COVID-19 pandemic MESHD COVID-19 pandemic MESHD. Binding of the viral spike protein PROTEIN (SARS-2-S) to cell surface receptor angiotensin-converting enzyme 2 ( ACE2 HGNC) mediates host cell infection MESHD. In the present study, we demonstrate that in addition to ACE2 HGNC, the S1 subunit of SARS-2-S binds to HDL and that SARS-CoV-2 hijacks the SR-B1 HGNC-mediated HDL uptake pathway to facilitate its entry. SR-B1 HGNC facilitates SARS-CoV-2 entry into permissive cells by augmenting virus attachment. MAb (monoclonal antibody)-mediated blocking of SARS-2-S-HDL binding and SR-B1 HGNC antagonists strongly inhibit HDL-enhanced SARS-CoV-2 infection MESHD. Notably, SR-B1 HGNC is co-expressed with ACE2 HGNC in human pulmonary and extrapulmonary tissues. These findings revealed a novel mechanism for SARS-CoV-2 entry MESHD and could provide a new target to treat SARS-CoV-2 infection MESHD.

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MeSH Disease
HGNC Genes
SARS-CoV-2 Proteins


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