Abstract
The majority of epidemic models are described by non-linear differential equations which do not have a closed-form solution. Due to the absence of a closed-form solution, the understanding of the precise dynamics of a virus is rather limited. We solve the differential equations of the N-intertwined mean-field approximation of the susceptible-infected-susceptible epidemic process with heterogeneous spreading parameters around the epidemic threshold for an arbitrary contact network, provided that the initial viral state vector is small or parallel to the steady-state vector. Numerical simulations demonstrate that the solution around the epidemic threshold is accurate, also above the epidemic threshold and for general initial viral states that are below the steady-state.
Keywords: NIMFA differential equations, SIS process, Epidemic models, Viral state dynamics
Introduction
Epidemiology originates from the study of infectious diseases such as gonorrhoea, cholera and the flu (Bailey 1975; Anderson and May 1992). Human beings do not only transmit infectious diseases from one individual to another, but also opinions, on-line social media content and innovations. Furthermore, man-made structures exhibit epidemic phenomena, such as the propagation of failures in power networks or the spread of a malicious computer virus. Modern epidemiology has evolved into the study of general spreading processes (Pastor-Satorras et al. 2015; Nowzari et al. 2016). Two properties are essential to a broad class of epidemic models. First, individuals are either infected with the disease (respectively, possess the information, opinion, etc.) or healthy. Second, individuals can infect one another only if they are in contact (e.g., by a friendship). In this work, we consider an epidemic model which describes the spread of a virus between groups of individuals.
We consider a contact network of N nodes, and every node corresponds to a group1 of individuals. If the members of two groups i, j are in contact, then group i and group j can infect one another with the virus. We denote the symmetric adjacency matrix by A and its elements by . If there is a link between node i and node j, then , and otherwise. Hence, the virus directly spreads between two nodes i and j only if . We stress that in most applications it holds that , since infected individuals in group i usually do infect susceptible individuals in the same group i. At any time , we denote the viral state of node i by . The viral state is in the interval [0, 1] and is interpreted as the fraction of infected individuals of group i. N-intertwined mean-field approximation (NIMFA) with heterogeneous spreading parameters (Lajmanovich and Yorke 1976; Van Mieghem and Omic 2014) assumes that the curing rates and infection rates depend on the nodes i and j.
Definition 1
(Heterogeneous NIMFA) At any time , the NIMFA governing equation is
1 |
for every group , where is the curing rate of node i, and is the infection rate from node j to node i.
For a vector , we denote the diagonal matrix with x on its diagonal by . We denote the curing rate matrix . Then, the matrix form of (1) is a vector differential equation
2 |
where is the viral state vector at time t, the infection rate matrix B is composed of the elements , and u is the all-one vector. In this work, we assume that the matrix B is symmetric.
Definition 2
(Steady-State Vector) The steady-state vector is the non-zero equilibrium of NIMFA, which satisfies
3 |
In its simplest form, NIMFA (Van Mieghem et al. 2009) assumes the same infection rate and curing rate for all nodes. More precisely, for homogeneous NIMFA the governing equations (2) reduce to
4 |
For the vast majority of epidemiological, demographical, and ecological models, the basic reproduction number is an essential quantity (Hethcote 2000; Heesterbeek 2002). The basic reproduction number is defined (Diekmann et al. 1990) as “The expected number of secondary cases produced, in a completely susceptible population, by a typical infective individual during its entire period of infectiousness”. Originally, the basic reproduction number was introduced for epidemiological models with only group of individuals. Van den Driessche and Watmough (2002) proposed a definition of the basic reproduction number to epidemic models with groups. For NIMFA (1), the basic reproduction number follows (Van den Driessche and Watmough 2002) as , where denotes the spectral radius of a square matrix M. For the stochastic Susceptible-Infected-Removed (SIR) epidemic process on data-driven contact networks, Liu et al. (2018) argue that the basic reproduction number is inadequate to characterise the behaviour of the viral dynamics, since the number of secondary cases produced by an infectious individual varies greatly with time t. In contrast to the stochastic SIR process, for the deterministic NIMFA equations (1), the basic reproduction number is of crucial importance for the viral state dynamics. Lajmanovich and Yorke (1976) showed that there is a phase transition at the epidemic threshold criterion : If , then the only equilibrium of NIMFA (1) is the origin, which is globally asymptotically stable. Else, if , then there is a second equilibrium, the steady-state , whose components are positive, and the steady-state is globally asymptotically stable for every initial viral state . For real-world epidemics, the regime around epidemic threshold criterion is of particular interest. In practice, the basic reproduction number cannot be arbitrarily great, since natural immunities and vaccinations lead to significant curing rates and the frequency and intensity of human contacts constrain the infection rates . Beyond the spread of infectious diseases, many real-world systems seem to operate in the critical regime around a phase transition (Kitzbichler et al. 2009; Nykter et al. 2008).
The basic reproduction number only provides a coarse description of the dynamics of NIMFA (1). Recently (Prasse and Van Mieghem 2019), we analysed the viral state dynamics for the discrete-time version of NIMFA (1), provided that the initial viral state v(0) is small (see also Assumption 2 in Sect. 3). Three results of Prasse and Van Mieghem (2019) are worth mentioning, since we believe that they could also apply to NIMFA (1) in continuous time. First, the steady-state is exponentially stable. Second, the viral state is (almost always) monotonically increasing. Third, the viral state v(t) is bounded by linear time-invariant systems at any time t. In this work, we go a step further in analysing the dynamics of the viral state v(t), and we focus on the region around the threshold . More precisely, we find the closed-form expression of the viral state for every node i at every time t when , given that the initial state v(0) is small or parallel2 to the steady-state vector .
We introduce the assumptions in Sect. 3. Section 4 gives an explicit expression for the steady-state vector when . In Sect. 5, we derive the closed-form expression for the viral state vector v(t) at any time . The closed-form solution for gives an accurate approximation also for as demonstrated by numerical evaluations in Sect. 6.
Related work
Lajmanovich and Yorke (1976) originally proposed the differential equations (1) to model the spread of gonorrhoea and proved the existence and global asymptotic stability of the steady-state for strongly connected directed graphs. In Lajmanovich and Yorke (1976), Fall et al. (2007), Wan et al. (2008), Rami et al. (2013), Prasse and Van Mieghem (2018) and Paré et al. (2018), the differential equations (1) are considered as the exact description of the virus spread between groups of individuals. Van Mieghem et al. (2009) derived the differential equations (1) as an approximation of the Markovian Susceptible-Infected-Susceptible (SIS) epidemic process (Pastor-Satorras et al. 2015; Nowzari et al. 2016), which lead to the acronym “NIMFA” for “N-Intertwined Mean-Field Approximation” (Van Mieghem 2011; Van Mieghem and Omic 2014; Devriendt and Van Mieghem 2017). The approximation of the SIS epidemic process by NIMFA is least accurate around the epidemic threshold (Van Mieghem et al. 2009; Van Mieghem and van de Bovenkamp 2015). Thus, the solution of NIMFA when , which is derived in this work, might be inaccurate for the description of the probabilistic SIS process.
Fall et al. (2007) analysed the generalisation of the differential equations (1) of Lajmanovich and Yorke (1976) to a non-diagonal curing rate matrix S. Khanafer et al. (2016) showed that the steady-state is globally asymptotically stable, also for weakly connected directed graphs. Furthermore, NIMFA (1) has been generalised to time-varying parameters. Paré et al. (2017) consider that the infection rates3 depend continuously on time t. Rami et al. (2013) consider a switched model in which both the infection rates and the curing rates change with time t. NIMFA (1) in discrete time has been analysed in Ahn and Hassibi (2013), Paré et al. (2018), Prasse and Van Mieghem (2019) and Liu et al. (2020).
In Van Mieghem (2014b), NIMFA (4) was solved for a special case: If the adjacency matrix A corresponds to a regular graph and the initial state is the same4 for every node i, then NIMFA with time-varying, homogeneous spreading parameters has a closed-form solution. In this work, we focus on time-invariant but heterogeneous spreading parameters . We solve NIMFA (1) for arbitrary graphs around the threshold criterion and for an initial viral state v(0) that is small or parallel to the steady-state vector .
Notations and assumptions
The basic reproduction number is determined by the infection rate matrix B and the curing rate matrix S. Thus, the notation is imprecise, since there are infinitely many matrices B, S such that the basic reproduction number equals 1. To be more precise, we consider a sequence of infection rate matrices and curing rate matrices that converges5 to a limit , such that and
For the ease of exposition, we drop the index n and replace and by the notation B and S, respectively. In particular, we emphasise that the assumptions below apply to every element of the sequence. In Sects. 4 to 6, we formally abbreviated the limit process by the notation . For the proofs in the appendices, we use the lengthier but clearer notation . Furthermore, we use the superscript notation to denote the limit of any variable that depends on the infection rate matrix B and the curing rate matrix S. For instance, denotes the limit of the curing rate of node i when . The Landau-notation as denotes that for some constant as . For instance, it holds that as .
In the remainder of this work, we rely on three assumptions, which we state for clarity in this section.
Assumption 1
For every basic reproduction number , the curing rates are positive and the infection rates are non-negative, i.e., and for all nodes i, j. Furthermore, in the limit , it holds that and for all nodes i.
We consider Assumption 1 a rather technical assumption, since only non-negative rates and have a physical meaning. Furthermore, if the curing rates were zero, then the differential equations (1) would describe a Susceptible-Infected (SI) epidemic process. In this work, we focus on the SIS epidemic process, for which it holds that .
Assumption 2
For every basic reproduction number , it holds that and for every node . Furthermore, it holds that for at least one node i.
For the description of most real-world epidemics, Assumption 2 is reasonable for two reasons. First, the total number of infected individuals often is small in the beginning of an epidemic outbreak. (Sometimes, there is even a single patient zero.) Second, a group i often contains many individuals. For instance, the viral state could describe the prevalence of virus in municipality i. Thus, even if there is a considerable total number of infected individuals in group i, the initial fraction would be small.
Assumption 3
For every basic reproduction number , the infection rate matrix B is symmetric and irreducible. Furthermore, in the limit , the infection rate matrix B converges to a symmetric and irreducible matrix.
Assumption 3 holds if and only if the infection rate matrix B (and its limit) corresponds to a connected undirected graph (Van Mieghem 2014a).
The steady-state around the epidemic threshold
We define the effective infection rate matrix W as
5 |
In this section, we state an essential property that we apply to solve the NIMFA equations (1) when the basic reproduction number is close to 1: The steady-state vector converges to a scaled version of the principal eigenvector of the effective infection rate matrix W when .
Under Assumptions 1 and 3, the effective infection rate matrix W is non-negative and irreducible. Hence, the Perron–Frobenius Theorem (Van Mieghem 2014a) implies that the matrix W has a unique eigenvalue which equals the spectral radius . As we show in the beginning of Appendix B, the eigenvalues of the effective infection rate matrix W are real and satisfy . In particular, under Assumptions 1 and 3, the largest eigenvalue , the spectral radius and the basic reproduction number are the same quantity, i.e., .
In Van Mieghem (2012, Lemma 4) it was shown that, for homogeneous NIMFA (4), the steady-state vector converges to a scaled version of the principal eigenvector of the adjacency matrix A when . We generalise the results of Van Mieghem (2012) to heterogeneous NIMFA (1):
Theorem 1
Under Assumptions 1 and 3, the steady-state vector obeys
6 |
where the scalar equals
7 |
and the vector satisfies when the basic reproduction number approaches 1 from above.
Proof
Appendix B.
The viral state dynamics around the epidemic threshold
In Sect. 5.1, we give an intuitive motivation of our solution approach for the NIMFA equations (1) when . In Sect. 5.2, we state our main result.
Motivation of the solution approach
For simplicity, this subsection is confined to the homogeneous NIMFA equations (4). In numerical simulations (Prasse and Van Mieghem 2018), we observed that the viral state matrix , for arbitrary observation times , is severely ill-conditioned. Thus, the viral state v(t) at any time approximately equals the linear combination of orthogonal vectors , and we can write , see also Prasse and Van Mieghem (2020). Here, the functions are scalar. We consider the most extreme case by representing the viral state v(t) by a scaled version of only vector , which corresponds to for a scalar function c(t). The viral state v(t) converges to the steady-state vector as . Hence, a natural choice for the vector is , which implies that as . If and , then the approximation is accurate at all times due to two intuitive reasons.
- If when , then NIMFA (4) is approximated by the linearisation around zero. Hence, it holds that
when . The state v(t) of the linear system (8) converges rapidly to a scaled version of the principal eigenvector of the matrix . Furthermore, Theorem 1 states that when . Thus, the viral state v(t) rapidly converges to a scaled version of the steady-state :8 - Suppose that the viral state v(t) approximately equals to a scaled version of the steady-state vector . (In other words, the viral state v(t) is “almost parallel” to the vector .) Then, it holds that
for some scalar c(t). We insert (9) into the NIMFA equations (4), which yields that9
For homogeneous NIMFA (4), the steady-state equation (3) becomes10
We substitute (11) in (10) and obtain that11
Since around the epidemic threshold, it holds that . Hence, we obtain that12
Left-multiplying (13) by and dividing by yields that13
The logistic differential equation (14) has been introduced by Verhulst (1838) as a population growth model and has a closed-form solution.14
Due to the two intuitive steps above, NIMFA (4) reduces around the threshold to the one-dimension differential equation (14). Solving (14) for the function c(t) gives an approximation of the viral state v(t) by (9). The solution approach is applicable to other dynamics on networks, see for instance (Devriendt and Lambiotte 2020).
However, the reasoning above is not rigorous for two reasons. First, the viral state vector v(t) is not exactly parallel to the steady state . To be more specific, instead of (9) it holds that
15 |
for some error vector which is orthogonal to the steady-state vector . In Sect. 5.2, we use (15) as an ansatz for solving NIMFA (1).
Second, the steady-state vector is not exactly parallel to the principal eigenvector . More precisely, we must consider the vector in (6). Since , the step from (12) to (13) is affected by an error.
The solution around the epidemic threshold
Based on the motivation in Sect. 5.1, we aim to solve the NIMFA differential equations (1) around the epidemic threshold criterion . The ansatz (15) forms the basis for our solution approach. From the orthogonality of the error vector and the steady-state vector , it follows that the function c(t) at time t equals
16 |
The error vector at time t follows from (15) and (16) as
17 |
Our solution approach is based on two steps. First, we show that6 the error term satisfies at every time t when . Hence, the error term converges to zero uniformly in time t. Second, we find the solution of the scalar function c(t) at the limit .
Assumption 2 implies that7 the viral state v(t) does not overshoot the steady-state :
Lemma 1
Under Assumptions 1 to 3, it holds that for all nodes i at every time . Furthermore, it holds that at every time .
Proof
Appendix C.
Theorem 2 states that the error term converges to zero in the order of when .
Theorem 2
Under Assumptions 1 to 3, there exist constants such that the error term at any time is bounded by
18 |
when the basic reproduction number approaches 1 from above.
Proof
Appendix D.
Under Assumption 2, the steady-state is exponentially stable for NIMFA in discrete time (Prasse and Van Mieghem 2019). If the steady-state is exponentially stable, then the error vector goes to zero exponentially fast, since is orthogonal to . Thus, the first addend on the right-hand side in (18) is rather expectable, under the conjecture that the steady-state is exponentially stable also for continuous-time NIMFA (1). Regarding this work, the most important implication of Theorem 2 is that uniformly in time t when , provided the initial value of the error vector is negligibly small.
We define the constant , which depends on the initial viral state v(0), as
19 |
Furthermore, we define the viral slope w, which determines the speed of convergence to the steady-state , as
Then, building on Theorems 1 and 2, we obtain our main result:
Theorem 3
Suppose that Assumptions 1 to 3 hold and that, for some constant , when . Furthermore, define
20 |
Then, there exists some constant such that
21 |
where , when the basic reproduction number approaches 1 from above.
Proof
Appendix E.
We emphasise that Theorem 3 holds for any connected graph corresponding to the infection rate matrix B. Theorem 3 is in agreement with the universality of the SIS prevalence (Van Mieghem 2016). The bound (21) states a convergence of the viral state v(t) to the approximation which is uniform in time t. Furthermore, since both the viral state v(t) and the approximation converge to the steady-state , it holds that when . At time , we obtain from Theorem 3 and (17) that
Since and, by Theorem 1, , we obtain that
Hence, for general the approximation error does not converge to zero faster than , and the bound (21) is best possible (up to the constant ) when . With (17), the term in Theorem 2 can be expressed explicitly with respect to the initial viral state v(0) and the steady-state . In particular, it holds that . Furthermore, if the initial viral state v(0) is parallel to the steady-state vector , then it holds that . Thus, if the initial viral state v(0) is small or parallel to the steady-state vector , then it holds that and the bound (21) on the approximation error vector becomes
22 |
The time-dependent solution to NIMFA (1) at the epidemic threshold criterion depends solely on the viral slope w, the steady-state vector and the initial viral state v(0). The viral slope w converges to zero as . Thus, Theorem 3 implies that the convergence time to the steady-state goes to infinity when , even though the steady-state converges to zero. More precisely, it holds:
Corollary 1
Suppose that Assumptions 1 and 3 hold and that the initial viral state v(0) equals for some scalar . Then, for any scalar , the largest time at which the viral state satisfies for every node i converges to
when the basic reproduction number approaches 1 from above.
Proof
Appendix F.
Corollary 2
Suppose that Assumptions 1 to 3 hold and that, for some constant , when . Furthermore, define
23 |
Then, there exists some constant such that
where , when the basic reproduction number approaches 1 from above.
In contrast to Theorem 3, the approximation error in Corollary 2 does not converge to zero when , since we replaced the steady-state by the first-order approximation of Theorem 1. Corollary 2 implies that
24 |
at every time t when , provided that the initial viral state v(0) is small or parallel to the steady-state vector . From (24) it follows that, around the epidemic threshold criterion , the eigenvector centrality (Van Mieghem 2010) fully determines the “dynamical importance” of node i versus node j.
For homogeneous NIMFA (4), the infection rate matrix B and the curing rate matrix S reduce to and , respectively. Hence, the effective infection rate matrix becomes , and the principal eigenvector of the effective infection rate matrix W equals the principal eigenvector of the adjacency matrix A. Furthermore, the limit process reduces to , with the effective infection rate and the epidemic threshold . For homogeneous NIMFA (4), Theorem 3 reduces to:
Corollary 3
Suppose that Assumptions 1 to 3 hold and consider the viral state v(t) of homogeneous NIMFA (4). Furthermore, suppose that for some constant when and define
25 |
Then, there exists some constant such that
where , when the effective infection rate approaches the epidemic threshold from above.
Proof
Appendix G.
From Corollary 3, we can obtain the analogue to Corollary 2 for NIMFA (4) with homogeneous spreading parameters . Furthermore, the approximation defined by (25) equals the exact solution (Van Mieghem 2014b) of homogeneous NIMFA (4) on a regular graph, provided that the initial state is the same for every node i. In particular, the net dose , a crucial quantity in Van Mieghem (2014b); Kendall (1948), is related to the viral slope w via .
Theorem 3 and Corollary 3 suggest that, around the epidemic threshold criterion , the dynamics of heterogeneous NIMFA (1) closely resembles the dynamics of homogeneous NIMFA (4). In particular, we pose the question: Can heterogeneous NIMFA (1) be reduced to homogeneous NIMFA (4) around the epidemic threshold criterion by choosing the homogeneous spreading parameters and the adjacency matrix A accordingly?
Theorem 4
Consider heterogeneous NIMFA (1) with given spreading parameters . Suppose that Assumptions 1 to 3 hold and that, for some constant , when the basic reproduction number approaches 1 from above. Define the homogeneous NIMFA system
26 |
where the homogeneous curing rate equals
27 |
the homogeneous infection rate equals
28 |
with the variable defined by (7), and the self-infection rates equal
Then, if , there exists some constant such that
where , when the basic reproduction number approaches 1 from above.
Proof
Appendix H.
In other words, when , for any contact network and any spreading parameters , heterogeneous NIMFA (1) can be reduced to homogeneous NIMFA (4) on a complete graph plus self-infection rates . We emphasise that the sole influence of the topology on the viral spread is given by the self-infection rates . Thus, under Assumptions 1to 3, the network topology has a surprisingly small impact on the viral spread around the epidemic threshold.
Numerical evaluation
We are interested in evaluating the accuracy of the closed-form expression , given by (20), when the basic reproduction number is close, but not equal, to one. We generate an adjacency matrix A according to different random graph models. If , then we set the infection rates to a uniformly distributed random number in [0.4, 0.6] and, if , then we set . We set the initial curing rates to a uniformly distributed random number in [0.4, 0.6]. To set the basic reproduction number , we set the curing rates to a multiple of the initial curing rates , i.e. for every node l and some scalar such that . Thus, we realise the limit process by changing the scalar . Only in Sect. 6.2, we consider homogeneous spreading parameters by setting and for all nodes i, j. Numerically, we obtain the “exact” NIMFA viral state sequence v(t) by Euler’s method for discretisation, i.e.,
29 |
for a small sampling time T and a discrete time slot . In Prasse and Van Mieghem (2019), we derived an upper bound on the sampling time T which ensures that the discretisation (29) of NIMFA (1) converges to the steady-state . We set the sampling time T to . Except for Sect. 6.3, we set the initial viral state to . We define the convergence time as the smallest time t at which
holds for every node i. Thus, at the convergence time the viral state has practically converged to the steady-state . We evaluate Theorem 3 with respect to the approximation error , which we define as
All results are averaged over 100 randomly generated networks.
Approximation accuracy around the epidemic threshold
We generate a Barabási–Albert random graph (Barabási and Albert 1999) with nodes and the parameters , . Figure 1 gives an impression of the accuracy of the approximation of Theorem 3 around the epidemic threshold criterion . For a basic reproduction number , the difference of the closed-form expression of Theorem 3 to the exact NIMFA viral state trace is negligible.
We aim for a better understanding of the accuracy of the closed-form expression of Theorem 3 when the basic reproduction number converges to one. We generate Barabási–Albert and Erdős–Rényi connected random graphs with nodes. The link probability of the Erdős–Rényi graphs (Erdős and Rényi 1960) is set to . Figure 2 illustrates the convergence of the approximation of Theorem 3 to the exact solution of NIMFA (1). Around the threshold criterion , the approximation error converges linearly to zero with respect to the basic reproduction number , which is in agreement with Theorem 3. The greater the network size N, the greater is the approximation error for Barabási–Albert networks. The greater the network size N, the lower is the approximation error for Erdős–Rényi graphs.
Impact of degree heterogeneity on the approximation accuracy
For NIMFA (4) with homogeneous spreading parameters , the approximation defined by (4) is exact if the contact network is a regular graph. We are interested how the approximation accuracy changes with respect to the heterogeneity of the node degrees. We generate Watts–Strogatz (Watts and Strogatz 1998) random graphs with nodes and an average node degree of 4. We vary the link rewiring probability from , which correspond to a regular graph, to , which corresponds to a “completely random” graph. Figure 3 depicts the approximation error versus the rewiring probability for homogeneous spreading parameters . Interestingly, the approximation error reaches a maximum and improves when the adjacency matrix A is more random.
Impact of general initial viral states on the approximation accuracy
Theorem 3 required that the initial error converges to zero, which means that the initial viral state v(0) must be parallel to the steady-state or, since , converge to zero. To investigate whether the approximation of Theorem 3 is accurate also when the initial error does not converge to zero, we set the initial viral state of every node i to a uniformly distributed random number in for some scalar . By increasing the scalar , the initial viral state v(0) is “more random”. Figure 4 shows that the approximation error is almost unaffected by an initial viral state v(0) that is neither parallel to the steady-state nor small. Figure 5 shows that the viral state v(t) converges rapidly to the approximation as time t increases.
For general initial viral states v(0) with , it holds that since the approximation is parallel to the steady-state vector . Hence, the approximation does not converge point-wise to the viral state v(t) when . However, based on the results shown in Figs. 4 and 5, we conjecture convergence with respect to the -norm for general initial viral states v(0) when .
Conjecture 1
Suppose that Assumptions 1 to 3 hold. Then, it holds for the approximation defined by (20) that
when the basic reproduction number approaches 1 from above.
Directed infection rate matrix
The proof of Theorem 3 relies on a symmetric infection rate matrix B as stated by Assumption 3. We perform the same numerical evaluation as shown in Fig. 2 in Sect. 6.1 with the only difference that we generate strongly connected directed Erdős–Rényi random graphs. Figure 6 demonstrates the accuracy of the approximation for a directed infection rate matrix B, which leads us to:
Conjecture 2
Suppose that Assumptions 1 and 2 hold and that the infection rate matrix B is irreducible but, in contrast to Assumption 3, not necessarily symmetric. Then, the viral state v(t) is “accurately described” by the approximation when the basic reproduction number approaches 1 from above.
Accuracy of the approximation of the convergence time
Corollary 1 gives the expression of the convergence time from the initial viral state to the viral state for any scalars around the epidemic threshold criterion . We set the scalars to and and define the approximation error
where denotes the exact convergence time and denotes the approximate expression of Corollary 1. We generate Barabási–Albert and Erdős–Rényi random graphs with nodes. Figure 7 shows that Corollary 1 gives an accurate approximation of the convergence time when the basic reproduction number is reasonably close to one.
Reduction to a complete graph with homogeneous spreading parameters
Theorem 4 states that, around the epidemic threshold, heterogeneous NIMFA (1) on any graph can be reduced to homogeneous NIMFA (4) on a complete graph. Figures 8 and 9 show the approximation accuracy of Theorem 4 for Erdős–Rényi and Barabási–Albert random graphs, respectively. To accurately approximate heterogeneous NIMFA on Barabási–Albert graphs by homogeneous NIMFA on a complete graph, the basic reproduction number must be closer to 1 than for Erdős–Rényi graphs.
Conclusion
We solved the NIMFA governing equations (1) with heterogeneous spreading parameters around the epidemic threshold when the initial viral state v(0) is small or parallel to the steady-state , provided that the infection rates are symmetric (). Numerical simulations demonstrate the accuracy of the solution when the basic reproduction number is close, but not equal, to one. Furthermore, the solution serves as an accurate approximation also when the initial viral state v(0) is neither small nor parallel to the steady-state . We observe four important implications of the solution of NIMFA around the epidemic threshold.
First, the viral state v(t) is almost parallel to the steady-state for every time . On the one hand, since the viral dynamics approximately remain in a one-dimensional subspace of , an accurate network reconstruction is numerically not viable around the epidemic threshold (Prasse and Van Mieghem 2018). Furthermore, when the basic reproduction number is large, then the viral state v(t) rapidly converges to the steady-state , which, again, prevents an accurate network reconstruction. On the other hand, only the principal eigenvector of the effective infection rate matrix W and the viral slope w are required to predict the viral state dynamics around the epidemic threshold. Thus, around the epidemic threshold, the prediction of an epidemic does not require an accurate network reconstruction.
Second, the eigenvector centrality (with respect to the principal eigenvector of the effective infection rate matrix W) gives a complete description of the dynamical importance of a node i around the epidemic threshold. In particular, the ratio of the viral states of two nodes i, j does not change over time t.
Third, around the epidemic threshold, we gave an expression of the convergence time to approach the steady-state . The viral state v(t) converges to the steady-state exponentially fast. However, as the basic reproduction number approaches one, the convergence time goes to infinity.
Fourth, around the epidemic threshold, NIMFA with heterogeneous spreading parameter on any graph can be reduced to NIMFA with homogeneous spreading parameters on the complete graph plus self-infection rates.
Potential generalisations of the solution of NIMFA to non-symmetric infection rate matrices B or time-dependent spreading parameters stand on the agenda of future research.
Acknowledgements
We are grateful to Karel Devriendt for his help in proving Theorem 4.
Appendices
Nomenclature
The eigenvalues of the effective infection rate matrix W are denoted, in decreasing order, by . The principal eigenvector of unit length of the matrix W is denoted by and satisfies . The greatest and smallest curing rate in are denoted by and , respectively. The numerical radius r(M) for an matrix M is defined as (Horn and Johnson 1990)
30 |
where is the conjugate transpose of a complex vector z. For a square matrix M, we denote the 2-norm by , which equals the largest singular value of M. In particular, it holds that the 2-norm of the curing rate matrix S equals . Table 1 summarises the nomenclature.
Table 1.
Infection rate from node j to node i | |
B | Infection rate matrix; |
c(t) | Projection of the viral state v(t) on the steady-state ; see (16) |
Curing rate of node i | |
diagonal matrix with on its diagonal | |
I | identity matrix |
k-th eigenvalue of the matrix W; | |
N | Number of nodes |
2-norm of a matrix M: largest singular value of M | |
r(M) | Numerical radius of a square matrix M; see (30) |
Basic reproduction number; | |
Spectral radius of a square matrix M | |
S | Curing rate matrix; |
u | all-one vector |
v(t) | viral state vector v(t) at time ; for |
Steady-state vector, see Definition 2 | |
w | The viral slope; |
W | Effective infection rate matrix ; |
Symmetric matrix | |
k-th eigenvector of the matrix W; | |
Viral state component that is orthogonal to ; |
Proof of Theorem 1
The steady-state solely depends on the effective infection rate matrix W: By left-multiplication of (3) with the diagonal matrix , we obtain that
31 |
In general, the effective infection rate matrix W, defined in (5) as , is asymmetric, which prevents a straightforward adaptation of the proof in Van Mieghem (2012, Lemma 4). However, the matrix W is similar to the matrix
32 |
Since the infection rate matrix B is symmetric under Assumption 3, the matrix is symmetric. Hence, the matrix , and also the effective infection rate matrix W, are diagonalisable. With (32), we write the steady-state (31) with respect to the symmetric matrix as
33 |
We decompose the matrix as
34 |
where the eigenvalues of are real and equal to with the corresponding normalized eigenvectors denoted by . Then, the steady-state vector can be expressed as linear combination
where the coefficients equal . To prove Theorem 1, we would like to express the coefficients as a power series around . However, in the limit process , the eigenvectors of the matrix are not necessarily constant. Hence, the coefficients depend on the full matrix and not only on the basic reproduction number . To overcome the challenge of non-constant eigenvectors in the limit process , we define the symmetric auxiliary matrix
35 |
for a scalar . Thus, the matrix M(z) is obtained from the matrix by replacing the largest eigenvalue of by z. In particular, the definition of the matrix M(z) in (35) and (34) illustrate that . When the matrix is formally replaced by the matrix M(z), the steady-state equation (33) becomes
36 |
where the vector denotes the solution of (36). Since , the solution of (36) at and the solution to (33) coincide, i.e., . Lemma 2 expresses the solution of the equation (36) as a power series.
Lemma 2
Suppose that Assumptions 1 and 3 hold. If (B, S) is sufficiently close to , then the vector which satisfies (36) equals
37 |
where the vector satisfies for some scalar when z approaches 1 from above.
Proof
The proof is an adaptation of the proof (Van Mieghem 2012, Lemma 4). We express the solution of (36) as linear combination of the vectors , i.e.,
38 |
Since the diagonal matrix is full rank, the vectors , where , are linearly independent. Furthermore, we express the coefficients as a power series
39 |
where for every , since (Lajmanovich and Yorke 1976) it holds that when . We denote the eigenvalues of the matrix M(z) by
40 |
By substituting (38) into (36), we obtain that
and left-multiplying with the eigenvector , for any , yields
41 |
We define
Then, we rewrite (41) as
42 |
First, we focus on the left-hand side of (42), which we denote by
With the power series (39), we obtain that
Further rewriting yields that
43 |
Second, we rearrange the right-hand side of (42) as
By the definition of in (40) it holds that , and we obtain that
44 |
where
Introducing the power series (39) into (44) and executing the Cauchy product for yields
We shift the index j in the first term and obtain
45 |
Finally, we equate powers in in (43) and (45), which yields for that
46 |
for every . The spectral radius of the limit of the effective infection rate matrix W equals 1. Furthermore, the limit is a non-negative and irreducible matrix. Thus, the eigenvalues of the limit obey for every , which implies that for every provided that (B, S) is sufficiently close to . With the definition of in (40), we obtain from (46) that when provided that (B, S) is sufficiently close to , since .
For , equating powers in (45) yields that
47 |
In particular, for the case , we obtain
48 |
since for all and . Since , we obtain for from (48) that
and, hence,
Since for , we obtain that the power series (38) for the solution of (36) becomes
49 |
where the vector equals
Thus, it holds when z approaches 1 from above, which proves Lemma 2.
We believe that, based on (47), a recursion for the coefficients can be obtained for powers , similar to the proof of Van Mieghem (2012, Lemma 4). The radius of convergence of the power series (49) is an open problem, see also He and Van Mieghem (2020). To express the solution in (37) in terms of the principal eigenvector of the effective infection rate matrix W, we propose Lemma 3.
Lemma 3
Under Assumptions 1 and 3, it holds that
50 |
Proof
From (32), it follows that the principal eigenvector of the matrix and the principal eigenvector of the effective infection rate matrix W are related via
or, component-wise,
Then, we rewrite the left-hand side of (50) as
which simplifies to
Writing out the quadratic form in the numerator completes the proof.
The basic reproduction number converges to 1 when . Hence, if (B, S) is sufficiently close to , then the basic reproduction number is smaller than the radius of convergence of the power series (38). Thus, if (B, S) is sufficiently close to , then the solution to (36) at follows with Lemma 2 as
where the last equality follows from Lemma 3 and the definition of the scalar in (7). We emphasise that Lemma 2 implies that and, hence, as . Since , the solution of (36) at and the solution to (33) coincide, i.e., . Thus, from the definition of the vector in (6), we obtain that
51 |
when . Lemma 2 states that as . Hence, we obtain from (51) that
52 |
for some scalar when .
Furthermore, when (B, S) converge to the limit , the scalar converges to some limit . Hence, by defining the constant
for some , it holds that
for all (B, S) which are sufficiently close to . Finally, we obtain from (52) that
when (B, S) approaches .
Proof of Lemma 1
We divide Lemma 1 into two parts. In Sect. C.1, we prove that the viral state v(t) does not overshoot the steady-state . In Sect. C.2, we show that the function c(t) lies in the interval [0, 1].
Absence of overshoot
The proof follows the same reasoning as Prasse and Van Mieghem (2019, Corollary 1). Assume that at some time it holds for some node i and that for every node j. Since , the NIMFA equation (1) yields that
Since for every node j, we obtain that
where the last equality follows from the steady-state equation (3). Thus, implies that , which means that, at time , the viral state does not increase. Hence, the viral state cannot exceed the steady-state at any time .
Boundedness of the function c(t)
Relation (16) indicates that
53 |
Section C.1 shows that Assumption 2 implies that for all nodes i and every time t. Thus, we obtain from (53) that
Analogously, since for all nodes i and every time t, we obtain from (53) that .
Proof of Theorem 2
By inserting the ansatz (15) into the NIMFA equations (2), we obtain that
54 |
Here, the function is given by
which simplifies, with the steady-state equation (3), to
55 |
The function is given by
With , we obtain that
56 |
To show that the error term converges to zero at every time t when , we consider the squared Euclidean norm . The convergence of the squared norm to zero implies the convergence of the error term to zero. The derivative of the squared norm is given by
Thus, we obtain from (54) that
57 |
since by definition of . We do not know how to solve (57) exactly, and we resort to bounding the two addends on the right-hand side of (57) in Sects. D.1 and D.2, respectively. In Sect. D.3 we complete the proof of Theorem 2 by deriving an upper bound on the squared norm .
Upper bound on
We obtain an upper bound on the projection of the function onto the error vector , which is linear with respect to the norm :
Lemma 4
Under Assumptions 1 to 3, it holds at every time that
Proof
From (55) and the definition of the matrix W in (5) it follows that
With Theorem 1, we obtain
The triangle inequality yields that
58 |
With the Cauchy–Schwarz inequality, the first addend in (58) is upper-bounded by
since and the matrix S is symmetric. The matrix 2-norm is sub-multiplicative, which yields that
Thus, (58) gives that
59 |
since and . We consider the second addend in (59), which we write with (32) as
From the Cauchy–Schwarz inequality and the sub-multiplicativity of the matrix norm we obtain
The triangle inequality and the symmetry of the matrix imply that
Thus, we can upper bound the second added in (59) by
since . Hence, (59) yields the upper bound
Finally, Lemma 1 states that , which implies that
and completes the proof.
Upper bound on
Lemma 5 states an intermediate result, which we will use to bound the projection of the function onto the error vector .
Lemma 5
Suppose that Assumptions 1 to 3 hold. Then, at every time , it holds that
Proof
From (56) it follows that
60 |
To simplify (60), we aim to bound the last addend of (60) by an expression that is quadratic in the error vector . The last addend equals
61 |
Since and for every node i at every time t, it holds that
62 |
By inserting (62) in (61), the last addend of (60) is upper bounded by
which simplifies to
63 |
By applying the upper bound (63) to (60), we obtain that
With the definition of the matrix in (32), we obtain
and further rearranging completes the proof.
For any scalar and any vector , we define
Then, we obtain from Lemma 5 that
64 |
To upper-bound the term , we make use of (parts of) the results of Issos (1966), which are analogues of the Perron–Frobenius Theorem for the numerical radius of a non-negative, irreducible matrix:
Theorem 5
(Issos 1966) Let M be a real irreducible and non-negative matrix. Then, there is a positive vector of length such that . Furthermore, if holds for a vector of length , then either or .
We refer the reader to Issos (1966), Maroulas et al. (2002) and Li et al. (2002) for further results on the numerical radius of non-negative matrices. We apply Theorem 5 to obtain:
Lemma 6
Denote the set of vectors with at least one positive and at least one negative component as
Then, it holds for every scalar and for every vector .
Proof
By introducing the vector
and by using (32), we rewrite the term as
65 |
For every scalar the matrix is irreducible and non-negative. Since and the matrix S is a diagonal matrix with non-negative entries, it holds that and for some i, j. Hence, at least two components of the vector have different signs, and Theorem 5 implies that (65) is upper-bounded by
Since the matrix is irreducible and for every , where the inequality holds element-wise, it holds (Li et al. 2002, Corollary 3.6.) that
The matrix is symmetric, and, hence, the numerical radius equals the spectral radius , which yields that
Finally, we obtain a bound on the projection of the function onto the error vector :
Lemma 7
Under Assumptions 1 to 3, there is some constant such that
holds at every time when approaches .
Proof
We denote the maximum of the function with respect to and by
66 |
As a first step, we consider the value of at the limit . Since the steady-state equals to zero at the limit , we obtain from (65) that
67 |
where we denote . Since it holds at the limit , Lemma 6 implies that
68 |
As a second step, we consider that the infection rate matrix B and the curing rate matrix S do not equal the respective limit and . Thus, there are non-zero matrices and such that , , and . Then, we obtain from (65) that
which is upper-bounded by
69 |
Maximising every addend in (69) independently yields an upper bound on as
70 |
In the following, we state upper bounds for each of the three addends in (67) separately. With (67), we write the first addend in (70) as
71 |
where the last equality follows from the definition of in (66). Regarding the second addend in (70), it holds that
where the last equality follows from the definition the numerical radius. Hence, the second addend in (70) is upper-bounded by
72 |
for some . Similarly, we obtain an upper bound on the third addend in (70) as
73 |
for some . With (71), (72) and (73), we obtain from (70) that
74 |
The numerical radius r(M) is a vector8 norm (Horn and Johnson 1990) on the space of matrices M. Thus, the numerical radius r(M) converges to zero if the matrix M converges to zero. Since and as and are bounded, the last two addends in (74) converge to zero as . Hence, for every scalar there is a such that and implies that
75 |
We choose the scalar , which is positive due to (68). Then, the right-hand side of (75) becomes
Thus, we obtain from (75) that
76 |
holds for all (B, S) which are sufficiently close to the limit .
By definition, the error vector at any time is orthogonal to the steady-state vector . Since the steady-state is positive, the error vector has at least one positive and one negative element, and, hence, it holds that . Thus, we obtain from the definition of the term in (66) that
With (76), we obtain from (64) that
From the sub-multiplicativity of the matrix norm, we obtain
which completes the proof, since .
Bound on the error vector
With Lemma 4 and Lemma 7, we upper-bound (57) by
From
it follows that
We denote
77 |
and we obtain that
78 |
The upper bound (78) is a linear first-order ordinary differential inequality, which is solved by (Arfken and Weber 1999)
which simplifies to
The triangle inequality yields that
79 |
Furthermore, since at every time , we obtain from (79) that
80 |
The maximum of the curing rates converges to some limit when . Hence, for any it holds that when approaches . For some , we set the constant
Then, it holds that when approaches , and we obtain from (80) that
81 |
Theorem 1 states that and when approaches . Thus, it follows from the definition of the term in (77) that . Hence, there is a constant such that (81) yields
when approaches .
Proof of Theorem 3
By projecting the differential equation (54) onto the steady-state vector , we obtain that
since by definition of the error term . We divide by and obtain with (55) that
82 |
The first addend in the differential equation (82) can be expressed in a simpler manner when approaches :
Lemma 8
Under Assumptions 1 and 3, it holds
83 |
where when approaches .
Proof
With Theorem 1 and the definition of the matrix W in (5), the numerator of the left-hand side of (83) becomes
where the last equality follows from . Thus, it holds that
84 |
Under Assumption 3, both matrices B and S are symmetric, which implies that
Hence, we obtain from (84) that
Since and , we finally rewrite the numerator of the left-hand side of (83) as
85 |
With Theorem 1, the denominator of the left-hand side of (83) equals
86 |
Combining the approximate expressions for the numerator (85) and the denominator (86) completes the proof.
We define the viral slope w as
87 |
and the function n(t) as
88 |
Then, we obtain from (82) that
89 |
The function n(t) is complicated and depends on the error vector . Hence, we cannot solve the differential equation (89) for the function c(t) without knowing the solution for the error vector . However, as , the function n(t) converges to zero uniformly in time t as stated by the bound in Lemma 9.
Lemma 9
Under Assumptions 1 to 3, it holds at every time that
for some constants when (B, S) approaches .
Proof
Regarding the first addend in the definition of the function n(t) in (88), Lemma 1 implies that at every time t. Hence, Lemma 8 yields that there is a constant such that
at every time t when (B, S) approaches . Regarding the second addend of the function n(t) defined in (88), it follows from the definition of the function in (56) that
since . Thus, it holds that
With the definition of the matrix in (32), we obtain that
The Cauchy–Schwarz inequality yields an upper bound as
With and the triangle inequality, we obtain
90 |
In the following, we consider the three addends in (90) separately. Regarding the first addend, we obtain with the definition of the matrix in (32) that
where the last equality follows from Theorem 1. Thus, the triangle inequality yields
With the sub-multiplicativity of the matrix 2-norm, we obtain
since . Since and when , there is a constant such that
91 |
when (B, S) approaches . Regarding the second addend in (90), it holds that
Since when , it follows that there is a constant such that
92 |
when (B, S) approaches . Regarding the third addend in (90), it holds per definition of the matrix 2-norm that
where the last inequality follows from , as stated by Lemma 1, and the definition of the effective infection rate matrix W in (5). Hence, we obtain the upper-bound
93 |
for some constant when (B, S) approaches . We apply the three upper bounds (91), (92) and (93) to (90) and obtain that
when (B, S) approaches . Since when , there is a constant such that, as (B, S) approaches , it holds
at every time t. Thus, we have obtained an upper bound, which is proportional to the norm of the error vector . Finally, we apply Theorem 2 to bound the norm , which completes the proof.
Lemma 9 suggests that, since when , the differential equation (89) for the function c(t) is approximated by the logistic differential equation
94 |
To make the statement (94) precise, we define the function , for any scalar x with , as
95 |
where the constant is set such that , i.e.,
Lemma 10 states an upper and a lower bound on the function c(t).
Lemma 10
Suppose that Assumptions 1 to 3 hold and that
96 |
for some constants and when approaches . Then, the function c(t) is bounded by
where the scalar equals with and some constant as approaches .
Proof
With (96), Lemma 9 implies that it holds
for some constants . Since , we obtain that at every time t, where we define the scalar
with the constants and . With , we obtain from the differential equation (89) for the function c(t) that
97 |
The upper and lower bound (97) give rise to a Riccati differential equation, which can be solved exactly, and we obtain that the function c(t) is bounded by
and
at every time .
When approaches , Theorem 2 states that the error term is negligible and, furthermore, Lemma 10 states that the function c(t) converges to . Thus, based on the ansatz (15), we approximate the viral state v(t) by
With the definition of the function in (95), it holds that
Then, it follows from the ansatz (15) that the difference of the exact viral state v(t) to the approximation equals
98 |
The norm of the error term is bounded by Theorem 2. Thus, it remains to bound the first addend of (98). With Lemma 10, the difference of the function c(t) to is bounded by
99 |
Furthermore, the scalar converges to zero when approaches . Hence, if we show that, as the scalar converges to zero, the upper bound converges to the lower bound then (99) implies that the function c(t) converges to . Furthermore, we must show that the upper bound converges to the lower bound uniformly in time t, since the upper bound on the approximation error in Theorem 3 does not depend on time t. From the definition of the function in (95) we obtain that
100 |
where we denote
101 |
Lemma 10 states that for some when approaches . Furthermore, Lemma 8 states that . Hence, it holds that when approaches . For small x, the series expansion of the square root yields that
Thus, for small values of , we obtain from (100) that
Since the magnitude of the hyperbolic tangent is bounded by 1, it follows from the definition of the function in (101) that
which yields that
102 |
since . The last two addends of (102) are independent of time t. Thus, it remains to show that first addend, i.e., the difference , converges to zero uniformly in time t as .
Lemma 11
Under Assumptions 1 to 3, there is some constant such that
at every time when the scalar approaches zero from above.
Proof
The mean value theorem gives that
for some . Thus, it holds that
for some and , which yields that
103 |
To express the derivative of the function , we write the function g(t, x) as
where we define the function as
Then, the derivative of the function with respect to the scalar is given by
which is upper-bounded by
104 |
With the derivative of the function , i.e.
we obtain from (104) that
The right-hand side of (104) is finite at every time . Furthermore, for every scalar , the right-hand side of (104) converges to zero when . Hence, we can upper-bound the derivative by some constant for every time t. Thus, we obtain from (103) that
With Lemma 11, we obtain from (102) that there is a constant such that
Since and when approaches , we obtain that there exists some constant such that
Thus, it follows from (98) that
Hence, we obtain an upper bound as
Then, the upper bound on the error vector in Theorem 2 implies that there are constants such that
By assumption it holds that for some constant , and it holds that as stated by Theorem 1. Thus, we obtain that
for some constants , since . By using the definition of the scalar s, we complete the proof.
Proof of Corollary 1
By assumption, it holds that , which implies that . Thus, we obtain from (22) that
when approaches . From the definition of the approximation in (20), we obtain that for every node i is equivalent to
With the definition of the term in (19), it follows that
From , we obtain that
The inverse hyperbolic tangent equals
which completes the proof.
Proof of Corollary 3
For NIMFA (4) with homogeneous spreading parameters , the effective infection rate matrix reduces to . Hence, the basic reproduction number reproduction becomes
where the last equation follows from the definition of the effective infection rate and the epidemic threshold . Furthermore, it holds that for every node l and , since the principal eigenvector is of unit length. Thus, the definition of the approximation in (20) yields that
Proof of Theorem 4
We acknowledge the help of Karel Devriendt, who constructed an effective infection rate matrix of homogeneous NIMFA with a given principal eigenvector . The idea of proving Theorem 4 is based on Corollary 2: When , the viral state dynamics of heterogeneous NIMFA (1) are determined by the four variables . Thus, we aim to show that the corresponding four variables of the homogeneous NIMFA system (26), which we denote by and , are the same as the variables of heterogeneous NIMFA (1).
Lemma 12
The homogeneous NIMFA system (26) and heterogeneous NIMFA (1) have the same principal eigenvector , the variable and viral slope .
Proof
First, we consider the principal eigenvector . The effective infection rate matrix of the homogeneous NIMFA system (26) equals
105 |
We show that the principal eigenvector of heterogeneous NIMFA (1) is also the principal eigenvector of the matrix . Indeed,
Thus, is an eigenvector of the effective infection rate matrix of the homogeneous NIMFA system (26). The corresponding eigenvalue equals
106 |
The effective infection rate matrix is non-negative and irreducible, by definition (105). Thus, the Perron–Frobenius Theorem (Van Mieghem 2010) yields that the eigenvalue to the positive eigenvector equals the spectral radius and that . Second, we consider the variables , in Theorem 1. By definition (7) and since is a vector of length 1, it holds that
where the last equality follows from (106). With (28), we obtain further that
Thus, the variable of the homogeneous NIMFA (26) equals the variable of heterogeneous NIMFA (1). Third, we show that the viral slope of the homogeneous NIMFA (26) equals the viral slope w of heterogeneous NIMFA (1). From the definition (87), the variable of the homogeneous NIMFA system (26) follows as
With (106), we obtain that
Then, the definition of the infection rate in (28) yields that
which simplifies with the definition of in (27) to
Then, the definition of in (7) yields that
Thus, the viral slope of the homogeneous NIMFA system (26) equals the viral slope w of heterogeneous NIMFA (1), which completes the proof.
In contrast to the variables in Lemma 12, the two variables and , given by definition (19), are not necessarily equal, since the steady states and might be different. For the homogeneous NIMFA system (26) and heterogeneous NIMFA (1), we denote the viral state approximations of Corollary 2 by and , respectively. The difference of the viral state vectors v(t) and can be written as
With the triangle inequality, we obtain that
107 |
Corollary 2 states that there is some constant , such that, at every time , it holds that
as , since by Theorem 1. Similarly, Corollary 2 implies that as . Thus, (107) yields that
108 |
In the following, we bound the first addend on the right side of (108). We insert the expression (23) for the approximations and to obtain that
where the second equality follows from Lemma 12. From Abramowitz and Stegun (1965, 4.5.45), it follows that
Since for every time t and the eigenvector has length 1, we obtain that
Thus, the difference of the viral states v(t) and in (108) is bounded by
109 |
To bound the hyperbolic sine on the right side of (109), we introduce:
Lemma 13
Suppose that Assumptions 1 to 3 hold. Furthermore, assume that the initial viral states of the homogeneous NIMFA system (26) and heterogeneous NIMFA (1) are the same, i.e., . Then, as , it holds that
Proof
The series expansion (Abramowitz and Stegun 1965, 4.5.62) of the hyperbolic sine yields that
110 |
In the following, we consider the difference . Since by the assumption, it follows from the definition of the variable in (19) that
111 |
where we define
112 |
and
113 |
The Taylor series of around reads
Thus, we obtain from (111) that
114 |
Hence, to bound the difference , we aim to bound the variable . The definition of in (113) yields with (112) that
The Cauchy–Schwarz inequality gives that
Under Assumption 2, it holds that , and hence
which can be rewritten as
The triangle inequality yields that
which becomes
115 |
Since, by Lemma 12, and , Theorem 1 implies that
116 |
for some vector that satisfies as . Thus, with (6) and (116), we obtain from (115) that
Finally, since , , , and , we obtain that
as , which completes the proof in combination with (110) and (114).
With Lemma 13 and , we obtain from (109) that
since, by definition, . Since by Theorem 1, it holds that
as , which completes the proof.
Footnotes
In this work, we use the words node and group interchangeably.
The initial state vector v(0) is parallel to the steady-state vector if for some scalar .
More precisely, Paré et al. (2017) assume that the adjacency matrix A(t) is time-varying but not necessarily symmetric nor binary-valued, which is equivalent to time-varying infection rates .
The steady-state is the same for every node i in a regular graph for homogeneous spreading parameters . Hence, the initial state is the same for every node i if and only if the initial state v(0) is parallel to the steady-state vector .
By convergence of the sequence of tuples to the limit , we mean that, for all , there exists an such that both and holds for all .
Theorem 1 implies that the steady-state satisfies when . Thus, also at every time t. Thus, a linear convergence of the error term to zero, i.e., , would not be sufficient to show that the viral state v(t) converges to when .
In Prasse and Van Mieghem (2019), an analogous statement has been proved for the discrete-time version of the NIMFA equations (2).
The numerical radius is not a matrix norm, since the numerical radius is not sub-multiplicative.
Publisher's Note
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Contributor Information
Bastian Prasse, Email: b.prasse@tudelft.nl.
Piet Van Mieghem, Email: p.f.a.vanmieghem@tudelft.nl.
References
- Abramowitz M, Stegun IA. Handbook of mathematical functions: with formulas, graphs, and mathematical tables. North Chelmsford: Courier Corporation; 1965. [Google Scholar]
- Ahn HJ, Hassibi B (2013) Global dynamics of epidemic spread over complex networks. In: Proceedings of 52nd IEEE conference on decision and control, CDC, IEEE, pp 4579–4585
- Anderson RM, May RM. Infectious diseases of humans: dynamics and control. Oxford: Oxford University Press; 1992. [Google Scholar]
- Arfken GB, Weber HJ. Mathematical methods for physicists. Am J Phys. 1999;67:165. [Google Scholar]
- Bailey NTJ. The mathematical theory of infectious diseases and its applications. 2. London: Charles Griffin & Company; 1975. [Google Scholar]
- Barabási AL, Albert R. Emergence of scaling in random networks. Science. 1999;286(5439):509–512. doi: 10.1126/science.286.5439.509. [DOI] [PubMed] [Google Scholar]
- Devriendt K, Lambiotte R (2020) Non-linear network dynamics with consensus-dissensus bifurcation. arXiv preprint arXiv:2002.08408
- Devriendt K, Van Mieghem P. Unified mean-field framework for susceptible-infected-susceptible epidemics on networks, based on graph partitioning and the isoperimetric inequality. Phys Rev E. 2017;96(5):052314. doi: 10.1103/PhysRevE.96.052314. [DOI] [PubMed] [Google Scholar]
- Diekmann O, Heesterbeek JAP, Metz JA. On the definition and the computation of the basic reproduction ratio in models for infectious diseases in heterogeneous populations. J Math Biol. 1990;28(4):365–382. doi: 10.1007/BF00178324. [DOI] [PubMed] [Google Scholar]
- Van den Driessche P, Watmough J. Reproduction numbers and sub-threshold endemic equilibria for compartmental models of disease transmission. Math Biosci. 2002;180(1–2):29–48. doi: 10.1016/s0025-5564(02)00108-6. [DOI] [PubMed] [Google Scholar]
- Erdős P, Rényi A. On the evolution of random graphs. Publ Math Inst Hung Acad Sci. 1960;5(1):17–60. [Google Scholar]
- Fall A, Iggidr A, Sallet G, Tewa JJ. Epidemiological models and Lyapunov functions. Math Model Nat Phenom. 2007;2(1):62–83. [Google Scholar]
- He Z, Van Mieghem P. Prevalence expansion in NIMFA. Physica A. 2020;540:123220. [Google Scholar]
- Heesterbeek JAP. A brief history of and a recipe for its calculation. Acta Biotheor. 2002;50(3):189–204. doi: 10.1023/a:1016599411804. [DOI] [PubMed] [Google Scholar]
- Hethcote HW. The mathematics of infectious diseases. SIAM Rev. 2000;42(4):599–653. [Google Scholar]
- Horn RA, Johnson CR. Matrix analysis. Cambridge: Cambridge University Press; 1990. [Google Scholar]
- Issos JN (1966) The field of values of non-negative irreducible matrices. PhD thesis, Auburn University
- Kendall DG. On the generalized birth-and-death process. Ann Math Stat. 1948;19(1):1–15. [Google Scholar]
- Khanafer A, Başar T, Gharesifard B. Stability of epidemic models over directed graphs: a positive systems approach. Automatica. 2016;74:126–134. [Google Scholar]
- Kitzbichler MG, Smith ML, Christensen SR, Bullmore E. Broadband criticality of human brain network synchronization. PLoS Comput Biol. 2009;5(3):e1000314. doi: 10.1371/journal.pcbi.1000314. [DOI] [PMC free article] [PubMed] [Google Scholar]
- Lajmanovich A, Yorke JA. A deterministic model for gonorrhea in a nonhomogeneous population. Math Biosci. 1976;28(3–4):221–236. [Google Scholar]
- Li CK, Tam BS, Wu PY. The numerical range of a nonnegative matrix. Linear Algebra Appl. 2002;350(1–3):1–23. [Google Scholar]
- Liu QH, Ajelli M, Aleta A, Merler S, Moreno Y, Vespignani A. Measurability of the epidemic reproduction number in data-driven contact networks. Proc Natl Acad Sci. 2018;115(50):12680–12685. doi: 10.1073/pnas.1811115115. [DOI] [PMC free article] [PubMed] [Google Scholar]
- Liu F, Cui S, Li X, Buss M (2020) On the stability of the endemic equilibrium of a discrete-time networked epidemic mode. arXiv preprint arXiv:2001.07451
- Maroulas J, Psarrakos P, Tsatsomeros M. Perron-Frobenius type results on the numerical range. Linear Algebra Appl. 2002;348(1–3):49–62. [Google Scholar]
- Nowzari C, Preciado VM, Pappas GJ. Analysis and control of epidemics: a survey of spreading processes on complex networks. IEEE Control Syst Mag. 2016;36(1):26–46. [Google Scholar]
- Nykter M, Price ND, Aldana M, Ramsey SA, Kauffman SA, Hood LE, Yli-Harja O, Shmulevich I. Gene expression dynamics in the macrophage exhibit criticality. Proc Natl Acad Sci. 2008;105(6):1897–1900. doi: 10.1073/pnas.0711525105. [DOI] [PMC free article] [PubMed] [Google Scholar]
- Paré PE, Beck CL, Nedić A. Epidemic processes over time-varying networks. IEEE Trans Control Netw Syst. 2017;5(3):1322–1334. [Google Scholar]
- Paré PE, Liu J, Beck CL, Kirwan BE, Başar T. Analysis, estimation, and validation of discrete-time epidemic processes. IEEE Trans Control Syst Technol. 2018;28(1):79–93. [Google Scholar]
- Pastor-Satorras R, Castellano C, Van Mieghem P, Vespignani A. Epidemic processes in complex networks. Rev Mod Phys. 2015;87(3):925. [Google Scholar]
- Prasse B, Van Mieghem P (2018) Network reconstruction and prediction of epidemic outbreaks for NIMFA processes. arXiv preprint arXiv:1811.06741
- Prasse B, Van Mieghem P. The viral state dynamics of the discrete-time NIMFA epidemic model. IEEE Trans. Netw. Sci. Eng. 2019;7(3):1667–1674. [Google Scholar]
- Prasse B, Van Mieghem P (2020) Predicting dynamics on networks hardly depends on the topology. arXiv preprint arXiv:2005.14575
- Rami MA, Bokharaie VS, Mason O, Wirth FR (2013) Stability criteria for SIS epidemiological models under switching policies. arXiv preprint arXiv:1306.0135
- Van Mieghem P. Graph spectra for complex networks. Cambridge: Cambridge University Press; 2010. [Google Scholar]
- Van Mieghem P. The N-intertwined SIS epidemic network model. Computing. 2011;93(2–4):147–169. [Google Scholar]
- Van Mieghem P. The viral conductance of a network. Comput Commun. 2012;35(12):1494–1506. [Google Scholar]
- Van Mieghem P. Performance analysis of complex networks and systems. Cambridge: Cambridge University Press; 2014. [Google Scholar]
- Van Mieghem P. SIS epidemics with time-dependent rates describing ageing of information spread and mutation of pathogens. Delft Univ Technol. 2014;1(15):1–11. [Google Scholar]
- Van Mieghem P (2016) Universality of the SIS prevalence in networks. arXiv preprint arXiv:1612.01386
- Van Mieghem P, van de Bovenkamp R. Accuracy criterion for the mean-field approximation in susceptible-infected-susceptible epidemics on networks. Phys Rev E. 2015;91(3):032812. doi: 10.1103/PhysRevE.91.032812. [DOI] [PubMed] [Google Scholar]
- Van Mieghem P, Omic J (2014) In-homogeneous virus spread in networks. arXiv preprint arXiv:1306.2588
- Van Mieghem P, Omic J, Kooij R. Virus spread in networks. IEEE/ACM Trans Netw. 2009;17(1):1–14. [Google Scholar]
- Verhulst PF. Notice sur la loi que la population suit dans son accroissement. Corresp Math Phys. 1838;10:113–126. [Google Scholar]
- Wan Y, Roy S, Saberi A. Designing spatially heterogeneous strategies for control of virus spread. IET Syst Biol. 2008;2(4):184–201. doi: 10.1049/iet-syb:20070040. [DOI] [PubMed] [Google Scholar]
- Watts DJ, Strogatz SH. Collective dynamics of “small-world” networks. Nature. 1998;393(6684):440. doi: 10.1038/30918. [DOI] [PubMed] [Google Scholar]