Fig. 9: Diagram depicting RSV-driven cholesterol reprogramming in lysosomes to facilitate viral replication. | Nature Communications

Fig. 9: Diagram depicting RSV-driven cholesterol reprogramming in lysosomes to facilitate viral replication.

From: Cholesterol-rich lysosomes induced by respiratory syncytial virus promote viral replication by blocking autophagy flux

Fig. 9

RSV reprograms cholesterol metabolism in infected cells. In brief, RSV blocks cholesterol transport from lysosomes to the ER by reducing LAL activity, activates the SREBP2–LDLR axis, and promotes the uptake and accumulation of exogenous cholesterol in lysosomes in infected cells. The high cholesterol level in infected cells triggers the minus-end transport of autophagosomes and autolysosome formation by altering ORP1L function. On the other hand, cholesterol-rich lysosomes show acidification inhibition and dysfunction and impair autolysosome degradation and autophagic flux, which create sites for RSV-F protein storage. Inhibition of LDLR effectively reverses RSV-induced increase in cholesterol content, thereby blocking RSV infection.

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