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Abstract
We present a model of contagion that unifies and generalizes existing models of the spread of social influences and
microorganismal infections. Our model incorporates individual memory of exposure to a contagious entity (e.g. a rumor or disease),
variable magnitudes of exposure (dose sizes), and heterogeneity in the susceptibility of individuals. Through analysis and simulation,
we examine in detail the case where individuals may recover from an infection and then immediately become susceptible again
(analogous to the so-called SIS model). We identify three basic classes of contagion models which we call epidemic threshold,
vanishing critical mass, and critical mass classes, where each class of models corresponds to different strategies for prevention or
facilitation. We find that the conditions for a particular contagion model to belong to one of the these three classes depend only on
memory length and the probabilities of being infected by one and two exposures, respectively. These parameters are in principle
measurable for real contagious influences or entities, thus yielding empirical implications for our model. We also study the case
where individuals attain permanent immunity once recovered, finding that epidemics inevitably die out but may be surprisingly
persistent when individuals possess memory.
r 2004 Elsevier Ltd. All rights reserved.
Keywords: Contagion; Epidemic; Memory; Treshold; Dose response; Critical mass; Universality; Bifuraction
0022-5193/$ - see front matter r 2004 Elsevier Ltd. All rights reserved.
doi:10.1016/j.jtbi.2004.09.006
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588 P.S. Dodds, D.J. Watts / Journal of Theoretical Biology 232 (2005) 587–604
1
(a) (b)
0.8
0.6
0.4
0.2
0
0 2 4 6 8 10 12 0 2 4 6 8 10 12
Pinf
1 1
(c) (d)
0.8 0.8
0.6 0.6
0.4 0.4
0.2 0.2
0 0
0 2 4 6 8 10 12 0 2 4 6 8 10 12
K
Fig. 2. Examples of dose–response, i.e. Pinf ðKÞ; the probability an individual becomes infected due to K exposures in the last Tð¼ 12Þ time steps [see
Eq. (2)]. The plots correspond to (a) independent interaction (or disease-like) models with homogeneous dose sizes and thresholds [p ¼ 0:25; dose
distribution f ðdÞ ¼ dðd 1Þ; and threshold distribution gðd Þ ¼ dðd 1Þ]; (b) deterministic threshold models with homogeneous dose sizes and
thresholds [p ¼ 1; f ðdÞ ¼ dðd 1Þ; and gðd Þ ¼ dðd 5Þ]; (c) stochastic threshold models with heterogeneous doses and homogeneous thresholds
[p ¼ 0:9; doses distributed lognormally with unit mean and standard deviation 0:5; and gðd Þ ¼ dðd 5Þ]; and (d), same as (c) but with heterogeneity
in thresholds introduced via a lognormal distribution with mean of 5 as per (c) and standard deviation of 10.
0.6
3. Homogeneous SIS contagion models
φ*
3.1. Epidemic threshold models 0.4
¼1 : ð10Þ
1 ð1 pf Þð1 rÞ
0.4
Fig. 3 shows a comparison between the above equation
and simulation results for T ¼ 2; r ¼ 12; and d¯ ¼ 1:
0.2
Taking the limit of small f in Eq. (6) we find the
epidemic threshold to be
0
r 1 0 0.2 0.4 0.6 0.8 1
pc ¼ ¼ : (11) p
1 þ rðT 1Þ T þ 1=r 1
Checking the special cases of the preceding calculations, Fig. 4. Comparison between simulation (circles) and theory (lines, Eq.
we find pc ¼ r when T ¼ 1 and pc ¼ 1=T when r ¼ 1: (13)) for T ¼ 12; d¯ ¼ 3; and r ¼ 1: For d¯ 41; the homogeneous SIS
contagion model exhibits a saddle-node bifurcation. Shown are the
Denoting the mean time to recovery of an infected, non-zero stable and unstable points. For the theoretical curves, solid
isolated individual by t; we observe t ¼ 1=r 1 and lines represent stable points and dashed ones unstable points. All
Eq. (11) becomes points on the line f ¼ 0 are stable points. The arrows show
trajectories of the system for three example initial conditions.
1 Simulations details are as per Fig. 3. The location of the unstable
pc ¼ : (12)
T þt fixed point curve is determined by binary search.
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(or backwards bifurcations) have also been observed in of individuals whose dose counts are below threshold but
a number of unrelated epidemiological multi-group are still infected since they have not yet recovered. For the
models, arising from differences between groups and d¯ ¼ 1 case, this was straightforward since the only way to
inter-group contact rates (Hadeler and Castillo-Chávez, stay below threshold was to experience a sequence of null
1995; Hadeler and van den Driessche, 1997; Dushoff et exposures. Nevertheless, for ro1; we can formally modify
al., 1998; Kribs-Zaleta and Velasco-Hernandez, 2000; the expression for f given in Eq. (13):
Greenhalgh et al., 2000; Kribs-Zaleta, 2002).
T
X
Although it is not generally possible to obtain an T
expression for f ðpÞ from Eq. (13), we are able to write
f ¼ Gðp; f ; r; TÞ þ ðpf Þi ð1 pf ÞTi ; (15)
¯ i
i¼d
down a closed-form expression involving the position of
the saddle-node bifurcation ðpb ; fb Þ (see Appendix A for where the additional term Gðp; f ; rÞ accounts for the
details): proportion of below threshold individuals who have not
T
X yet recovered. For small values of T and d¯ ; exact
T id¯
0¼ z ð1 zÞTi1 ½i 1 zðT 1Þ; (14) expressions for Gðp; f ; rÞ can be derived and then f can
¯ i be solved for numerically. In Appendix B, we consider two
i¼d
special cases, d¯ ¼ 2 for T ¼ 2 and 3, that illustrate the
where z ¼ pb fb : Using Eq. (14), we solve for z by process of constructing expressions for Gðp; f ; rÞ:
standard numerical means and then use Eq. (13) to These results allow us to explore the movement of the
obtain fb and hence pb : Fig. 5 shows positions of saddle- fixed points with decreasing r. Figs. 6A and B show
node bifurcation points computed for a range of values
of T and d¯ : In all cases, as d¯ increases, the bifurcation 1
point moves upward and to the right of the fixed point
diagram. For small values of d¯ and T, we are able to 0.8
determine ðpb ; fb Þ exactly. For example, for d¯ ¼ 2 and
T ¼ 3; we find that pb ¼ 89 and fb ¼ 27 0.6
32 and that the
φ*
bifurcation is parabolic.
As with epidemic threshold models, the analysis for 0.4
critical mass dynamics can be generalized to include a non-
trivial recovery rate ro1: Now, however, we are unable to 0.2
find a closed-form expression for the fixed points for
general T and d¯ : The difficulty in making such a (A) 0
computation lies in finding an expression for the number 1
1
0.8
0.8 0.6
φ*
0.6 0.4
φ*b
0.2
0.4
0
0.2 0 0.2 0.4 0.6 0.8 1
(B) p
0 Fig. 6. (A) Theory versus simulation for T ¼ 3; d¯ ¼ 2; and varying r.
0 0.2 0.4 0.6 0.8 1 Solid lines represent theoretically derived stable fixed points, dashed
pb lines represent unstable ones, and the squares indicate bifurcation
points (using Eqs. (15) and (46)). From left-to-right, we have r ¼
Fig. 5. Bifurcation points for d¯ 41; f 41; and r ¼ 1; determined 0:01; 0:05; 0:10; 0:15; . . . ; 1:00: The circles correspond to simulation
numerically using Eqs. (13) and (14). The data shown are for T ¼ 3 data for the case r ¼ 0:2 and matches the theoretical curves. (B)
(), T ¼ 6 (&), T ¼ 12 (/), T ¼ 24 (.), and T ¼ 96 (n). The solid Theoretical fixed point curves for T ¼ 2; d¯ ¼ 2; and varying r.
lines guide the eye for the range d¯ ¼ 2 to T 1 with d¯ increasing Bifurcations appear for ro0:3820 0:0001: Otherwise, ðp; f Þ ¼ ð1; 1Þ
with pb : The dashed lines connect to the transcritical bifurcation points is the only fixed point of the system with f 40: The values of r are as
() observed for d¯ ¼ 1: Note that no bifurcations occur when d¯ ¼ per the T ¼ 3 case in A. Circles correspond to simulation results for
T41 (the sole fixed point is f ¼ 1 when p ¼ 1) and when d¯ ¼ T ¼ 1 r ¼ 0:1: For all values of r, both of the above systems possess a line of
(the fixed points lie along the line p ¼ 1 and 0pfp1). stable fixed points described by 0ppo1 and f ¼ 0; i.e. the p-axis.
ARTICLE IN PRESS
594 P.S. Dodds, D.J. Watts / Journal of Theoretical Biology 232 (2005) 587–604
comparisons over a range of r between the solutions of Eq. the k-fold convolution
(15) and simulations for T ¼ 2 and 3, respectively, !
X k
confirming that the agreement is excellent. P d j ¼ d ¼ f f f ðdÞ ¼ f k% ðdÞ: (16)
j¼1
circumstances of the contact (duration, proximity, where we have averaged over all possible ways an
etc.). Our homogeneity assumption of the preceding individual may experience 1pkpT exposures in T
section is therefore unlikely to be justified in any real interactions.
application. Furthermore, as we show below, the more Next, in order to account for any variation d ; we
general case of heterogeneous populations, while pre- must incorporate another layer of averaging into Eq.
serving much of the structure of the homogeneous case, (18) as follows:
also yields a new class of dynamical behavior; thus the
inclusion of heterogeneity not only makes the model f
more realistic, but also provides additional qualitative Z !
1 X
T T
insight. ¼
dd gðd Þ
ðpf Þk ð1 pf ÞTk
While in principle all parameters in the model could 0 k¼1 k
Z 1
be assumed to vary across the population, we focus here
on two parameters—individual threshold d and dose Times dd f k% ðdÞ
d¼d
size d—which when generalized to stochastic variables, !
X
T T
embody the variations in individual susceptibility and ¼ ðpf Þk ð1 pf ÞTk Pk ; ð19Þ
contacts that we wish to capture. We implement these k¼1 k
two sources of heterogeneity as follows. In the case of
where Pk is defined by Eq. (3). An important insight that
thresholds, each individual is assigned a threshold
can be derived immediately from Eq. (19) is that all
drawn randomly from a specified probability distribu-
information concerning the distributions of dose sizes
tion gðd Þ at t ¼ 0 which remains fixed for all t. In effect,
and thresholds is expressed via the fPk g; hence the
this assumption implies that individual characteristics
details of the functions f and g are largely unimportant.
remain roughly invariant on the time-scale of the
In other words, many pairs of f and g can be constructed
dynamics, rather than varying from moment to mo-
to give rise to the same fPk g and hence the same fixed
ment. By contrast, in order to capture the unpredict-
points. For example, any desired fPk g can be realized by
ability of circumstance, we assign dose sizes
a uniform distribution of unit doses f ðdÞ ¼ dðd 1Þ;
stochastically, according to the distribution f ðdÞ; in-
along with a discrete distribution of thresholds
dependent both of time and the particular individuals
between whom the contact occurs. X
T 1
Again considering the more tractable r ¼ 1 version of gðd Þ ¼ P1 dðd 1Þ þ ðPkþ1 Pk Þdðd k 1Þ:
the SIS model, we first examine the effect of allowing k¼1
4.2. Universal classes of contagion Our generalized model therefore exhibits behavior
that falls into one of only three universal classes: class I
In the homogeneous version of the model, we (epidemic threshold), class II (vanishing critical mass),
determined the existence of two classes of dynamics— and class III (critical mass). As we show below, more
epidemic threshold and critical mass—with the former complicated fixed point curves exist (i.e. curves posses-
arising whenever d¯ ¼ 1; and the latter when d¯ X2: In sing two or more saddle-node bifurcation points) but
other words, in homogeneous populations, the condi- nevertheless belong to one of these three universal
tion for differentiating between one class of behavior classes, since together they include all possible behaviors
and another is a discrete one. Once heterogeneity is of the fixed point curves near p ¼ pc :
introduced, however, we observe a smooth transition In addition to identifying three universal classes of
between epidemic threshold and critical mass models behavior, it is also possible to specify the conditions that
governed by a continuous adjustment of the distribu- govern into which class any particular choice of model
tions f and d (or equivalently the fPk g). One consequence parameters will fall. For r ¼ 1; we can calculate when
of this now-continuous transition is the appearance of the transitions between universal classes occur in terms
an intermediate class of models, which we call vanishing of the parameters of interest; i.e. the fPk g (viz. f and g)
critical mass (see Fig. 7). As with pure critical mass and T. This exercise amounts to locating the transcri-
models, this new class is characterized by a saddle-node tical bifurcation and determining when it collides with
bifurcation, but now the lower unstable branch of fixed the saddle-node bifurcation. To locate the transcritical
points crosses the p-axis at pc ; in other words, the bifurcation, we examine the fixed point equation as
required critical mass ‘‘vanishes.’’ The collision of the f ! 0: Since, from Eq. (19),
unstable branch of the saddle node bifurcation with the
horizontal axis also effectively reintroduces a transcri- f ¼ Tpf P1 þ Oðf 2 Þ; (21)
tical bifurcation, in the manner of epidemic threshold we have
models. However, the transcritical bifurcation is differ-
ent from the one observed in epidemic threshold models 1
pc ¼ : (22)
because the rising branch of the bifurcation has TP1
negative, rather than positive, slope and comprises
The position of the transcritical bifurcation is therefore
unstable, rather than stable, fixed points. Vanishing
determined by the memory length T and the fraction of
critical mass dynamics are therefore qualitatively
individuals who are typically infected by one exposure,
distinct from both previously identified classes of
P1 : We see immediately that the transition between
behavior, exhibiting important properties of each: for
classes II and III contagion models occurs when pc ¼ 1;
popc ; they behave like critical mass models; and for
i.e. when
p4pc ; they behave like epidemic threshold models, in
the sense that an infinitesimal initial seed can spread. P1 ¼ 1=T: (23)
1
(a) (b) (c)
0.8
0.6
1 1
(d) (e)
φ*
0.4
0.5 0.5
0.2
0 0
0 0.5 1 0 0.5 1
0
0 0.5 1 0 0.5 1 0 0.5 1
p
Fig. 7. Fixed point curves for the three main classes of contagion models produced by the model, along with transitions between classes. All curves
are determined by numerical solution of Eq. (19) with an error tolerance of 1010 : Here, T ¼ 12; individual doses are lognormally distributed with
mean 1 and a variance of 0.6 for the underlying normal distribution, and thresholds are homogeneously distributed with gðd Þ ¼ dðd d¯ Þ: The
main plots correspond to (a) d¯ ¼ 0:4 (class I), (b) d¯ ¼ 1:5 (class II), and (c) d¯ ¼ 3 (class III). The insets plots (d) and (e), respectively, show fixed
point curves for models at the classes I–II transition (i.e. when P1 ¼ P2 =2 which occurs when d¯ ¼ 0:8600 . . .) and the classes II–III transition (i.e.
when pc ¼ 1 which occurs when d¯ ¼ 1:9100 . . .). In all plots except (e), the intersection between the fixed point curve and the p-axis is a transcritical
bifurcation. In plots (b), (c), and (e), the second bifurcation is a saddle-node bifurcation.
ARTICLE IN PRESS
596 P.S. Dodds, D.J. Watts / Journal of Theoretical Biology 232 (2005) 587–604
0.5
(a) (b)
0
φ*
0.5
(c) (d)
0
0 0.5 1 0 0.5 1
p
Fig. 9. Fixed point curves involving multiple bifurcations. In all four examples, T ¼ 20 , r ¼ 1; and dose size is uniformly held at unity. The different
curves are obtained by adjusting the threshold distribution g which in turn leads to changes in the fPk g [see Eq. (3)]. The curves correspond to (a)
gðdÞ ¼ 0:2dðd 1Þ þ 0:8dðd 6Þ; (b) gðdÞ ¼ 0:15dðd 1Þ þ 0:4dðd 5Þ þ 0:45dðd 12Þ; (c) gðdÞ ¼ 0:075dðd 1Þ þ 0:4dðd 2Þ þ 0:525dðd 12Þ; and
(d) gðdÞ ¼ 0:3dðd 3Þ þ 0:7dðd 12Þ: Note that example (d) consists of two separate fixed point curves. The curves were found numerically by
solving for pðf Þ using Eq. (19). Solid and dashed lines indicate stable and unstable fixed points, respectively.
We observe that when individuals possess a memory generalizes elements of contagion models from both the
of doses (i.e. T41), tmax diverges as p ! 1: Fig. 11 social sciences and epidemiology. A key feature of the
shows tmax ðpÞ for four sample systems with T ¼ 3; 4, 5, current model is that interdependencies between succes-
and 6. We find the divergence of tmax near p ¼ 1 to be sive exposures are introduced in a natural way by
well approximated by varying the length of memory that an individual
maintains of past exposures. Contagion models incor-
tmax / ð1 pÞðT1Þ ; (28)
porating memory correspond to standard notions of
where fits are shown in the inset of Fig. 11. Eq. (28) also contagion in the social sciences (although these models
shows that for a fixed p, the relaxation time increases rarely discuss the role of memory explicitly), while
exponentially with length of memory T for all p, i.e. memoryless contagion models correspond to traditional
models of disease spreading. Our model suggests,
tmax / eaT ; (29)
however, that in reality these two kinds of contagion
where a ¼ lnð1 pÞ40: models may not be entirely distinct. We venture the
Thus, when r ¼ 0; epidemics, while not ever achieving possibility that some infectious diseases may spread in a
a non-zero steady state as in the r40 case, can persist fashion similar to social contagion processes. For
for (arbitrarily) long periods of time. The introduction example, two exposures to an agent sufficiently close
of memory, which allows infected individuals to main- in time may infect an individual with higher probability
tain their dose count above their threshold by repeatedly than would be expected if the exposures acted as
infecting each other, creates an SIR model with independent events. The response of some individuals
strikingly different behavior to the standard memoryless to allergens where separate doses accumulate in the
SIR model. body may be an example of a disease with memory.
Although allergies are not contagious, they demonstrate
that such a phenomenon is biologically plausible—a
6. Concluding remarks possibility that has largely remained unexamined in the
microorganismal dose–response literature (Haas, 2002).
Our aim here has been to develop and analyse in The main result of our analysis is the identification
detail a model of contagion that incorporates and of three universal classes of contagion dynamics, along
ARTICLE IN PRESS
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The second and fourth terms on the right-hand side Appendix B. Exact solution for ro1; d ¼ 2; and T ¼ 2
disappear since dp=df ¼ 0; leaving and 3
@2 U d2 p @U
0¼ þ : (39) For ro1; we have individuals whose cumulative dose
2
@f df 2 @p is below the threshold d¯ but are still infected because
Upon rearrangement, we have they have not yet recovered. To find the proportion of
individuals in this category, we must calculate Gm ; the
d2 p @2 U=@f 2 fraction of individuals whose memory count D [number
¼ : (40)
df 2 @U=@p of successfully infecting interactions, Eq. (1)] last
equaled the threshold m time steps ago and has been
We first compute @U=@p: With U as defined in Eq. (30),
below the threshold since then. The fraction of these
we see that
! individuals still infected will be ð1 rÞm ; i.e. those who
@Uðp; f Þ @ 1 X T T have failed to recover at each subsequent time step. We
¼ Pk ðpf Þk ð1 pf ÞTk write the proportion of infected individuals below the
@p @p f k¼1 k
! threshold as
@ X T T
X
1
¼ Pk ðpf Þk ð1 pf ÞTk
@pf k¼1 k Gðp; f ; r; TÞ ¼ ð1 rÞm Gm ðp; f ; TÞ: (45)
! m¼1
@ X T T
¼ Pk zk ð1 zÞTk Once G is determined, a closed form expression for f ðpÞ
@z k¼1 k is obtained by inserting G into Eq. (15). To determine
!
XT T the fGm g; we explicitly construct all allowable length m
¼ Pk zk ð1 zÞTk1 sequences of 1’s and 0’s such that no subsequence of
k¼1 k length T has d ¼ 2 or more 1’s. The analysis is similar
½kð1 zÞ ðT kÞz for both the T ¼ 2 and 3 cases we consider in this
! appendix, and a generalization to all T is possible.
XT T
¼ Pk zk ð1 zÞTk1 ½k Tz: ð41Þ Below, we first show the forms of G for the two cases
k¼1 k and then provide details of the calculations involved.
Using Eqs. (30) and (35) (i.e. that we are at a bifurcation For T ¼ 3; we obtain
point), the above yields Gðp; f ; r; TÞ ¼ ðpf Þ2 ð1 pf Þ2
@Uðp; f Þ 1 X
1
¼ : ð42Þ 1rþ ð1 rÞm ½wð3Þ ð3Þ
@p p m1 þ wm2
m¼1
Using this result, Eq. (40) becomes
þ 2pf ð1 pf Þwð3Þ
m3
2
d p 2
@ U !
¼ p : (43)
df 2 @f 2
þ pf ð1 pf Þ2 wð3Þ
m4 ; ð46Þ
Next, we find
! where wðTÞm is defined as
2
@ U X
T T
¼ Pk zk3 ð1 zÞTk2 X m ðT 1Þk
½m=T
@f 2 k¼1 k wðTÞ
m ðp; f
Þ ¼ ð1 pf Þmk ðpf Þk :
k¼0
k
½ðk 1Þðk 2Þ 2zðk 1ÞðT 2Þ
(47)
þ z2 ðT 1ÞðT 2Þ: ð44Þ
Upon inserting G into Eq. (15), we have a closed form
As stated above, if the fPk g are parametrized in some expression for f involving p and r as parameters. This
way, and we are interested in finding at what parameter expression can then be solved for numerically yielding
values two bifurcations appear and begin to separate, the fixed point curves in Fig. 6.
then we need to determine when @U=@f ¼ 0 [Eq. (35)] For the T ¼ d¯ ¼ 2 case, we find
and when @2 U=@f 2 ¼ 0 [Eq. (44)].
If, however, the fPk g are fixed and we want to find all Gðp; f ; r; TÞ
bifurcation points along with whether they are forward X
1
or backward bifurcations, then we can check the latter ¼ ðpf Þ2 ð1 pf Þ ð1 rÞm ½wð2Þ ð2Þ
m1 þ pf wm2 : ð48Þ
by finding the sign of d2 p=df2 ¼ 0 [Eq. (43)]. Further m¼1
analysis of these equations may be possible to find We consider the case of d ¼ 2 and T ¼ 3 first. For
conditions on f and g, and thereby the fPk g; that would this specification of the model, there are two ways for an
ensure certain types of model behavior. individual to transition to being below the threshold, i.e.
ARTICLE IN PRESS
602 P.S. Dodds, D.J. Watts / Journal of Theoretical Biology 232 (2005) 587–604
the probability of being above the threshold and then Expanding Eq. (71) to second order about p ¼ pc and
having no reinfections may be written as f ¼ 0; and writing p~ ¼ p pc ; we obtain
becomes infinite. For the heterogeneous version of the We observe that for C 2 ¼ C 3 ¼ ¼ C n ¼ 0; a linearity
model with r ¼ 1 and variable fPk g; we are able to condition in the fPk g must hold, specifically, Pk ¼ kP1
determine the behavior near p ¼ pc as follows. We first for k ¼ 1; . . . ; n: To show this, we rearrange the fC m g
rearrange the right-hand side of Eq. (19) to obtain a given by Eq. (72) as follows, ignoring multiplicative
ARTICLE IN PRESS
604 P.S. Dodds, D.J. Watts / Journal of Theoretical Biology 232 (2005) 587–604
factors and substituting Pk ¼ kP1 : Greenhalgh, D., Diekmann, O., de Jong, M.C.M., 2000. Subcritical
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