2.1 Model structure
The model we used resembled the structure of a SEIR
(susceptible-exposed-infected-recovered) epidemiological model (Anderson
and May, 1992), with the inclusion of a spatially-explicit, stochastic,
individual-based structure. It mimics the structure of the model
presented in Lange et al. (2018), with a particular focus on the
mechanisms of virus transmission. We built it and ran it using the
software Netlogo 6.1.1 (Wilensky, 1999).
All processes took place in a grid of 120x120 km (area = 14,400
km2). We divided the grid into 1,600 3x3 km cells,
which represented the smaller simulated spatial unit. Such units,
covering an area of 9 km2, corresponded to a
reasonable estimate of a wild boar’s core home range (Leaper et al.,
1999). Each spatial unit was characterized by its local wild boar
density, defined as the number of individuals having their home range
centred in each cell. This state variable was then used as an input
parameter for the reproduction and dispersal processes.
Each wild boar was characterized by a series of state variables, which
defined its role and behaviour in the model. First, a wild boar was
assigned a sex and classified into one of the three age classes:
juveniles (0-1-year-old), yearlings (1-2 years old); adults (older than
2 years). Additional individual state variables were the reproductive
state (only for females) and the dispersal state (only for yearlings).
Finally, each individual could be classified in one of the eight model
compartments: susceptible, exposed, infected, convalescent, immune,
infectious carcass, non-infectious carcass, hunted. The “convalescent”
compartment included the individuals which survived the acute phase of
the disease and were passing through the recovery process. In such phase
they were still able to transmit the infection for a limited amount of
time, until total recovery. The duration of the infectious period in
convalescents was controlled by parameter χ, whose value was
determined through a numerical optimization process (see below for
details). The “infectious carcass” compartment included the
individuals which succumbed ASF and whose decomposing bodies could still
transmit the virus. Once a carcass lost its potential infectiousness it
was transferred to the absorbing “non-infectious carcass” state. The
duration of a carcass infectious period was controlled by parameterΙ, also derived from the optimization process. Such period was by
default 50% shorter in summer than in winter.
The analytical framework included two scenarios, one in which disease
transmission occurred only through direct contact between susceptible
and infected individuals, or between susceptible individuals and
infected carcasses, another in which we added a third possible
transmission route, which involved the role of ASF convalescents, while
keeping the other two transmission mechanisms in place. Transmission
routes are shown in Fig. 1.