AbstractIn their recent publication, Rossman et al.  describe how the inherent budding capability of its M2 protein allows influenza A virus to bypass recruitment of the cellular ESCRT machinery enlisted by several other enveloped RNA and DNA viruses, including HIV, Ebola, rabies, herpes simplex type 1 and hepatitis B. Studies from the same laboratory  and other laboratories [3–6] indicate that budding of plasmid-derived virus-like particles can be mediated by the influenza virus hemagglutinin and neuraminidase proteins in the absence of M2. These events are also independent of canonical ESCRT components [2,7]. Understanding how intrinsic properties of these influenza virus proteins permit ESCRT-independent budding expands our understanding of the budding process itself.
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Yondola, M.; Carter, C. Un-“ESCRT”-ed Budding. Viruses 2011, 3, 26-31.
Yondola M, Carter C. Un-“ESCRT”-ed Budding. Viruses. 2011; 3(1):26-31.Chicago/Turabian Style
Yondola, Mark; Carter, Carol. 2011. "Un-“ESCRT”-ed Budding." Viruses 3, no. 1: 26-31.