Explaining rapid reinfections in multiple-wave influenza outbreaks: Tristan da Cunha 1971 epidemic as a case study

Camacho, Anton; Ballesteros, Sébastien; Graham, Andrea L.; Carrat, Fabrice; Ratmann, Oliver; Cazelles, Bernard

-Although originally dismissed [13] , the first biological hypothesis (subsequently referred as the 2 Virus, or 2Vi, hypothesis) assumes that two separate viral agents, with different transmissibility, were introduced at the beginning of the epidemic. -The Mutation (Mut) hypothesis assumes that a single initiating virus mutated within an infected host during the first epidemic wave, leading to the emergence of a new antigenic variant [8] . -The All-or-Nothing (AoN) hypothesis assumes that following recovery from infection, some hosts did not develop a long-term protective immunity and remained fully susceptible to reinfection by the same strain [9, 11] . -The Partially Protective Immunity (PPI) hypothesis assumes that following recovery from infection, all hosts developed a long-term immunity that is not fully protective but reduces the risk of reinfection by the same strain [12] . -The In-Host (InH) hypothesis assumes that following infection some hosts were unable to completely eliminate the viral load and suffered from an intra-host recrudescence of infection [13] . -The Window-of-reinfection (Win) hypothesis assumes that following recovery, long-term protective immunity can take some time before becoming effective [9] , resulting in a time window of susceptibility to reinfection by the same strain.