Review 3: "A global lipid map reveals host dependency factors conserved across SARS-CoV-2 variants"

Dao Wen Wang

doi:doi:10.1162/2e3983f5.39fe1b90

Review 3: "A global lipid map reveals host dependency factors conserved across SARS-CoV-2 variants"

This preprint examines lipid droplet plasticity as a feature of infection that can be stopped by glycolipid biosynthesis inhibitors and finds that they are a host dependency factor supporting COVID-19. Reviewers found this study reliable and informative for virus evolution.

by Dao Wen Wang

Published onMar 30, 2022

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This Pub is a Review of

A global lipid map reveals host dependency factors conserved across SARS-CoV-2 variants

by Scotland E. Farley, Jennifer E. Kyle, Hans C. Leier, Lisa M. Bramer, Jules Weinstein, Timothy A. Bates, Joon-Yong Lee, Thomas O. Metz, Carsten Schultz, and Fikadu G. Tafesse

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dx.doi.org

Description

AbstractA comprehensive understanding of host dependency factors for SARS-CoV-2 remains elusive. We mapped alterations in host lipids following SARS-CoV-2 infection using nontargeted lipidomics. We found that SARS-CoV-2 rewires host lipid metabolism, altering 409 lipid species up to 64-fold relative to controls. We correlated these changes with viral protein activity by transfecting human cells with each viral protein and performing lipidomics. We found that lipid droplet plasticity is a key feature of infection and that viral propagation can be blocked by small-molecule glycerolipid biosynthesis inhibitors. We found that this inhibition was effective against the main variants of concern (alpha, beta, gamma, and delta), indicating that glycerolipid biosynthesis is a conserved host dependency factor that supports this evolving virus.

Review:

Authors mapped profiles of host lipids following SARS-CoV-2 infection by using nontar-20 geted lipidomics. They found significant changes in host lipid metabolism for 2-64 folds. Also, the manuscript showed that lipid droplet plasticity is a key feature of infection, which is confirmed by the application of small-molecule glycerolipid biosynthesis inhibitors to block the propagation of the virus, and especially this inhibition can protect against the main variants; thus, they conclude that glycerolipid biosynthesis is a conserved host dependency factor for virus evolving. This is an interesting study, and it can address some important issues about lipid and virus evolve.

Some issues need to be improved:

1. Some writings are not easy to understand.

2. The important absence is that they do not include some patient samples to test these lipid profiles. This will be key to linking human disease and scientific findings.