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. 2020 Sep 30;93(3):1512–1519. doi: 10.1002/jmv.26469

Figure 3.

Figure 3

Comparison of viral infections by SARS‐CoV‐2 and influenza virus (influenza virus A e.g.). (Left) SARS‐CoV‐2 (capsid in orange) owns an outer protein shell that encapsulates gRNAs (purple) and nucleoproteins, with a mixed coverage of M (pink), S (light brown), and E (teal) proteins. It binds to cell surface (lower part) rich of ACE2 (red) expression through a receptor‐mediated endocytosis (in close view), for intercellular trafficking and unleashing of genetic materials to replicate at ribosome, reassemble at Golgi apparatus, and finally end up with exocytosis. (Right) Influenza A virus has an envelope of bilayer lipids (tan) with HA (green) and NA (mustard) on surface, and enclosed were eight gRNA segments (magenta). When influenza virus attacks, HA binds to sialic acid on the host cell surface (in close view), being engulfed into endosomes. gRNAs were then liberated to enter nucleus for synthesis of mRNAs, being transported to cytoplasm to produce viral proteins, followed by reassembly and budding of new virions for exocytosis. 11 HA, hemagglutinin; mRNA, messenger RNA; NA, neuraminidase; SARS‐CoV‐2, severe acute respiratory syndrome coronavirus 2; gRNA, genomic RNA