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. 2020 Nov 11;133:111008. doi: 10.1016/j.biopha.2020.111008

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© 2020 The Authors

Since January 2020 Elsevier has created a COVID-19 resource centre with free information in English and Mandarin on the novel coronavirus COVID-19. The COVID-19 resource centre is hosted on Elsevier Connect, the company's public news and information website. Elsevier hereby grants permission to make all its COVID-19-related research that is available on the COVID-19 resource centre - including this research content - immediately available in PubMed Central and other publicly funded repositories, such as the WHO COVID database with rights for unrestricted research re-use and analyses in any form or by any means with acknowledgement of the original source. These permissions are granted for free by Elsevier for as long as the COVID-19 resource centre remains active.

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Fig. 1 — Illustration of replication mechanism and potential drug targets of SARS-CoV-2. The SARS-CoV-2 infects the host cell in two ways: either through the plasma membrane or endosomes or through the interaction between its spike protein (S) and cell receptor, ACE2. The SARS-CoV-2 may also enter the host cell through the interaction between its S protein and sialic acid receptors. The TMPRSS2 close to the ACE receptor activates the S protein in the endosome via followed by initiating the fusion of the SARS-CoV-2 membrane with the plasma membrane. The viral RNA is released and translated in the viral polyprotein followed by proteolysis to produce non-structural proteins (NSPs) and form a replication-transcription complex (RTC). The RTC drives the synthesis of (-) RNA. The full length (-) RNA copies of the genome provide the templates for full-length (+) RNA genomes. The transcription further produces a subset of subgenomic RNAs, including those encoding the accessory and structural proteins. The translated structural proteins (M, N, E, and S) and the genomic RNA are assembled into the viral nucleocapsid and envelope in the ER-Golgi intermediate compartment, which is subsequently released via exocytosis. The potential drug targets are shown in red such as inhibitors of viral entry to human cells: chloroquine (CQ)/hydroxychloroquine (HCQ), umifenovir; viral protease inhibitor: lopinavir/ritonavir, ivermectin; RNA-dependent RNA polymerase inhibitor: remdesivir, favipiravir; interleukin (IL)-6 inhibitor; IL-1 inhibitor: anakinra; Janus kinases inhibitor: baricitinib, ruxolitinib, upadacitinib; corticosteroid: dexamethasone; an inhibitor of the cellular serine protease TMPRSS2: camostat mesylate; antimicrobial/antibiotics: azithromycin (AZM); immunoglobulins: convalescent plasma; interferons (IFNs); angiotensin-converting enzyme inhibitor (ACEI); angiotensin II receptor blocker (ARB). Abbreviations: ACE2, angiotensin-converting enzyme 2; TMPRSS2, transmembrane protease serine 2; AT1R, angiotensin II type 1 receptor; SARS-CoV-2, severe acute respiratory syndrome coronavirus 2; RNA, ribonucleic acid; (+) RNA, Positive-strand (5′-to-3′) RNA; (-) RNA, negative-strand (3′-to-5′) RNA; N, nucleocapsid protein; M, matrix protein; E, envelope protein; S, spike protein.