Neuropilin-1 facilitates SARS-CoV-2 cell entry and infectivity

Cantuti-Castelvetri, Ludovico; Ojha, Ravi; Pedro, Liliana D.; Djannatian, Minou; Franz, Jonas; Kuivanen, Suvi; Meer, Franziska van der; Kallio, Katri; Kaya, Tuğberk; Anastasina, Maria; Smura, Teemu; Levanov, Lev; Szirovicza, Leonóra; Tobi, Allan; Kallio‐Kokko, Hannimari; Österlund, Pamela; Joensuu, Merja; Meunier, Frédéric A.; Butcher, S.J.; Winkler, Martin Sebastian; Mollenhauer, Brit; Helenius, Ari; Gökçe, Özgün; Teesalu, Tambet; Hepojoki, Jussi; Vapalahti, Olli; Stadelmann, Christine; Balistreri, Giuseppe; Simons, Mikael

doi:10.1126/science.abd2985

Cited by 1,554 publications

(1,714 citation statements)

References 39 publications

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“…Remarkably, also in five out of six COVID-19 patients, infection in the nasal olfactory neuroepithelium was demonstrated at autopsy, thus suggesting the existence of an NRP-dependent intranasal brain entry pathway that will be the focus of future inquiry. 145…”

Section: Covid-19 Associated Olfactory Dysfunction and Clinical Implimentioning

confidence: 99%

The central role of the nasal microenvironment in the transmission, modulation, and clinical progression of SARS-CoV-2 infection

et al. 2021

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The novel coronavirus SARS-CoV-2 enters into the human body mainly through the ACE2 + TMPRSS2+ nasal epithelial cells. The initial host response to this pathogen occurs in a peculiar immune microenvironment that, starting from the Nasopharynx-Associated Lymphoid Tissue (NALT) system, is the product of a long evolutionary process that is aimed to first recognize exogenous airborne agents. In the present work, we want to critically review the latest molecular and cellular findings on the mucosal response to SARS-CoV-2 in the nasal cavity and in NALT, and to analyze its impact in the subsequent course of COVID-19. Finally, we want to explore the possibility that the regulation of the systemic inflammatory network against the virus can be modulated starting from the initial phases of the nasal and nasopharyngeal response and this may have several clinical and epidemiological implications starting from a mucosal vaccine development.

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Section: Covid-19 Associated Olfactory Dysfunction and Clinical Implimentioning

confidence: 99%

The central role of the nasal microenvironment in the transmission, modulation, and clinical progression of SARS-CoV-2 infection

et al. 2021

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“…Recent work showed that the NTD of SARS-CoV-2 may bind cellular receptors other than ACE2 and mediate the entry of the virus into cells that do not express ACE2 [35]. Furthermore, the cell-surface protein neuropilin-1 has been reported to facilitate SARS-CoV-2 cell entry, especially into brain cells [36][37][38], although the mechanism is not fully understood.…”

Section: The Spike Glycoproteinmentioning

confidence: 99%

Spike Glycoprotein-Mediated Entry of SARS Coronaviruses

Wang

Xiang

2020

Viruses

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Severe acute respiratory syndrome coronavirus (SARS-CoV) and SARS-CoV-2 are enveloped, positive-sense, single-stranded RNA viruses and causes of epidemic diseases that have resulted in public health emergencies worldwide. Angiotensin-converting enzyme 2 (ACE2) is the receptor that allows the entry of these two viruses into host cells, a key step in the life cycle of the pathogens. The characterization of the interactions of ACE2 with the viral spike glycoproteins and structural studies of the ACE2-binding-induced conformational changes in the viral spike glycoproteins have furthered our understanding of the entry processes of these two viruses, and these studies provide useful information that will facilitate the development of antiviral agents and vaccines to control the diseases.

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“…Both receptors are expressed in the type II pneumocytes, which in turn are infected by both viruses. Apart from the ACE2 receptor, Neuropilin 1 has been recently identified as entry factor that function in concert with ACE2 to facilitate SARS-CoV-2 entry [15,16]. Notwithstanding, expression of ACE2 in combination with a host transmembrane serine protease has been shown to confer susceptibility to SARS-CoV-2.…”

Section: Entry Mechanismsmentioning

confidence: 99%

How SARS-CoV-2 (COVID-19) spreads within infected hosts — what we know so far

Sanyal

2020

Emerging Topics in Life Sciences

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Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the causative agent of the ongoing pandemic of coronavirus disease 2019 (COVID-19), belongs to the betacoronavirus genus and shares high homology to the severe acute respiratory syndrome coronavirus (SARS-CoV) that emerged in 2003. These are highly transmissible and pathogenic viruses which very likely originated in bats. SARS-CoV-2 uses the same receptor, angiotensin-converting enzyme 2 (ACE2) as SARS-CoV, and spreads primarily through the respiratory tract. Although several trials for vaccine development are currently underway, investigations into the virology of SARS-CoV-2 to understand the fundamental biology of the infectious cycle and the associated immunopathology underlying the clinical manifestations of COVID-19 are crucial for identification and rational design of effective therapies. This review provides an overview of how SARS-CoV-2 infects and spreads within human hosts with specific emphasis on key aspects of its lifecycle, tropism and immunopathological features.

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Neuropilin-1 facilitates SARS-CoV-2 cell entry and infectivity

Cited by 1,554 publications

References 39 publications

The central role of the nasal microenvironment in the transmission, modulation, and clinical progression of SARS-CoV-2 infection

The central role of the nasal microenvironment in the transmission, modulation, and clinical progression of SARS-CoV-2 infection

Spike Glycoprotein-Mediated Entry of SARS Coronaviruses

How SARS-CoV-2 (COVID-19) spreads within infected hosts — what we know so far

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