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Discrete SIR model on a homogeneous tree and its continuous limit

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Page 1 of 18 AUTHOR
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Discrete SIR model on a homogeneous tree and its

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continuous limit
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13 Alexander Gairat* and Vadim Shcherbakov„

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Abstract
18
19 We study a discrete Susceptible-Infected-Recovered (SIR) model for the spread of
20

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infectious disease on a homogeneous tree and the limit behavior of the model in the case
21
22 when the tree vertex degree tends to infinity. We obtain the distribution of the time it
23 takes for a susceptible vertex to get infected in terms of a solution of a non-linear integral
24 equation under broad assumptions on the model parameters. Namely, infection rates are
25
assumed to be time-dependent, and recovery times are given by random variables with a
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29
an
fairly arbitrary distribution. We then study the behavior of the model in the limit when
the tree vertex degree tends to infinity, and infection rates are appropriately scaled. We
show that in this limit the integral equation of the discrete model implies an equation
30
for the susceptible population compartment. This is a master equation in the sense that
31
32 both the infectious and the recovered compartments can be explicitly expressed in terms
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33 of its solution.
34
35 Keywords: SIR model; homogeneous tree; Bernoulli equation; non-linear equation; memory
36
37
effects; fractional SIR models
38
39
40 1 Introduction
41
42 Studying the spread of infectious disease has been of great interest for a long time and has
43
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44 motivated a lot of mathematical models. Susceptible-Infected-Recovered (SIR) type models

45 are among those that are commonly studied. A SIR model is a compartmental model, in
46 which a population of individuals is divided into three distinct groups (compartments). The
47
48 first compartment consists of individuals that are susceptible to the disease, but are not yet
49 infected. The second compartment is represented by infected individuals. Finally, the remaining
50 third compartment is a group of individuals, who have been infected and recovered from the
51
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52 disease.
53 In this paper we revisit a discrete stochastic SIR model and study its continuous limit (to
54 be explained). In the discrete setting a population is modeled by vertices of a graph, and
55
56 infection is transmitted from infected vertices to susceptible ones via edges of the graph. Such
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57 a model is usually studied under additional assumptions on the graph, infection rates and
58
* Gearquant. Email address: agairat@gearquant.com
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„ Royal Holloway, University of London. Email address: vadim.shcherbakov@rhul.ac.uk
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3 recovery times (e.g., see [1], [3], [7], [13], [14], [16], [18], and references therein). For example,
4 if the underlying graph is complete, infection rates are constant and the recovery times are
5
6 exponentially distributed, then the model is a discrete version of the classic SIR model of A.G.
7 McKendrick and W.O. Kermack ([11]).
8 We study the discrete SIR model on a homogeneous tree. The latter is an infinite connected

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10 constant vertex degree graph without cycles. The constant vertex degree means that each
11 vertex has the same number of adjacent vertices (neighbors). A homogeneous tree can serve as
12 a mathematical model for an infinite closed homogeneous population, in which all individuals
13
have the same number of social contacts. To the best of our knowledge the SIR model on a

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15 homogeneous tree has never been considered, despite many years of study of the SIR model on
16 graphs (networks).
17
18
The discrete model is studied under broad assumptions on both infection rates and recovery
19 times. In particular, we assume that an infected vertex emits germs according to a Poisson
20 process with a time-dependent rate. A susceptible vertex can be also infected by itself (according

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21
22
to another Poisson process), which can be interpreted as a source of infection outside of the
23 population. Infection rates are assumed to be time-dependent deterministic functions. An
24 infected vertex recovers in a period of time given by a random variable. Recovery times are
25
assumed to be independent identically distributed random variables with a fairly arbitrary
26
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29
common distribution.
an
Our main result for the discrete model is concerned with the distribution of the time it takes
for a susceptible vertex to get infected (the time to infection). We obtain a simple analytical
30
31 expression for this distribution in terms of a solution of a non-linear integral equation. In some
32 special cases this integral equation is equivalent to a differential equation of Bernoulli type
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33
(depending on a particular case). In one of these cases the corresponding differential equation
34
35 can be solved analytically.
36 The structure of a homogeneous tree plays an essential role in our analysis. The key obser-
37 vation is that a susceptible vertex splits the homogeneous tree into a finite number of identical
38
39 subgraphs, and infection processes on these subgraphs are independent and identically distrib-
40 uted.
41 We then study the discrete model in the limit, as the vertex degree of the tree tends to
42
43 infinity, and the infection rate decreases proportionally. We show that in this limit our results
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44 for the discrete model imply an equation for the susceptible compartment. We call it the
45 master equation, because both the infectious and the recovered compartments can be explicitly
46
47 expressed in terms of its solution. This generalizes the results in ([9], [10] and [12]), where
48 the system of equations of the classic Kermack-McKendrick SIR model was reduced to a single
49 equation.
50
51 The obtained continuous SIR model is fairly general and provides a flexible technical frame-
ce

52 work for modeling various infectious and recovery dynamics. In fact, the master equation
53 implies a family of continuous SIR models. A particular SIR model depends on the structure
54
55 and interpretation of the model parameters. For example, the Kermack-McKendrick SIR model
56 is a special case of our model. Another special case of the model coincides with the SIR model
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57 proposed in [6].
58
59
The rest of the paper is organized as follows. In Section 2 we consider the discrete SIR
60 model. The model is formally defined in Section 2.1. The main result for the discrete model is

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3 stated and proved in Section 2.2. In Section 3.1 we use this result to derive the master equation
4 for the susceptible compartment in the limit, as the tree vertex degree tends to infinity. We
5
6 discuss the continuous SIR model implied by the master equation in Section 3.2 and briefly
7 comment of the relationship of our model with fractional SIR models in Section 4. Finally, in
8 Section 5 we consider some special cases in which the integral equation of the discrete model

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10 can be written in the differential form.
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12
13 2 The discrete SIR model

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16 2.1 The model definition
17
18 We start with defining the discrete continuous time SIR model on a general graph (since a
19 particular structure of the graph is not important at the definition). Let T be a connected
20 (and possibly infinite) graph. With some abuse of notation, we will associate a graph with

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22 the set of its vertices. Given vertices x, y ∈ T we write x ∼ y, if these vertices are connected
23 by an edge, in which case we call them neighbors. Given a vertex its vertex degree is defined
24 as the number of its neighbors. A vertex can be either susceptible, or infected, or recovered
25
26 (and immune). At time t = 0 each vertex is either susceptible, or infected (in which case we
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29
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assume that it gets infected at time t = 0). When a vertex becomes infected, it starts emitting
infectious germs towards all of its neighbors and continues to do so until the moment of its
30 recovery from the disease. When a susceptible vertex gets a germ, it becomes infected, and all
31 subsequently arrived germs do not give any additional effect. An infected vertex emits germs
32 to a given neighbor according to a Poisson process with a time dependent rate. Namely, if
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33
34
a vertex y ∈ T becomes infected at time ty and recovers in a time given in the general case
35 by a random variable Hy , then, at time t ∈ [ty , ty + Hy ] it infects a susceptible neighbor with
36 the rate εt−ty , where (εt , t ≥ 0) is a non-negative deterministic function. A susceptible vertex
37
38
can be also infected by itself, according to a Poisson process with the time-dependent rate λt ,
39 where (λt , t ≥ 0) is a non-negative deterministic function. Thus, given ty , Hy = hy for y ∼ x,
40 a susceptible vertex x is infected at time t with the following total infection rate
41
42 X
43 λt + εt−ty · 1{ty ≤t≤ty +hy } . (1)
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44 y:y∼x
45
46 We assume that all random variables are realized on a certain probability space (Ω, F, P),
47 the expectation with respect to the probability P is denoted by E; all Poisson processes are
48
49
independent of each other, and they are also independent of the recovery times.
50 Both infection rates and recovery times can be fairly arbitrary. However, some minimal
51
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technical assumptions are required. These assumptions are as follows.

52
53 (A1) Functions (εt , t ≥ 0) and (λt , t ≥ 0) are bounded measurable functions.
54
55
56
(A2) Recovery times {Hy , y ∈ T } are given by independent identically distributed random
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57 variables. The common distribution of recovery times is either absolutely continuous, or

58 discrete, or a mixture of these two types of distributions. A special case is when the
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recovery time is given by a deterministic constant H (including the limit case H = ∞).

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7 10
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23

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10 12 3 5 21

11 13 20
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13 14 19

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susceptible infected immuned
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19 Figure 1: A finite fragment of a homogeneous tree, where n = 4 (i.e. each vertex has 5 neighbors).
20

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22 Remark 1. If εt ≡ const, the recovery time is exponentially distributed, the underlying graph
23 is complete (i.e. any two vertices are neighbors) and λt ≡ 0, then the corresponding discrete
24
25 SIR model is a discrete version of the classic Kermack-McKendrick model.
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Remark 2. Note that the case when the recovery time is given by a deterministic constant H
can be modeled by assuming that εt = 0 for t ≥ H. Setting formally H = ∞ gives the model,
30
in which an infected individual never recovers and stays infectious forever. This is not entirely
31 realistic. However, by considering a function ε, which decays to zero sufficiently fast, one can
32 model a situation, when contagiousness of a chronically infected individual practically vanishes
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in a finite time.
34
35
36
37
2.2 Distribution of the time to infection
38
In this section we state and prove the main result (Theorem 1 below) for the discrete SIR model
39
40 on a homogeneous tree.
41 Let ϕt be the probability that an infected at time 0 vertex does not emit a germ towards a
42
given neighbor until time t, and let ft be the probability that an initially susceptible vertex is
43
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44 not self-infected until time t. Then

45 
46
(
1, t < 0, 1, t < 0,
47 ϕt =  R t∧H  and f t = Rt (2)
48 E e− 0 εu du , t ≥ 0, e− 0 λu du , t ≥ 0,
49
50
where, for technical convenience, we define both probabilities by unity for t < 0, and H is a
51
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52 random variable that has the same distribution as the recovery times.
53
54 Theorem 1. Let T be a homogeneous tree with the vertex degree n + 1, where n ≥ 1. Assume
55 that at time t = 0 a vertex x ∈ T is infected with probability p and is susceptible with probability
56
1 − p independently of other vertices. Let τ be the time it takes for a susceptible vertex to get
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57
58 infected. Then
59 P (τ > t) = (1 − p)ft [st ]n+1 for t ≥ 0, (3)
60

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3 where the function st satisfies the integral equation
4
5 t
Z
6 st = ϕt − (1 − p) fu snu ϕ0t−u du, (4)
7 0
8
where functions ϕ and f are defined in (2) and ϕ0 is the derivative of ϕ.

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11 Proof of Theorem 1. Consider a susceptible vertex x ∈ T and define the probability
12
13 st = P(x not infected by a given neighbor before time t), (5)

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16 which does not depend on a neighbor due to homogeneity of both the tree and the initial
17 condition. Recall that infectious neighbors infect the vertex x independently of each other, and
18 there is an independent chance of self-infection. Therefore, we have that
19
20

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21 P(susceptible x not infected neither by its neighbors, nor by itself before time t)
(6)
22 = ft sn+1 for t ≥ 0,
t
23
24
and, hence,
25
26 P(τ > t) = (1 − p)ft sn+1
t for t ≥ 0, (7)
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29
where the factor ft is defined in (2).
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Further, recall that a rooted homogeneous tree with the vertex degree N ≥ 2 as a tree,
30 where one of the vertices, called the root, has N − 1 neighbors, while any other vertex has N
31
32 neighbors. Then, observe that removing the vertex x and all edges connecting x to its neighbors
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33 generates n + 1 subgraphs given by rooted trees with roots y1 , ..., yn+1 , that are neighbors of
34 x. Further, given a neighbor y ∼ x consider an auxiliary SIR model on the rooted tree Ty with
35
36 the root y. Assume that the auxiliary SIR model is specified by the same parameters as the
37 original SIR model on the tree T . In particular, we assume that at time t = 0 any vertex in
38 the auxiliary model is either infected with probability p or susceptible with probability 1 − p,
39
40 independently of other vertices. Let τe be the time to infection of the root vertex y in the
41 auxiliary SIR model on the graph Ty . Similarly to equations (6)-(7) in the original model, we
42 have that
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44
P(eτ > t) = (1 − p)ft snt for t ≥ 0. (8)
45
Further, observe that if the root y is not infected, then, due to the similarity of the rooted
46
47 trees, the time before infection of any of its susceptible neighbor has the same distribution as
48 the infection time τe. Combining this fact with the law of total probability with (8) gives the
49
following equation for the probability st
50
51
ce

Z t
52 st = pϕt − (1 − p) ϕt−u (fu snu )0u du + (1 − p)ft snt for t ≥ 0, (9)
53 0
54
55 where the function ϕ is defined in (2). Integrating by parts gives the equation
56
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57 Z t
58 st = ϕt − (1 − p) fu snu ϕ0t−u du, (10)
59 0
60

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3 which is the integral equation (4), as claimed.
4
5 Remark 3. Consider the SIR model on a homogeneous tree, in which recovery times are given
6 by i.i.d. random variables (including the degenerate case of deterministic recovery time). Recall
7 the function (ϕt , t ≥ 0) defined in (2) and let
8

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d
10 ε̃t = − (log(ϕt )) for t ≥ 0. (11)
11 dt
12
13 It is easy to see that, as long as one is interested in the distribution of the time to infection, they

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14 can consider an equivalent model with just susceptible and infected compartments, in which
15 the recovery mechanism is somehow embedded into the new infection rate given by the function
16
17 ε̃t = (ε̃t , t ≥ 0). For example, consider a SIR model with the infection rate εt = (εt , t ≥ 0)
18 such that εt > 0 for all t ≥ 0, and the deterministic recovery time given by a constant H > 0,
19 then
20
(
εt , for t ≤ H,

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21 ε̃t = (12)
22 0, for t > H.
23
24 Trivially, if H = ∞, then ε̃t = εt for all t ≥ 0. However, the function ε̃t can differ significantly
25 from the original function εt in the case of the random recovery time (e.g., see Corollary 3 in
26
27
28
29
Section 5).
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Remark 4. In some special cases, the obtained integral equation is equivalent to the Bernoulli
30 type differential equation, which can be solved analytically (see Section 5 for examples).
31
32
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33 3 Continuous limit of the discrete model
34
35
36 3.1 The master equation
37
38 In this section we analyze integral equation (4) in the limit, as the tree vertex degree goes to
39 infinity. Specifically, we show that in this limit the integral equation implies an equation for
40 the susceptible population proportion.
41
42 Theorem 2. Consider the discrete SIR model on the homogeneous tree T with the vertex degree
43
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n + 1. Suppose that an infected vertex infects a susceptible neighbor with the rate n+1 εt after
44
45 time t of being infected, where (εt , t ≥ 0) is a non-negative function. In addition, suppose
46 that the other model parameters (i.e. the recovery times and the rate of self-infection) do not
47 depend on n. Let St,n be the expected susceptible population in this SIR model. Let (St , t ≥ 0)
48
49 be a limit point of the sequence of functions (St,n , t ≥ 0), n ≥ 1, in the sense of the pointwise
50 convergence. Then the function (St , t ≥ 0) must satisfy the following equation
51
ce

52 t t
  Z Z
St
53 log =− λu du − (1 − Su )γt−u du, (13)
54 S0 0 0
55
56 where
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57 γt := εt P(H > t) for t≥0 (14)

58
59 and S0 = 1 − p (i.e. it is the probability for a vertex to be susceptible at time t = 0 in the
60 discrete model).

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3 Proof. Note first, that the corresponding ϕ-function (see equation (2)) is given by
4
5

1, t < 0,
6
ϕt,n =  1
R t∧H 
7 E e− n+1 0 εu du , t ≥ 0.
8

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10 By Theorem 1,
11 St,n = S0,n ft [st,n ]n+1 for t ≥ 0, (15)
12
13 where the function st,n satisfies the equation

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15 Z t
16 st,n = ϕt,n − S0,n fu snu,n ϕ0t−u,n du with S0,n = 1 − p = S0 . (16)
17 0
18
19 By (15)-(16),
20

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21 
St,n
1
 n+1
1
 
St,n
   
1
22 st,n = =1+ log − log(ft ) + o ,
23 S 0 ft n+1 S0 n
24
25 so that
26
27
28
29
log

St,n
S0

− log(ft ) = (n + 1)(ϕt,n − 1) −
an Zt
n 1
(Su,n ) n+1 (S0 fu ) n+1 [(n + 1)ϕ0t−u,n ]du. (17)
0
30
31
32 A direct computation (we skip detailes) gives that
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33  t∧H 
34 Z Z t
35 (n + 1)(ϕt,n − 1) = −E  εu du + o(1) =
 γu du + o (1) (18)
36 0
0
37 1
Rt
38 − n+1
(n + 1)ϕ0t,n = −γt e 0 εu du
= −γt (1 + o (1)) (19)
39
40 1
41 for any fixed t ≥ 0, where the function γt is defined in (14). In addition, note that (S0 fu ) n+1 → 1
n
42 and (Su,n ) n+1 → Su,n , as n → ∞. Combining this with (18)-(19) allows to rewrite (17) as follows
43
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44 Zt
  t
45
Z
St,n
46 log − log(ft ) = − γu du + Su,n γt−u du + o (1)
S0 0
47 0
48 (20)
Zt
49
50
=− (1 − Su,n )γt−u du + o (1) .
51
ce

0
52
53
Rt
Since log(ft ) = − 0
λu du, we obtain that
54
55
Zt
56 t
  Z
St,n
Ac

57 log =− λu du − (1 − Su,n )γt−u du + o (1) , (21)

58
S0 0
0
59
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1
2
3 which implies, by the dominated convergence theorem, equation (13) for any pointwise limit
4 point (St , t ≥ 0) for the sequence of functions (St,n , t ≥ 0), n ≥ 1, as claimed.
5
6 Differentiating (13) gives the master equation in the differential form
7
8 t
St0
Z

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9 = −λt − (1 − St )γ0 − 0
(1 − Su )γt−u du, (22)
10 St 0
11
12 or, equivalently,
13 St0 t
Z
Su0 γt−u du.

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14 = −λt − (1 − S0 )γt + (23)
15
St 0
16 Remark 5. The existence and the uniqueness of solution of equation (13) follows from general
17
18 results for integral equations with delay ([5]). It can be shown that the sequence of functions
19 (St,n , t ≥ 0), n ≥ 1, is equicontinuous. Therefore, there exists a subsequence that uniformly
20 converges to the solution of (13). We skip the technical details.

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21
22
23
Remark 6. It follows from equation 13 that stationary value S∞ satisfies the following equation
24   Z ∞ Z ∞
25 S∞
log =− λu du − (1 − S∞ ) γu du. (24)
26 S0
27
28
29
0
an 0

Remark 7. Note that equation (13) (or its differential equivalent (23)) is a standalone equa-
30
tion for the susceptible population St , namely that this equation does not involve neither the
31 infected, nor the recovered populations.
32
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33 Remark 8. It should be noted that all the information concerning the infection rates and
34 recovery times of the original discrete SIR model is included in (23) via the function γ. For
35
36 example, if the recovery time in the discrete SIR model is given by a deterministic constant H,
37 then (
38 εt , for t < H,
39 γt =
40 0, for t ≥ H,
41
42 where εt is the rate of infection in the discrete model. In particular, if H = ∞, then γt = εt .
43 In general, these two functions are different (see Example 2 below).
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44
45
46 3.2 Continuous SIR models implied by the master equation
47
48 In this section we show that the master equation (13) for the susceptible population implies
49 equations for other population compartments (which explains the term master equation). A
50
51 SIR model implied by the master equation (13) depends on the structure and its interpretation
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52 of the function γ. To clarify what is meant by ”interpretation” consider the case when γt = 0
53 for all t > H for some H > 0. This can be interpreted as an infected individual recovering after
54
55
time H since the moment of being infected (as in Remark 8). On the other hand, this can be
56 interpreted, as if an infected individual never recovers, but becomes not contagious to others
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57 after time H since the moment of being infected. In this case one can operate with just two
58
59
compartments, namely susceptible and infected ones. Below we consider examples, where this
60

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3 argument is reinforced. Note that for simplicity of exposition and without loss of generality we
4 assume throughout this section that
5
6 λt ≡ 0, (25)
7
8
i.e. there is no self-infection.

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10 3.2.1 The model with no recovery
11
12 The basic continuous SIR model implied by the master equation is a two-compartmental model,
13
in which the population is divided into two compartments, namely, the compartment of suscept-

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15 ible individuals, described by the variable St , and the compartment of infected ones, described
16 by the variable It , so that
17
18
1 = St + It and for t ≥ 0. (26)
19
Then St0 = −It0 , which allows to rewrite equation (23) as follows
20

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21  Z t 
22 St0 = −St I0 γt + 0
Iu γt−u du . (27)
23 0
24
25 Equation (27) describes the model, in which an individual infected at time u ≥ 0 infects any
26
27
28
29
model without recovery.
an
susceptible individual with the rate γt−u at time t > u. This model can be interpreted as the

30 Example 1 (The model with latent period). Suppose that an infected individual is latent for
31 a non-random period of time of length L > 0. In addition, suppose that the rate of infection
32
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33 is constant. Then γt = ε1{t≥L} , where ε is the rate of infection, and equation (27) becomes as
34 follows
35 St0 = −εSt It−L and It0 = −St0 .
36
37
38 3.2.2 Model with a constant rate of infection and random recovery
39
40 Suppose that the function γt is of the following form
41
42
γt = εβt for t ≥ 0, (28)
43
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44
45 where ε > 0 is a given constant and βt is a non-increasing positive function, such that β0 = 1 and
46 βt → 0, as t → ∞. Then, the master equation implies the continuous SIR model with the three
47
48
standard compartments, in which an infected individual recovers in a time given by random
49 variable ξ with the tail distribution P(ξ > t) = βt , and during its infectious period it infects
50 any susceptible one with the constant rate ε. Indeed, under these assumptions, equation (23)
51
ce

is as follows (recall that (25))

52
53  
54 Zt
55 St0 = −εSt I0 βt − Su0 βt−u du . (29)
56
0
Ac

57
58
59
60

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1
2
3 Define
4
5 Zt
6 It = I0 βt − Su0 βt−u du for t > 0 and I0 = 1 − S0 (30)
7
0
8

pt
9
10 and
11
12
Zt
13 Rt = I0 (1 − βt ) − Su0 (1 − βt−u )du for t > 0 and R0 = 0. (31)

cri
14 0
15
16 It is easy to see that
17
18 1 = St + It + Rt for t ≥ 0. (32)
19
20
Moreover, one can show that both It ≥ 0 and Rt ≥ 0 (we skip the details). Therefore, variables

us
21 It and Rt can be interpreted as the population proportions of infected and recovered individuals
22 respectively in the continuous SIR model with the constant rate of infection ε and the random
23
24
recovery time with the tail distribution given by the function β. Indeed, in this model the
25 infected compartment at time t consists of 1) those who were infected at time 0 and did not
26 recover before time t (which gives the first term I0 βt in (30)), and 2) those, who were infected
27
28
29
an
at time u ∈ (0, t] and did not recover before time t (integrating over time gives the integral
term in (30)). A similar argument gives (46), which also follows from (30) and (32) combined
30 with the initial condition S0 + I0 = 1. Differentiating both (30) and (31), and combining them
31
with (29), we get the following system of equations
32
dM
33
34 St0 = −εSt It , (33)
35 Zt
36
37 It0 = εSt It + I0 βt0 +ε 0
Su Iu βt−u du, (34)
38 0
39 Zt
40
41 Rt0 = −I0 βt0 − ε 0
Su Iu βt−u du. (35)
42 0
43
pte

44 Remark 9. The system of equations (33)-(35) is similar to the system of equations of the delay
45
model proposed in [6] for modeling the spread of Covid-19 in Italy.
46
47
48 Example 2 (The classic SIR model). Consider the discrete SIR model on a homogeneous tree
49 with the vertex degree n + 1. Assume that the infection rate is constant, i.e. εt ≡ ε for some
50 constant ε > 0, and that the recovery time H is exponentially distributed with parameter µ,
51
ce

52
i.e. P(H > t) = e−µt for t ≥ 0. In addition, assume that there is no self-infection, i.e. λt = 0
53 for t ≥ 0. Then Z t∧H 
54 ε
1 − e−µt ,


55 E εu du = εE(min(t, H)) =
0 µ
56
Ac

γt
57 so that γt = εe−µt for t ≥ 0. Setting βt = ε
= e−µt gives a special case of (28). The system of
58
59
60

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1
2
3 equations (33)-(35) becomes as follows
4
5 St0 = −εSt It , (36)
6
7 It0 = εSt It − µIt , (37)
8
Rt0 = µIt , (38)

pt
9
10
11 which is the system of equations of the classic Kermack-McKendrick model (with the infection
12 rate ε and the recovery rate µ).
13

cri
14
Remark 10. Note that in Example 2 it is probably more convenient to start with equation (13),
15
16 which in this case is as follows
17   Z t
18 St
log = −ε (1 − Su )e−µ(t−u) du. (39)
19 S0 0
20

us
21 Then, differentiating (39) gives that
22
23  Z t 
24 St0 = −εSt 1 − St − µ (1 − Su )e −µ(t−u)
du . (40)
25 0
26
27
28
29

an
Combining (40) with (39) we obtain the following equation
 
0 µ St
30 St = −εSt 1 − St + log , (41)
31 ε S0
32
dM
33 which is the master equation (in the differential
  form) corresponding to the Kermack-McKendrick
34 µ St
model. Setting It = 1 − St + ε log S0 , one can proceed as in Example 2 to get the equa-
35
36 tions (36)-(38).
37
38 Remark 11. It should be noted that the master equation (41) is well-known. For example, it
39 is the same as equation (22) in [12] and is also equivalent to equation (26) in [9].
40
41
Remark 12. Note that equating the time derivative to zero in equation (41), i.e. St0 = 0, gives
42
43 the known equation
pte

 
44 µ S
1 − S + log =0 (42)
45 ε S0
46
47 for the stationary population proportion of susceptible individuals S in the SIR model (e.g.
48 see equation (7) in [4] and references therein). In particular, this equation shows that the
49
50
stationary value S depends only on the ratio µ/ε = 1/R0 , where R0 is the basic reproduction
51 number in the classic SIR model. Note also that equation (42) is just a special case of more
ce

52 general equation (24) for the stationary susceptible state.

53
54 Example 3 (Constant rate of infection and deterministic recovery). Consider a model, in which
55
56 the infection rate is given by a constant ε > 0, and the recovery time is given by a deterministic
Ac

57 constant H > 0. This model can be obtained by setting γt = ε for t ∈ [0, H] and γt = 0 for
58
59
60

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1
2
3 t > H. This gives the following model equations
4
5 St0 = −εSt It ,
6
7 It0 = εSt It − εSt−H It−H ,
8
Rt0 = εSt−H It−H ,

pt
9
10
11 where St = It = 0 for t < 0.
12
13
3.2.3 The general case: time-varying infection rate and random recovery

cri
14
15
16
In this section we generalize SIR models considered in Sections 3.2.1 and 3.2.2.
17 Suppose that the function γ is of the following form
18
19 γt = w t β t for t ≥ 0, (43)
20

us
21
22 where (wt , t ≥ 0) is a non-negative function and the function (βt , t ≥ 0) is the tail distribution
23 of some positive random variable (i.e. similarly to what we assumed in Section 3.2.2). Arguing
24 as in Section 3.2.2, we obtain the continuous SIR model described by the following equations
25
26
27
28
29
log
 
St
S0
Z t

0
an
= − (1 − Su )γt−u du, (44)
Zt
30
31 It = I0 βt − Su0 βt−u du, (45)
32 0
dM
33 Zt
34
35
Rt = I0 (1 − βt ) − Su0 (1 − βt−u )du, (46)
36 0
37
38 where, St , It and Rt are population proportions of susceptible, infected and recovered individuals
39 respectively, so that 1 = St + It + Rt for t ≥ 0. As before, we assumed that R0 = 0. In this
40
41 model an infected individual recovers in a random time given by a random variable ξ with the
42 tail distribution P(ξ > t) = βt and, if it is infected at time u, then it infects any susceptible
43
pte

one with the rate wt at the time u + t. Recall, that we also assume (25).
44
45 In the differential form the model equations are as follows
46  Z t 
47 0 0
St = St −I0 γt + Su γt−u du , (47)
48 0
49 Z t
50 0 0 0
It = −St + I0 βt − Su0 βt−u
0
du, (48)
51
ce

0
52 Z t
0 0
53 Rt = −I0 βt + Su0 βt−u
0
du. (49)
54 0
55
56 Remark 13. By choosing appropriate functions (wt , t ≥ 0) and (βt , t ≥ 0) one can model
Ac

57 various infection rates and recovery distributions. For example, using the power law functions
58
allows to model memory effects observed in real data (e.g. see [2] and references therein).
59
60 In the rest of this section we use the idea from [2] in order to rewrite equations (47)-

12
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1
2
3 (49) in terms of a certain kernel. The idea is based on the fact that these equations contain
4 convolutions, which makes it possible to apply the Laplace transform.
5
6 Let (L{g}t , t ∈ R+ ) be the Laplace transform of a function (gt , t ∈ R+ ). It follows from (48)
7 that
8 L{I}t = I0 L{β}t − L{S 0 }t L{β}t ,

pt
9
10 and, hence,
11 L{I}t
12 L{S 0 }t = I0 − .
13
L{β}t

cri
14 Thus, for any appropriate function (gt , t ∈ R+ ) we have that
15
16 Z t
17 Su0 gt−u du = L−1 [L{S 0 }t L{g}t ]
18 0
(50)
19
    
−1 L{I}t −1 L{g}t
20 =L I0 − L{g}t = I0 gt − L L{I}t .
L{β}t L{β}t

us
21
22
23 Since L−1 (L{a}L{b}) is equal to the convolution a ∗ b, we can rewrite (50) as follows
24
t t
25
Z Z
26 Su0 gt−u du = I0 gt − Iu K(g)t−u du, (51)
27
28
29
where K is a kernel defined by
0
an 0

30  
31 −1 L{g}t
K(g)t := L . (52)
32 L{β}t
dM
33
34 Finally, using (51) with gt = −γt in (47), and with gt = −βt0 in (48) and (49) gives the system
35
of the model equations in the kernel form
36
37 Z t
38 St0 = −St Iu K(γ)t−u du, (53)
39 0
40 Z t Z t
0
41 It = St Iu K(γ)t−u du − Iu K(β 0 )t−u du, (54)
42
Z t0 0
43
pte

44 Rt0 = Iu K(β 0 )t−u du. (55)

45 0
46
47 Remark 14. It should be noted that equation (52) is an analogue of equation (16) in [2].
48
49
50 4 Remark on fractional SIR models
51
ce

52
One of the recognized drawbacks of the classic SIR model is that both the infection rate and
53
54 the recovery rate do not depend on the state of the system, i.e. the model is memoryless. A
55 popular approach to modeling memory effects consists in using fractional SIR models (e.g.,
56
see [17] and references therein). Some of these models are obtained by formal replacement
Ac

57
58 of ordinary derivatives by fractional derivatives of a certain type. This gives a system of
59 fractional differential equations that is equivalent to a system of integro-differential equations
60

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1
2
3 with a power-law kernel. For example, replacing ordinary derivatives in the classic SIR model
4 by Caputo fractional derivatives gives a system of fractional differential equations, which are
5
6 equivalent to the following system of integro-differential equations
7 Z t
8
St0= −ε Iu Su Kt−u du, (56)

pt
9 0
10 Z t
11 0
It = (εIu Su − µIu ) Kt−u du, (57)
12 0
13 Z t

cri
0
14 Rt = µ Iu Kt−u du, (58)
15 0
16 α−2
y
17 with the kernel Ky = Γ(α−1) , where α ∈ (0, 1] and Γ is the Gamma-function. However, it is not
18 quite clear what physical/biological process is described by equations (56)-(58). In contrast,
19
20 equations (47)-(49) and their equivalents in the kernel form, i.e. equations (53)-(55), can be

us
21 naturally interpreted in terms of the interaction between compartments. Indeed, using the
22 terminology of [2], one can say that, for example, the flux into the infected compartment is
23
24 equal to the flux out of the susceptible compartment (in the absence of any external factors
25 and self-infection). The susceptible compartment decreases at the rate proportional to its
26 current value St . The value K(γ)t−u (in (53)-(55)) describes the impact made on the susceptible
27
28
29
an
compartment at time t by those individuals, who were infected earlier and is still infectious.
Rt
The coefficient of proportionality, i.e. the integral term 0 Iu K(γ)t−u du, measures the total
30 impact of the infected compartment on the susceptible one over the time period [0, t]. This
31
32 generalizes the interaction between susceptible and infected compartments in the classic SIR
dM
33 model, where only the current value It is taken into account.
34 It should be also noted that the continuous SIR model in the present paper is obtained by
35
36
passing to the limit in the discrete stochastic SIR model. This is in line with SIR models in the
37 kernel form that are derived from stochastic processes based on natural biological assumptions
38 (e.g., see [2], [6] and references therein).
39
40
41
42 5 Appendix. Special cases of the discrete SIR model
43
pte

44 In this section, we consider some special cases of the discrete SIR model on the homogeneous
45 tree with the vertex degree n + 1. In these cases the integral equation (4) can be rewritten in
46
47 an equivalent differential form, which is of interest on its own right.
48 For simplicity of notations we assume that all vertices are initially susceptible (i.e. p = 0 in
49 Theorem 1).
50
51
ce

Corollary 1. Suppose that there is no recovery, i.e. H = ∞, εt = ε1{t≥0} and λt = λ1{t≥0} ,

52
53 where ε > 0 and λ > 0 are given constants. Then
54
55
2ε
st = e− λ (e −1+λt) , if n = 1;
−λt

56 1
(59)
Ac

57
  n−1
ε(n − 1) + λ
58 st = , if n ≥ 2,
ε(n − 1)e−λt + λeε(n−1)t
59
60

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1
2
3 so that
4
5 2ε
P(τ > t) = e−λt e− λ (e −1+λt) , if n = 1;
−λt
(60)
6
n+1
7
  n−1
ε(n − 1) + λ
8 P(τ > t) = e−λt , if n ≥ 2. (61)
ε(n − 1)e−λt + λeε(n−1)t

pt
9
10
11 Proof of Corollary 1. Since εt = ε1{t≥0} and λt = λ1{t≥0} , we have that
12
13
( (
1, t < 0, 1, t < 0,

cri
14 ϕt = and ft = (62)
15 e−εt , t ≥ 0, e−λt , t ≥ 0,
16
17 and ϕ0t = −εe−εt for t ≥ 0. The integral equation (4) in this case is as follows
18
19 Z t
20 st = e −εt
+ε e−λu snu e−ε(t−u) du. (63)

us
21 0
22
23 Differentiating (63) and simplifying gives the following differential equation
24
25
26 s0t = −εst + εe−λt snt . (64)
27
28
29
an
It is easy to verify that the function defined in (59) is a solution of equation 64.
30 Remark 15. The equation (64) is the well known Bernoulli equation (e.g., see [15]). Under
31
32 assumptions of Corollary 1 the model was originally considered in [8].
dM
33
34 Remark 16. It follows from equation (61) that
35
36  n+1
 n−1
−λt ε(n − 1) + λ
37 P(τ > t) = e
38 ε(n − 1)e−λt + λeε(n−1)t
39 
ε(n − 1) + λ

1+ λ
−λt ε(n−1)
40 ∼e = λ
41 ε(n − 1)e−λt + λeε(n−1)t 1+ ε(n−1)
e(ε(n−1)+λ)t
42
43
pte

for sufficiently large n. Further, if ε = εn , where εn n → c > 0, as n → ∞, then

44
45 λ (c+λ)t
e − λc
 
λ 1 λ
46 1 − P(τ > t) = P(τ ≤ t) → c
= 1+ c −(c+λ)t − , as n → ∞. (65)
47 1 + λc e(c+λ)t c 1 + λe c
48
49 In other words, the probability P(τ ≤ t) converges to a linear transformation of the logistic
50 1
51 curve c −(c+λ)t .
ce

1 + λe
52
53
Corollary 2. Suppose that the recovery time is given by a deterministic constant H > 0,
54
55 λt = λ1{t≥0} and εt = ε1{0≤t≤H} , where ε > 0 and λ > 0 are given constants. Then integral
56 equation (4) is equivalent to the following differential equation
Ac

57
58
s0t = −εst + εe−λt snt for t ≤ H,
59 (66)
60 s0t = −εst + εe−λt snt + εe −εH
− εe−λ(t−H)−εH snt−H for t > H.

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1
2
3 Proof of Corollary 2. In this case we have that ft = e−λt and ϕt = e−ε min(t,H) for t ≥ 0, and
4 equation (4) becomes as follows
5
6 ( Rt
7 ϕt + ε e−λu snt ϕt−u du for t < H,
8
st = R0t (67)
ϕt + ε e−λu snu ϕt−u u for t ≥ H.

pt
9 t−H
10
11 A direct computation gives that
12
t
13
Z
s0t = −εϕt + εe−λt snt +ε 2
e−λu snu ϕt−u du = −εst + εe−λt snt for t < H,

cri
14
0
15
16
which is the first equation in (66).
17
18 Further, if t > H, then ϕt = ϕH = e−εH , and, hence,
19
t
20
Z
s0t εe−λt snt εe−λ(t−H)−εH snt−H 2
f (u)snu ϕt−u du

us
21 = − −ε
t−H
22
23 = εe−λt snt − εe −λ(t−H)−εH n
st−H − ε(st − ϕH )
24 −λt n −εH
= −εst + εe st + εe − εe−λ(t−H)−εH snt−H ,
25
26
27
28
29
and this is the second equation in (66), as claimed.
an
We are going to consider an example of the model with a random recovery time.
30
31 Corollary 3 (Exponential recovery time). Suppose that the recovery time is exponentially dis-
32
tributed with the parameter µ and functions (εt , t ∈ R+ ) and (λt , t ∈ R+ ) are as in Corollaries 1
dM
33
34 and 2. Then integral equation (4) is equivalent to the following differential equation
35
36 s0t = −(µ + ε)st + εe−λt snt + µ. (68)
37
38
39 Proof of Corollary 3. Start with computing the corresponding function ϕ
40 Z t Z ∞
41 −ε min(t,H) −εu −µu −εt
e−µu du


ϕt = E e =µ e e du + µe
42
43
0 t (69)
pte

µ ε −(µ+ε)t
44 = + e for t ≥ 0.
µ+ε µ+ε
45
46
47
Recall Remark 3 and define
48
ε(µ + ε)
49 ε̃t := − (log(ϕt ))0 = 1{t≥0} for t ≥ 0, (70)
50 µe(µ+ε)t + ε
51
ce

52 so that ϕ0t = −ε̃t ϕt for t ≥ 0. A direct computation gives that

53
54 ε̃0t − ε̃2t = −(µ + ε)e
γt for t > 0.
55
56
Ac

57
58
59
60

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1
2
3 Using the equation in the preceding display and differentiating equation (4) gives that
4
5 t
Z
s0t εft snt f (u)snu ϕt−u ε̃0t−u − ε2t−u du


6 = −ε̃t ϕ(t) + +
7 0
Z t
8 n
= −ε̃t ϕt + εft st − (µ + ε) fu snu ϕt−u ε̃t−u du

pt
9
0
10
11 = −ε̃t ϕ(t) + εft snt − (µ + ε)(st − ϕt )
12 = −(µ + ε)st + εft snt + (µ + ε − ε̃t )ϕt .
13

cri
14
15 Noting that
16   
17 ε(µ + ε) µ ε −(µ+ε)t
18 (µ + ε − ε̃t )ϕt = µ + ε − (µ+ε)t + e = µ,
µe +ε µ+ε µ+ε
19
20
gives the equation s0t = −(µ+ε)st +εft snt +µ, which is the Bernoulli equation with the additional

us
21
22 term µ, as claimed.
23
24
25 References
26
27
28
29
an
[1] Andersson, H., and Britton, T. (2000). Stochastic epidemic models and their statistical
analysis. Lecture Notes in Statistics, 151, Springer, New York.
30
31 [2] Angstmann, C.N., Henry, B. I., and McGann, A.V. (2016). A Fractional Order Recovery
32
dM
SIR Model from a Stochastic Process. Bulletin of Mathematical Biology, 78, pp. 468–499.
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34
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[3] Ball, F., Britton, T., Larédo, C., Pardoux, E., Sirl, D., and Tran, V.C. (2019). Stochastic
36 Epidemic Models with Inference. Lecture Notes in Mathematics, Mathematical Biosciences,
37 Vol. 2255.
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39 [4] Barlow, N. S., and Weinstein, S. J. (2020). Accurate closed-form solution of the SIR epi-
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41 demic model. Physica D: Nonlinear Phenomena, 408, 132540.
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43 [5] Burton, T.A. and Purnaras, I. K. (2017).Global existence and uniqueness of solutions of
pte

44 integral equations with delay: progressive contractions. Electronic Journal of Qualitative

45
Theory of Differential Equations, 49, pp. 1–6.
46
47
48 [6] Dell’Anna, L. (2020). Solvable delay model for epidemic spreading: the case of Covid-19 in
49 Italy. Scientific Reports, 10, 15763.
50
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ce

[7] Fabricius, G., and Maltz, A. (2020). Exploring the threshold of epidemic spreading for a
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stochastic SIR model with local and global contacts. Physica A: Statistical Mechanics and
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54 Applications, 504, 123208.
55
56 [8] Gairat, A. (1994). Contact process without revival on tree. In Theoretical and applied
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57 aspects of mathematical researches: a collection of scientific works. Preprint, Moscow State

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59 University pp. 97–101. (In Russian).
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2
3 [9] Harko, T., Lobo, F.S.N. and Mak, M.K. (2014). Exact analytical solutions of the
4 Susceptible-Infected-Recovered (SIR) epidemic model and of the SIR model with equal
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6 death and birth rates. Applied Mathematics and Computation, 236, pp. 184–194.
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8 [10] Kendall, D. (1956). Deterministic and stochastic epidemics in closed populations. Proceed-

pt
9 ings of the Third Berkeley Symposium on Mathematical Statistics and Probability, vol. IV,
10 pp. 149–165. University of California Press, Berkeley and Los Angeles, Calif., 1956.
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[11] Kermack, W.O. and McKendrick, A.G. (1927). A contribution to the mathematical theory

cri
14 of epidemics. Proceedings of Royal Society A, 115, pp. 700–721.
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16 [12] Kröger, M. and Schlickeiser (2021). Analytical solution of the SIR-model for the temporal
17 evolution of epidemics. Part A: time-dependent reproduction factor. Journal of Physics A:
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19 Mathematical and Theoretical. 53, 505601. pp. 1–38.
20

us
21 [13] Montagnon, P. (2019). A stochastic SIR model on a graph with epidemiological and pop-
22 ulation dynamics occurring over the same time scale. Journal of Mathematical Biology, 79.
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24 [14] Moreno, Y., Pastor-Satorras, R. and Vespignani, A. (2002). Epidemic outbreaks in com-
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26 plex heterogeneous networks. European Physical Journal B, 26.
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[15] Parker, A.E. (2013). Who solved the Bernoulli differential equation and how did they do
it? The College Mathematics Journal, 44:2.
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31 [16] Schutz, G.M., Brandaut, M., and Trimper, S. (2008). Exact solution of a stochastic
32
dM
33 susceptible-infectious-recovered model. Physical Review E, 78, 061132.
34
35 [17] Yuli Chen, Fawang Liu, Qiang Yu, Tianzeng Li (2021). Review of fractional epidemic
36 models. Applied Mathematical Modelling, 97(4).
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38 [18] Zhang, Z., Zhou, Z., Zou, T. and Chen, G. (2008). Fractal scale-free networks resistant to
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