Abstract

Viruses rely on the cellular machinery to replicate and propagate within newly infected individuals. Thus, viral entry into the host cell sets up the stage for productive infection and disease progression. Different viruses exploit distinct cellular receptors for viral entry; however, numerous viral internalization mechanisms are shared by very diverse viral families. Such is the case of Ebola virus (EBOV), which belongs to the filoviridae family, and the recently emerged coronavirus SARS-CoV-2. These two highly pathogenic viruses can exploit very similar endocytic routes to productively infect target cells. This convergence has sped up the experimental assessment of clinical therapies against SARS-CoV-2 previously found to be effective for EBOV, and facilitated their expedited clinical testing. Here we review how the viral entry processes and subsequent replication and egress strategies of EBOV and SARS-CoV-2 can overlap, and how our previous knowledge on antivirals, antibodies, and vaccines against EBOV has boosted the search for effective countermeasures against the new coronavirus. As preparedness is key to contain forthcoming pandemics, lessons learned over the years by combating life-threatening viruses should help us to quickly deploy effective tools against novel emerging viruses.

Highlights

  • Published: 18 January 2021SARS-CoV-2 was identified on 7 January, 2020 as the etiological agent responsible for COVID-19, a severe respiratory disease currently causing a global pandemic

  • EBOV: Ebola virus; C-type lectins (CLECs): C-type lectin receptors; T-cell immunoglobulin and mucin domain (TIM): T-cell immunoglobulin and mucin receptors; TAM: Tyro3-Axl-Mer receptors; Siglec-1: sialic acid-binding Ig-like lectin 1; Niemann-Pick C1 (NPC1): Niemann-Pick receptor C1; SARS-CoV-2: severe acute respiratory syndrome coronavirus 2; angiotensin converting enzyme 2 (ACE2): angiotensin-converting enzyme 2; NRP1/2: neuropilin 1/2; TMPRSS2: transmembrane protease serine 2

  • The host factors that participate in EBOV assembly and budding include a number of components of the endosomal complex required for transport (ESCRT), such as the tumor susceptibility gene 101 (TSG101) and the vacuolar protein sorting-associated 4 (VPS-4) [68]

Read more

Summary

Introduction

SARS-CoV-2 was identified on 7 January, 2020 as the etiological agent responsible for COVID-19, a severe respiratory disease currently causing a global pandemic. EBOV life cycle, therapeutic neutralizing antibodies, and vaccine strategies All these tools laid the foundations to better cope with future viral zoonotic infections. Some of these strategies have been deployed against SARS-CoV-2, and the early efficacy shown in vitro has demonstrated key similitudes between both zoonotic viruses. We compare the life cycle of the filovirus EBOV and the beta-coronavirus SARS-CoV-2, which are very distant RNA-based viruses, focusing on the therapeutic strategies that tackle key steps shared by both viruses. Similitudes between EBOV and SARS-COV-2 highlight the importance of applying previous knowledge and key tools generated in preceding epidemics as a way to boost preparedness and confront new emerging viruses

Setting the Stage for Infection
EBOV Entry Converges with the Endosomal Route of SARS-CoV-2
Transcription and Replication of EBOV and SARS-CoV-2
EBOV Egress and Common Gateways to SARS-CoV-2
Repurposing Drugs against EBOV and SARS-CoV-2: A Shared Strategy to Find
Antiviral
How the Development of EBOV Treatments Based on Monoclonal Antibodies
Vaccines for EBOV and for SARS-CoV-2 Infection
Conclusions and Future Perspectives
Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call