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. 2022 May 2;33(8):554–568. doi: 10.1016/j.tem.2022.04.011

Figure 2.

Figure 2

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) targets lipid depot and secretory machinery of host cell.

SARS-CoV-2 usurps the host’s lipid metabolism to maximize the replication process by targeting LDs of host cells, the major cellular neutral lipid depot, to obtain energy substrates for sustaining their replication cycles. The virus also uses the host cell’s secretory machinery for egress. Newly synthesized coronavirus proteins in the ER are packaged into mature virions in Golgi compartments. After reaching the Golgi apparatus, SARS-CoV-2 virions traffic to lysosomes and use exocytic lysosomes to egress. These exosomes are deacidified compared with normal lysosomes that do not contain the virions. The virus may undertake (1) a direct route from the Golgi apparatus to lysosomes via the late endosomes or MVBs (orange broken lines) or may adopt (2) a more roundabout path that involves retrograde transport back to the ER/ERGIC to finally reach the lysosomes (orange broken lines). If SARS-CoV-2 enters lysosomes through the late endosomes or MVBs, it is likely that viral contents and exosomes come into physical contact before the extracellular release of exosomes. Orange unbroken lines indicate the path of SARS-CoV-2 egress; broken lines represent possible paths. Blue unbroken lines represent the path of exosome formation leading to their final extracellular release. Abbreviations: ER, endoplasmic reticulum; ERGIC, ER-Golgi intermediate compartment; LD, lipid droplet; MVB, multivesicular body.