HDL-scavenger receptor B type 1 facilitates SARS-CoV-2 entry

Wei, Congwen; Wan, Luming; Yan, Qiulin; Wang, Xiaolin; Zhang, Jun; Yang, Xiaopan; Zhang, Yanhong; Chen, Fan; Li, Dongyu; Deng, Yong-Qiang; Sun, Jin; Gong, Jing; Yang, Xiaoli; Wang, Yufei; Wang, Xuejun; Li, Jianmin; Yang, Huan; Li, Huilong; Zhang, Zhe; Wang, Rong; Du, Peng; Zong, Yulong; Yin, Feng; Zhang, Wanchuan; Wang, Nan; Peng, Yumeng; Lin, Hanqing; Feng, Jiangyue; Qin, Cheng‐Feng; Chen, Wei; Gao, Qi; Zhang, Rui; Cao, Yuan; Zhong, Hui

doi:10.1038/s42255-020-00324-0

Cited by 218 publications

(230 citation statements)

References 40 publications

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“…Whilst the tissue-specific factors controlling SARS-CoV-2 infection are poorly understood, there is an increasing recognition of the role of additional accessory receptors in viral entry. It has been shown that the high-density lipoprotein scavenger receptor B type 1 (SR-B1) helps facilitate ACE2-dependent coronavirus attachment in vitro 26 , reminiscent of hepatitis C virus infection 27 . Furthermore, treatments targeting SR-B1 reduced the lipoprotein-mediated enhancement…”

Section: Hepatotropism Of Sars-cov-2mentioning

confidence: 99%

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COVID-19 and liver disease: mechanistic and clinical perspectives

Marjot

Webb

Barritt

et al. 2021

Nat Rev Gastroenterol Hepatol

293

306

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Our understanding of the hepatic consequences of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection and its resultant coronavirus disease 2019 (COVID-19) has evolved rapidly since the onset of the pandemic. In this Review, we discuss the hepatotropism of SARS-CoV-2, including the differential expression of viral receptors on liver cell types, and we describe the liver histology features present in patients with COVID-19. We also provide an overview of the pattern and relevance of abnormal liver biochemistry during COVID-19 and present the possible underlying direct and indirect mechanisms for liver injury. Furthermore, large international cohorts have been able to characterize the disease course of COVID-19 in patients with pre-existing chronic liver disease. Patients with cirrhosis have particularly high rates of hepatic decompensation and death following SARS-CoV-2 infection and we outline hypotheses to explain these findings, including the possible role of cirrhosis-associated immune dysfunction. This finding contrasts with outcome data in pharmacologically immunosuppressed patients after liver transplantation who seem to have comparatively better outcomes from COVID-19 than those with advanced liver disease. Finally, we discuss the approach to SARS-CoV-2 vaccination in patients with cirrhosis and after liver transplantation and predict how changes in social behaviours and clinical care pathways during the pandemic might lead to increased liver disease incidence and severity.

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Section: Hepatotropism Of Sars-cov-2mentioning

confidence: 99%

“…of SARS-CoV-2 infection 26 . However, the histological assessment of liver tissue in this study confirmed only sparse hepatic ACE2 expression.…”

Section: Key Pointsmentioning

confidence: 99%

COVID-19 and liver disease: mechanistic and clinical perspectives

Marjot

Webb

Barritt

et al. 2021

Nat Rev Gastroenterol Hepatol

293

306

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“…Although ACE2 has been identified as the receptor for SARS-CoV2, other receptors are being uncovered. These include Neuropilin 12,13 , CD147 14 , Heparan Sulphate proteoglycans 15 and HDL scavenger receptors 16 . Additionally, the highly glycosylated nature of Spike protein could also confer the ability to interact with yet unidentified receptors.…”

Section: Discussionmentioning

confidence: 99%

Niclosamide inhibits SARS-CoV2 entry by blocking internalization through pH-dependent CLIC/GEEC endocytic pathway

Prabhakara

Godbole

Sil

et al. 2020

Preprint

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Many viruses utilize the host endo-lysosomal network to infect cells. Tracing the endocytic itinerary of SARS-CoV2 can provide insights into viral trafficking and aid in designing new therapeutic targets. Here, we demonstrate that the receptor binding domain (RBD) of SARS-CoV2 is internalized via the clathrin and dynamin-independent, pH-dependent CLIC/GEEC (CG) endocytic pathway. Endosomal acidification inhibitors like BafilomycinA1 and NH4Cl, which inhibit the CG pathway, strongly block the uptake of RBD. Using transduction assays with SARS-CoV2 Spike-pseudovirus, we confirmed that these acidification inhibitors also impede viral infection. By contrast, Chloroquine neither affects RBD uptake nor extensively alters the endosomal pH, yet attenuates Spike-pseudovirus entry, indicating a pH-independent mechanism of intervention. We screened a subset of FDA-approved acidification inhibitors and found Niclosamide to be a potential SARS-CoV2 entry inhibitor. Niclosamide, thus, could provide broader applicability in subverting infection of similar category viruses entering host cells via this pH-dependent endocytic pathway.

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“…The first step in cellular infection by SARS-CoV-2 is the binding of S protein to the host cell surface entry factors such as the membrane associated and soluble ACE2 receptor (38) which may be preceded by weaker binding of the S protein to attachment factors such as heparan sulphate (39). Other entry factors that facilitate attachment or entry include neuropilin-1 (40,41), the tyrosine-protein kinase receptor UFO (AXL) (42), CD147 (43), high-density lipoprotein (HDL) scavenger receptor B type 1 (SR-B1) (44), integrins (45,46), angiotension II receptor 1 (AT1) and vasopressin receptor 2, but their role in natural infection is currently unclear. Proteases such as surface TMPRSS2 and endosomal cathespsin L (46) cleave the S protein to activate SARS-CoV-2 entry by endocytosis and membrane fusion (22).…”

Section: Stages Of the Replication Cycle Of Sars-cov-2 Have Been Rapimentioning

confidence: 99%

Lessons learned 1 year after SARS-CoV-2 emergence leading to COVID-19 pandemic

Sridhar

Chiu

et al. 2021

Emerging Microbes & Infections

227

145

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Without modern medical management and vaccines, the severity of the Coronavirus Disease 2019 (COVID-19) pandemic caused by severe acute respiratory syndrome(SARS) coronavirus 2 (SARS-CoV-2) might approach the magnitude of 1894-plague (12 million deaths) and 1918-A(H1N1) influenza (50 million deaths) pandemics. The COVID-19 pandemic was heralded by the 2003 SARS epidemic which led to the discovery of human and civet SARS-CoV-1, bat SARS-related-CoVs, Middle East respiratory syndrome(MERS)-related bat CoV HKU4 and HKU5, and other novel animal coronaviruses. The suspected animal-to-human jumping of 4 betacoronaviruses including the human coronaviruses OC43(1890), SARS-CoV-1(2003), MERS-CoV(2012), and SARS-CoV-2(2019) indicates their significant pandemic potential. The presence of a large reservoir of coronaviruses in bats and other wild mammals, culture of mixing and selling them in urban markets with suboptimal hygiene, habit of eating exotic mammals in highly populated areas, and the rapid and frequent air traffic from these areas are perfect ingredients for brewing rapidly exploding epidemics. The possibility of emergence of a hypothetical SARS-CoV-3 or other novel viruses from animals or laboratories, and therefore needs for global preparedness should not be ignored. We reviewed representative publications on the epidemiology, virology, clinical manifestations, pathology, laboratory diagnostics, treatment, vaccination and infection control of COVID-19 as of 20 January 2021, which is one year after person-to-person transmission of SARS-CoV-2 was announced. The difficulties of mass testing, labour-intensive contact tracing, importance of compliance to universal masking, low efficacy of antiviral treatment for severe disease, possibilities of vaccine or antiviral-resistant virus variants and SARS-CoV-2 becoming another common cold coronavirus are discussed. The chronology of the pandemic An outbreak of acute community-acquired atypical pneumonia of unknown aetiology was reported in Wuhan, the capital of Hubei province in central China, in December 2019. The initial cluster of cases was related to the Huanan seafood wholesale market where wild game animals were also sold (1). During subsequent investigation, severe acute respiratory syndrome (SARS) coronavirus 2 (SARS-CoV-2) was detected in 33 out of 585 environmental samples taken from the market (2). However, 45% of the cases with onset before 1 January 2020 had no apparent link to this market (3). Retrospective molecular clock inference studies using phylogenetic analysis suggested that the earliest cases likely emerged between October and November 2019 (4, 5). The culprit virus was identified using next-generation sequencing on bronchoalveolar lavage fluids of three Wuhan patients (6). The complete genome sequences of SARS-CoV-2 clustered in a distinct clade from SARS-CoV within the genus Sarbecovirus. The draft genome sequence was released on 10 Jan 2020, 10 days after the outbreak was announced. As an escalating number of local cases was reported in Wuhan, a f...

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HDL-scavenger receptor B type 1 facilitates SARS-CoV-2 entry

Cited by 218 publications

References 40 publications

COVID-19 and liver disease: mechanistic and clinical perspectives

COVID-19 and liver disease: mechanistic and clinical perspectives

Niclosamide inhibits SARS-CoV2 entry by blocking internalization through pH-dependent CLIC/GEEC endocytic pathway

Lessons learned 1 year after SARS-CoV-2 emergence leading to COVID-19 pandemic

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