Lipid droplets: A hallmark of SARS-CoV-2 infection and a potential target for novel antiviral therapeutics
Since its emergence, severe acute respiratory syndrome-coronavirus 2 (SARS-CoV-2) has infected over 110.7 million people and killed over 2.4 million people worldwide. Currently, Remdesivir is the only antiviral approved by the Food and Drug Administration (FDA) to treat the disease caused by SARS-CoV-2, coronavirus disease 2019 (COVID-19). With millions of new COVID-19 cases reported weekly, efficient, and broad-acting antiviral treatments are urgently needed. Host lipid metabolic reprograming and the formation of lipid droplets (LDs) may play a role in SARS-CoV-2 replication and pathogenesis—opening new perspectives for therapeutic strategies against COVID-19. This paper will review the current knowledge on LDs in the SARS-CoV-2 lifecycle and its potential functions in viral replication, assembly, and pro-inflammatory cell moderation. This paper will also highlight key research areas in the field that remain to be understood, including, (i) the possible moonlighting activities of LD-associated viral proteins in the host-cell nucleus of SARS-CoV-2 infected cells, (ii) the potential ability for SARS-CoV-2 to escape or exploit autophagic machinery to enhance viral fitness and survival, and (iii) the impact of diet on one’s susceptibility to SARS-CoV-2 infection. Overall, a better understanding of the SARS-CoV-2 lifecycle and host cell interactions will clarify mechanisms of infection at various levels, inform the design of novel and effective therapeutics and vaccines, and reduce the impact of the COVID-19 pandemic on public health.