Shin Jen Lin

TL;DR: It is shown that an AHPND-causing strain of V. parahaemolyticus contains a 70-kbp plasmid with a postsegregational killing system, and that the ability to cause disease is abolished by the natural absence or experimental deletion of the plasmids-encoded homologs of the Photorhabdus insect-related toxins PirA and PirB.

TL;DR: The phylogenetic tree of viral DNA pols further supports the suggestion that WSSV is a distinct virus (likely at the family level) that does not belong to any of the virus families that are currently recognized.

TL;DR: A model of how the host and virus both attempt to regulate apoptosis to their respective advantage is constructed and it is shown that if WSSV succeeds in replicating in sufficient numbers, this will result in the death of the infected penaeid shrimp host.

TL;DR: By analyzing their structures, a possible cytotoxic mechanism, as well as strategies for anti-AHPND drug design, is proposed.

TL;DR: A heterotetrameric interaction model of this binary toxin complex is proposed that provides insight of how conformational changes might activate the PirBvp N-terminal pore-forming domain and should be helpful for devising effective anti-AHPND strategies in the future.