Biomedical Engineering Reference
In-Depth Information
tective effects are amplified when sick individuals selectively withdraw contacts
from their most socially distant partners (5C).
All disease-reactive network dynamics fundamentally stem from individual
biological immune responses (see Part III, section 4, this volume). Inflammatory
biology generates the illness signs that prompt the healthy to withdraw from the
sick, the sickness behaviors that prompt the sick to withdraw from the healthy,
and the leukocyte responses that modulate host resistance. Even when the im-
mune response fails to save the individual from disease (e.g., Ebola virus), it
may still effectively protect a population by triggering changes in social contact.
An ironic corollary is that the diseases most disastrous for an individual may be
the least dangerous to society as a whole because their spectacular visibility in-
duces the most pronounced changes in network structure. A more sobering cor-
ollary suggests that pathogens that acquire the capacity to undermine behavioral
responses to illness might enjoy a powerful selective advantage. Sickness behav-
ior and the reception of cytokine signals by the brain appear to constitute one
example in which evolution has encoded a critical emergent property of the en-
tire social network in the molecular biology of the individual.
3.2.2. Host Resistance Dynamics
In addition to changing social behavior, individual physiologic processes
also influence host resistance to disease. One example of this involves the ef-
fects of physical or psychological stress, which can impair leukocyte function
and render individuals more vulnerable to infectious diseases (7,8). Reduced
resistance is tantamount to increasing the number of exposures that can transmit
full-blown disease, and thus functionally increases the connectivity of a disease-
transmission network in the vicinity of a stressed individual. Dynamic host resis-
tance can be modeled by varying the probability of infection given an exposure,
as shown in Figure 6. In addition to intra-individual dynamics, between-host
heterogeneity in resistance can also have significant implications. Figure 6B
shows that assigning all individuals a constant resistance of .5 (50% probability
of infection given exposure) produces rapidly bifurcating disease trajectories,
with either hosts or pathogens quickly going extinct. In Figure 6C individual
resistance varies randomly between 0 and 100%, with the same mean level
(50%) as in 6B. This damps the explosive kinetics of 6B, producing fewer popu-
lation extinctions despite the fact that the mean trajectory remains constant. Un-
der these conditions, the addition of illness-reactive link dynamics can be
especially decisive. If uninfected individuals evade one visibly sick contact per
unit time, disease penetrance is substantially retarded (Figure 6D). However,
reducing contact with sick individuals can also have unintended negative effects
if host resistance depends in part on the number of social contacts realized. So-
cial relationships are major sources of individual sustenance, and host resistance
