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. 2018 Mar 5;217(3):813–822. doi: 10.1083/jcb.201706157

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© 2018 Cadwell and Debnath

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Figure 2. — LC3-conjugated membranes support viral exit. (A) Picornavirus (circles), such as poliovirus and CVB, promote the formation of LC3-II⁺ double membrane vesicles. LC3-conjugated membranes support viral replication as well as autophagosome-mediated exit without lysiss (AWOL), the exocytic release of multiple virions within a LC3⁺ membrane-bound coat. (B) For certain enveloped viruses (hexagons), such as the herpesviruses Epstein-Barr virus (EBV) and varicella-zoster virus (VZV), LC3-coupled membranes are incorporated into the viral envelope and promote viral release during lytic infection. (C) During IAV (stars) infection, the viral product matrix protein 2 (M2, diamonds) interacts with lipidated LC3 (LC3-II) to block autophagosome-to-autolysosome maturation in the host cell as well as redirect LC3-II to the cell surface. The translocation of LC3-conjugated membranes to the plasma membrane is important for the filamentous budding of IAV and the stability of virions in the extracellular milieu.