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In the DEB model, cVDPVs emerge when population immunity to transmission becomes so low that OPV-related viruses introduced through RI or SIAs can sustain transmission in the population and evolve to successive reversion stages with increasingly high basic reproduction numbers (R0 values) and paralysis-to-infection ratios (PIRs).
When the prevalence in the last of 20 reversion stages chosen to adequately represent the OPV evolution process [ 9, 22] exceeds a given transmission threshold, then fully-reverted VDPVs with assumed equal R0 and PIR as homotypic WPV circulate in the population and a cVDPV outbreak can occur.
Rn in a subpopulation depends on the baseline R0 of the subpopulation and the virus strain (i.e., different R0 values for different serotypes and reversion stages) [ 47, 48] and changes with time depending on vaccination policies, any immunity derived from LPV exposure, and seasonality.
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Whenever the CEI of a reversion stage reaches a certain exportation threshold (E*) we trigger a potentially effective introduction of virus from the same reversion stage into another subpopulation and reset the CEI to zero.
Specifically, we track the cumulative number of effective infections (CEI, defined as the cumulative prevalence of infectiousness-weighted infectious people) in each subpopulation, by virus reversion stage.
The model includes a 6-stage infection process, a 5-stage immunity waning process, and a 20-stage poliovirus reversion process for both fecal-oral and oropharyngeal routes of transmission.
That goes against the tendency in recent years, as does a reversion to longer mountain stages.
To estimate contact VAPP cases, the model tracks all infections in fully susceptible people with OPV-related viruses that did not yet evolve to fully-reverted VDPVs, and assumes that the serotype-specific VAPP rates increase logarithmically with each of 19 stages of reversion toward the serotype-specific paralysis-to-infection rates for VDPV (assumed to be equivalent to homotypic WPV) [ 35].
In 1871, Erasmus Darwin's grandson Charles published "Descent of Man," in which he speculated that the anomalous occurrence in humans of extra nipples represented a reversion to an earlier stage of evolution.
Addition of numerous epiossifications, acquisition of parietal fenestrae at a very late ontogenetic stage, and reversion of adult bone texture to mottled bone texture and finally a return to adult texture during ontogeny are unlikely (although certainly not impossible).
The return of favourable conditions is stimuli for activating metabolic pathways accompanied with excystment (i.e., reversion into the trophozoite stage) leading to reproduction of their species.
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Justyna Jupowicz-Kozak
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