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. 2021 Apr 24;147:110983. doi: 10.1016/j.chaos.2021.110983

Time-dependent probability distribution for number of infection in a stochastic SIS model: case study COVID-19

Olusegun Michael Otunuga 1
PMCID: PMC8112579  PMID: 33994678

Abstract

We derive the time-dependent probability distribution for the number of infected individuals at a given time in a stochastic Susceptible-Infected-Susceptible (SIS) epidemic model. The mean, variance, skewness, and kurtosis of the distribution are obtained as a function of time. We study the effect of noise intensity on the distribution and later derive and analyze the effect of changes in the transmission and recovery rates of the disease. Our analysis reveals that the time-dependent probability density function exists if the basic reproduction number is greater than one. It converges to the Dirac delta function on the long run (entirely concentrated on zero) as the basic reproduction number tends to one from above. The result is applied using published COVID-19 parameters and also applied to analyze the probability distribution of the aggregate number of COVID-19 cases in the United States for the period: January 22, 2020-March 23, 2021. Findings show that the distribution shifts concentration to the right until it concentrates entirely on the carrying infection capacity as the infection growth rate increases or the recovery rate reduces. The disease eradication and disease persistence thresholds are calculated.

Keywords: Stochastic differential equation, COVID-19, Infection, Probability density function, Laguerre function, Whittaker function, Hypergeometric, Kummer

1. Introduction

Several advances have been made in the field of mathematical modeling in studying the behavior of certain dynamical systems whose state evolves with time [1], [10], [23], [38], [43], [44], [49], [51], [54], [56], [57]. Most of these dynamical processes in nature are far from equilibrium and so using stationary distribution to describe and analyze the evolution of such processes has a great limitation [8], [9], [30], [55]. Although studying the evolution of such random dynamical systems using time-dependent probability density function is challenging, significant analysis and estimates about the process can be deduced from such study. The exact solutions in terms of probability density function of dynamical systems can only be obtained for a restricted class of dynamical systems [12], [13], [21], [31], [41].

Apart from Fokker-Planck equation (FPE), a partial differential equation that describes the time evolution of probability density function, there are other methods such as the moment or cumulant equations approach [17] that can be used to analyze the distribution of nonlinear systems under random perturbations. Because of the complexity of solving partial differential equations, many approximate methods have been developed numerically to solve the FPE equation for situations far from equilibrium. A simple thermodynamically consistent matrix numerical method (MNM) is developed by Holubec et al. [26] for solving over-damped FPEs with time-dependent coefficients. Paola at al. [17] proposed an approximate method called the Taylor moments for the probabilistic description of response of nonlinear system driven by a stochastic process. Other methods such as the stochastic linearization (SL) method [53], the equivalent non-linear equations method (ENLE) [14], the moment differential equation method (MDE) Monte Carlo simulation using a non-Gaussian closure approximation [40], the path integral approach, perturbation technique and Galerkin method [32], [35], [60] have been developed for approximating the time-dependent probability density of some general first-order and second-order non-linear stochastic systems.

In this work, we develop the time-dependent probability density function for the number of infections of certain diseases satisfying a particular stochastic SIS epidemic model. The state transition probability density function for the dynamic process is governed by the FPE equation [19], [58]. The result obtained is used to analyze the distribution of the aggregate daily infection count of COVID-19 cases for the United States collected from the Center of Disease Control and Prevention (CDC) for the period: 01/22/2020-03/23/2021.

The organization of the paper is as follows. In Section 2, we formulate a stochastic differential equation (SDE) used in modeling the number of infection at a given time by extending the well known deterministic SIS epidemic model with vital dynamics to a stochastic case. The existence and uniqueness of the solution of the SDE is also discussed. The threshold under which the disease dies out using the SDE model is obtained and analyzed. In Section 3, we derive the closed form time-dependent probability density function for the number of infection at a given time t for the stochastic SIS model. Properties of the distribution, namely, mean, variance, skewness, kurtosis functions are also derived in Section 3. Special cases of the distribution are also discussed in this section. Numerical results are carried out in Section 4 to verify our claim. Discussion and summary of the work done are presented in Section 5.

2. Formulation of model

Our main focus in this work is on the derivation of time-dependent probability density function for the number of infected individuals following the general stochastic SIS model. To do this, we first study the SIS deterministic epidemic model

dS=(ΛNβSINμS+γI)dt,S(t0)=S0,dI=(βSIN(μ+γ)I)dt,I(t0)=I0, (2.1)

where I and S represent the population of infected and susceptible individuals, respectively, S0>0, I00, and Λ>0 is the recruitment rate, β is the transmission rate, μ is the natural death rate and γ is the temporary recovery rate. To maintain a constant population, we assume Λ=μ. With this, the population size N remains constant over time so that S+I=N. This reduces the model governing I in (2.1) to the form

dI=(βN(NI)I(μ+γ)I)dt,I(t0)=I0. (2.2)

The model (2.1) has been studied extensively by Brauer et al. [11], Hethcote and Yorke [25], Lajmanovich and Yorke [33] and Nold [45].

Many factors such as pneumonia seasonality, mobility, testing rates, mask use per capital weather [27], social behavior, strain-specific factors [42], and public health intervention [34] can act as external fluctuations affecting the contact/transmission rate of the disease. For this reason, we assume the contact/transmission rate β of the disease is affected by environmental perturbations, such as stated above, changing the infection transmission rate β to the form

βdt=βdt+σdW(t), (2.3)

where each infected individual makes βdt infectious contacts with each other in the interval [t,t+dt), W(t) is a standard Wiener process on a filtered probability space (Ω,Ft,(Ft)t0,P), the filtration function (Ft)t0 is right-continuous and each Ft with t0 contains all P-null sets in Ft. By substituting (2.3) into (2.1), we reduce the deterministic epidemic model (2.1) to the Stratonovich stochastic model

{dS=(μNβSINμS+γI)dtσSINdW(t),S(t0)=S0,dI=(βSIN(μ+γ)I)dt+σSINdW(t),I(t0)=I0, (2.4)

where denotes the Stratonovich integral [2]. We used the Stratonovich calculus instead of the Itô calculus following the arguments made in [7], [37]. We also assume the initial process (S0,I0) is Ft0 measurable and independent of W(t)W(t0). The solution of (2.4) with Itô calculus has been studied extensively by Gray [22]. In their work, Dalal et al. [16] showed that the introduction of stochastic noise can stabilize system that is unstable. In this work, we are interested in studying how the system behaves in the presence of noise in the transmission rate of the disease. This behavior is studied by analyzing the time-dependent probability density function of the process S(t) and I(t). The stochastic differential equation has a unique positive solution [22], [39], [47], [59] in the feasible region

T:={(S,I)R+2|0S+IN} (2.5)

for all t0 with probability one.

The model governing I in (2.4) reduces to the Itô form

dI=(βN(NI)(μ+γ)+σ22N2(NI)(N2I))Idt+σN(NI)IdW(t),I(t0)=I0. (2.6)

Define

R0=βμ+γ,R0=β+σ2/2μ+γ. (2.7)

The number R0 is referred to the reproduction number for (2.1). This is the average number of infection cases produced by an infectious individual when introduced into a completely susceptible population. The number R0 is the stochastic version of R0 for the model (2.6).

It was shown in Méndez et al. [39] and Otunuga [48] that the boundaries I=0 and I=N of (2.6) are unattainable at all times if R0>1, regardless of the noise intensity. Following a similar Theorem in [22], we show in Theorem 1 that the disease will die out exponentially almost surely on the long run in the presence of noise if R01.

Theorem 1

For any given initial conditionI0(0,N),the solutionI(t)of the stochastic differential Eq.(2.6)tends to zero exponentially almost surely ifR01.

Proof

It follows from (2.6) that

dlnI=(βN(NI)(μ+γ)σ22N2(NI)I)dt+σN(NI)IdW(t).

If R01, we have from (2.5) that

lnI(t)=lnI0+(β(μ+γ))(tt0)t0t(βN+σ22N2(NI(s)))I(s)ds+σNt0t(NI(s))I(s)dW(s),<lnI0+(μ+γ)(R01)(tt0)+σNt0t(NI(s))I(s)dW(s),lnI0+σNt0t(NI(s))I(s)dW(s).

The result follows from the fact that

lim supt1tln(I(t))<0,

using the large number theorem for martingales [24]. □

We see in Theorem 1 that replacing the condition R0<1 with the condition R0<1 for the disease to die out exponentially almost surely is also valid. We note here that epidemic advances can still grow initially, leading to transient epidemic advance if

1σ22(μ+γ)<R0<1.

A numerical result is derived later in Section 4 to confirm Theorem 1 by showing that the stationary probability distribution of I concentrates entirely on zero if R01 (which also implies R01). Likewise, it can be shown that the stochastic differential Eq. (3.2) has a unique stationary distribution if R0>1. The proof of this is similar to the proof given in Theorem 6.2 of the work of Gray et al. [22], so we omit the proof here. We give the closed form representation of the time-dependent and stationary probability density function for I in the next section and confirm that these distributions exist if R0>1.

It was shown in Otunuga [48] that the solution (S(t),I(t)) of the system (2.4) is obtained as

I(t)=N1+C¯(NI0C¯I0Φ(t,t0)+σ22Φ(t,t0)t0tΦ1(s,t0)ds),S(t)=NI(t), (2.8)

where

Φ(t,t0)=eσ22(A¯+1)(tt0)σ(W(t)W(t0)), (2.9)

and

A¯=2σ2(β(μ+γ)σ2/2),C¯=2σ2(μ+γ). (2.10)

Let pI(I|t,I0) be the probability density for the process I satisfying (2.6) at time t given initial point I0. In his work, Otunuga [48] derived the probability density function pI(I|t,I0) for the specific case where the resulting Fokker Planck differential equation for pI(I|t,I0) has only discrete eigen-values rrn and λ satisfying

λ=1σ2(β(μ+γ)(β(μ+γ))22σ2r),

is a non-negative integer. In this work, we extend the work of Otunuga [48] to include both discrete and continuous eigen-values.

3. Derivation of time-dependent probability distribution for the general stochastic SIS epidemic model

Using the transformation

S=SN,I=IN, (3.1)

we reduce (2.4) to the form

{dS=(ΛβSIμS+γI)dtσSIdW(t),S(t0)=S0,dI=(βSI(μ+γ)I)dt+σSIdW(t),I(t0)=I0. (3.2)

By setting S=1I, the stochastic differential equation governing I in (3.2) reduces to the Stratonovich stochastic differential equation

dI=(β(1I)I(μ+γ)I)dt+σ(1I)IdW(t),I(t0)=I0. (3.3)

The Itô equivalent of (3.3) is given by

dI=(β(1I)I(μ+γ)I+σ22(1I)I(12I))dt+σ(1I)IdW(t),I(t0)=I0. (3.4)

Using the change of state variable

x=C¯I1I (3.5)

in (3.4), we obtain the Itô stochastic differential equation

dx=σ22x(A¯+2x)dt+σxdW(t),x(t0)=x0, (3.6)

where A¯ and C¯ are defined in (2.10).

Let pX(x|t,x0) be the probability density function for the process x satisfying (3.6) at time t given initial point x0, and let pXs(x) denotes the corresponding limiting or stationary distribution. We give the closed form expression for pXs(x) and pX(x|t,x0) in the following theorem.

Theorem 2

Assumex0>0andA¯+1>0. Then the solutionx(t)satisfying(3.6)has a unique stationary and time-dependent probability density functionpXs(x)andpX(x|t,x0),respectively, obtained as

pXs(x)=1Γ(A¯+1)xA¯ex,0<x<,pX(x|t,x0)=xA¯exn=0Mn!αnΓ(αn+n+1)ernt(xx0)nLnαn(x0)Lnαn(x)+1Γ(A¯+1)xA¯ex0er(η)th(η;x0)h(η;x)dη,0<x<,

where

rn=σ22n(A¯+1n),forn=0,1,2,M,A¯+121M<A¯+12,r(η)=σ22((A¯+12)2+η2),η0,αn=A¯+12n,forn=0,1,2,M,A¯+121M<A¯+12,G(η)=Γ(A¯+1)ηsinh(2πη)Γ(A¯+12+iη)Γ(A¯+12iη)π2,h(η;x)=G(η)x1A¯2ex2WhittakerW1+A¯2,iη(x),

Lnαn(x)is the Laguerre polynomial[46]

Lnαn(x)=m=0n(αn+m+1)nm(nm)!m!(x)m,

(a)b=a(a+1)(a+2)(a+b)is the Pochhammer symbol[5], andWhittakerWk,θ(x)is the Whittaker function[46].

Proof

It follows from (3.6) and the Fokker Planck equation that pX(x|t,x0) satisfies

tpX=x{σ22x(A¯+2x)pX}+122x2{σ2x2pX},0<x<, (3.7)

with boundary condition

[σ22x(A¯+2x)pX(x,t)+σ22x(x2pX(x,t))]x=0,=0. (3.8)

We assume a solution of the form

pX(x|t,x0)=ψ(x|x0)ert, (3.9)

where r0 is a constant. The stationary density function pXs(x) corresponding to (3.7) is obtained as

pXs(x)=1Γ(A¯+1)xA¯ex, (3.10)

provided that

A¯+1>0,orequivalentlyR0>1. (3.11)

We convert (3.7)-(3.8) to Sturm-Liouville equation

{σ22ddx(x2pXs(x)ddxh(x))+rpXs(x)h(x)=0,[x2pXs(x)ddxh(x)]x=0,=0, (3.12)

by substituting ψ(x|x0)=h(x)pXs(x). By substituting (3.10) into (3.12), we see that the differential equation in (3.12) reduces to

σ22x2d2hdx2+σ22(A¯+2x)xdhdx+rh=0. (3.13)

Using the transformation

h(x)=ex2x1A¯2g(x), (3.14)

we further reduce (3.13) into a differential equation of the form

d2gdx2+(14+θx+14ν2x2)g=0, (3.15)

where

θ=1+A¯2,v=(A¯+12)22rσ2. (3.16)

The differential Eq. (3.15) is the well known Whittaker differential equation (see Section 13.14 of [46]) with solution

g(x)=B1WhittakerMθ,v(x)+B2WhittakerWθ,v(x), (3.17)

where B1, B2 are constants and WhittakerMθ,v(x); WhittakerWθ,v(x) are the Whittaker functions [5], [46]. It now follows from (3.14) that the function h(x) satisfying (3.12) is obtained as

h(x)=B1ex2x1A¯2WhittakerMθ,v(x)+B2ex2x1A¯2WhittakerWθ,v(x). (3.18)

Using relations 6.9.2 and 6.9.4 in Bateman [5], the Sturm-Liousville equation (3.12) has M+1 eigenvalues

rn=σ22n(A¯+1n),forn=0,1,2,M,A¯+121M<A¯+12, (3.19)

with corresponding eigenfunction

hn(x)=CnxnLnαn(x), (3.20)

where

αn=A¯+12n>0, (3.21)

Lnαn(x) is the Laguerre polynomial of degree n, and Cn is a normalizing factor obtained as

Cn=n!αnΓ(A¯+1)Γ(αn+n+1). (3.22)

The Sturm-Liouville equation also has continuous range of eigenvalue

r(η)=σ22((A¯+12)2+η2),η0, (3.23)

with corresponding eigenfunction

h(η;x)=C(η)x12A¯2+iηU(12A¯2+iη,1+2iη,x),=G(η)x1A¯2ex2WhittakerW1+A¯2,iη(x), (3.24)

where U(a,b;x) is the Kummer function [46], i is the imaginary unit, and G(η) is a constant derived using the orthogonal condition

0pXs(x)hm(x)hn(x)dy=δm,n,0pXs(x)h(η;x)h(η;x)dx=δ(ηη), (3.25)

where δ(.) is the Dirac delta function. According to Szmytkowski [52], the functions Wκ,iθ(z)WhittakerWκ,iθ(z) and Wκ,iθ(z)WhittakerWκ,iθ(z), with θ,θ>0, are orthogonal on the positive real semi-axis with the weight z2 in the sense

0z2Wκ,iθ(z)Wκ,iθ(z)dz=π2θsinh(2πθ)Γ(12κ+iθ)Γ(12κiθ)δ(θθ). (3.26)

It follows immediately from (3.25) and (3.26) that

G(η)=Γ(A¯+1)ηsinh(2πη)Γ(A¯+12+iη)Γ(A¯+12iη)π2.

The principal solution pX(x|t,x0) is obtained as

pX(x|t,x0)=xA¯exn=0Mn!αnΓ(αn+n+1)ernt(xx0)nLnαn(x0)Lnαn(x)+1Γ(A¯+1)xA¯ex0er(η)th(η;x0)h(η;x)dη. (3.27)

 □

Remark 1

We note here that the distribution pXs(x) is the Gamma distribution with shape parameter A¯. Since r0=0 and r(η)>0, it follows from (3.27) that

limtpX(x|t,x0)=1Γ(A¯+1)xA¯ex=pXs(x).

Using the fact that the distribution pXs(x) is the Gamma distribution, it follows immediately that the limiting mean, mode, variance, skewness, kurtosis function of x(t) are obtained as

limtE[x(t)]=A¯+1,limtmodex(t)=A¯,limtvarx(t)=A¯,limtskx(t)=2A¯+1,limtKurtx(t)=6A¯+1, (3.28)

respectively.

Using the following integrals regarding Laguerre polynomial (these follows from the Chu-Vandermonde identities (see [46] Section 16.1.1)),

0xν1exLnαn(x)dx=Γ(ν)Γ(αn+n+1)n!Γ(αn+1)(αn+1ν)n(αn+1)n,ifν>0,0xA¯2nexLnαn(x)2dx=Γ(αn+n+1)n!αn, (3.29)

where (a)n is the Pochhammer’s symbol, it can be shown that pX(x|t,x0)>0 and

0pX(x|t,x0)dx=n=0Mn!αnΓ(αn+n+1)erntx0nLnαn(x0)0xA¯nexL(n,αn,x)dx+1Γ(A¯+1)0er(η)th(η;x0)0xA¯exh(η;x)dxdη=n=0Mn!αnΓ(αn+n+1)erntx0nLnαn(x0)Γ(A¯n+1)Γ(αn+n+1)n!Γ(αn+1)(αn+1(A¯n+1))n(αn+1)n+1Γ(A¯+1)0er(η)th(η;x0)G(η)Γ(A¯+12+iη)Γ(A¯+12iη)2F1(A¯+12iη,A¯+12+iη;0;0)=n=0Mn!αnΓ(αn+n+1)erntx0nLnαn(x0)Γ(A¯n+1)Γ(αn+n+1)n!Γ(αn+1)(1n)n(αn+1)n=1,

where 2F1(a,b;c;z) is the Hypergeometric regularized function [46]. □

Remark 2

In order to confirm the validity of the solution (3.27), we show that the solution pX(x|t,x0) corresponds to an initial value δ(xx0). That is, for any real valued continuous function f(x), we have 0f(x)pX(x|t=0,x0)dx=f(x0). To do this, we show that for m0, 0xmpX(x|t=0,x0)dx=x0m. We use (3.29) and equation (44) in Becker [6] to show that

0xmpX(x|t=0,x0)dx=n=0Mn!αnΓ(αn+n+1)x0nLnαn(x0)0xA¯+mnexLnαn(x)dx+1Γ(A¯+1)0h(η;x0)0xA¯/2+m1ex/2WhittakerW1+A¯/2,iη(x)dxdη=n=0M(1)nαnΓ(m+αn+n)Γ(m+n)Γ(αn+n+1)Γ(m)x0nLnαn(x0)+x0mn=0M(1)nαnΓ(m+αn+n)Γ(m+n)Γ(αn+n+1)Γ(m)x0nLnαn(x0)=x0m.

 □

Let pI(I|t,I0) and pS(S|t,S0) be the time-dependent probability density function for the number of infected and susceptible individuals at time t given initial points I0 and S0, respectively. Also, let

Y(S)=C¯(NS)S

and pIs(I) be the corresponding stationary density function. We give the closed form expression for pI(I|t,I0), pS(S|t,S0), and pIs(I) in the following theorem.

Theorem 3

AssumeI0>0,S0>0,andA¯+1>0. Then the solution(I(t),S(t))given in(2.8)and satisfying(2.4)has a unique stationary and time-dependent probability density functionpIs(I),(pI(I|t,I0),pS(S|t,S0)),respectively, obtained as

pIs(I)=NΓ(A¯+1)C¯A¯+1IA¯(NI)A¯+2eC¯INI,0<I<N,pI(I|t,I0)=C¯N(NI)2(C¯INI)A¯eC¯INI[n=0Mn!αnΓ(αn+n+1)ernt(C¯INIC¯I0NI0)nLnαn(C¯I0NI0)Lnαn(C¯INI)+1Γ(A¯+1)0er(η)th(η;C¯I0NI0)h(η;C¯INI)dη],0<I<N,pS(S|t,S0)=C¯NS2(Y(S))A¯eY(S)[n=0Mn!αnΓ(αn+n+1)ernt(Y(S)Y(S0))nLnαn(Y(S0))Lnαn(Y(S))+1Γ(A¯+1)0er(η)th(η;Y(S0))h(η;Y(S))dη],0<S<N. (3.30)

Proof

Using the transformation

x(I)=C¯I1I,0<I<1

in (3.5), we obtain the probability stationary function pIs(I) and the density function pI(I|t,I0) of the number of infection I at a given time time t with initial condition I0 as

pIs(I)=pXs(x(I))×|dxdI|=1Γ(A¯+1)C¯A¯+1IA¯(1I)A¯+2eC¯I1I,0<I<1, (3.31)

and

pI(I|t,I0)=pX(x(I),t|x(I0))|dxdI|=C¯(1I)2x(I)A¯ex(I)[n=0Mn!αnΓ(αn+n+1)ernt(x(I)x(I0))nLnαn(x(I0))Lnαn(x(I))+1Γ(A¯+1)0er(η)th(η;x(I0))h(η;x(I))dη],0<I<1. (3.32)

Let Y(S)=Y(NS). Since S=1I, it follows that the density probability function pS(S|t,S0) of the number of susceptible individuals at time t0 with initial condition S0 can be obtained as

pS(S|t,S0)=pI(I=1S,t|I0)|dIdS|=C¯S2(Y(S))A¯eY(S)[n=0Mn!αnΓ(αn+n+1)ernt(Y(S)Y(S0))nLnαn(Y(S0))Lnαn(Y(S))+1Γ(A¯+1)0er(η)th(η;Y(S0))h(η;Y(S))dη],0<S<1. (3.33)

Eq. (3.30) follows using the transformation (3.1)  □

Remark 3

The condition A¯+1>0 given in (3.10) is equivalent to R0>1. It follows that the probability distribution pIs(I) and pI(I|t,I0) do not exist if R01.

Following similar approach in Remark 1, it can be shown that pI(I|t,I0)>0 and 0NpI(I|t,I0)dI=1. Also, using the substitution u=I/(NI), it can be shown that 0NpIs(I)dI=1.

3.1. Properties of the stationary distribution pIs(I)

One can easily check that

limtpI(I|t,I0)=pIs(I). (3.34)

The cummulative density function, Ps(I) for the distribution pIs(I) in (3.30) is obtained as

PIs(I)=1Γ(A¯+1)γ(A¯+1,C¯INI),0<I<N, (3.35)

where γ(a,z)=0zta1etdt is the lower incomplete gamma distribution.

The mean and variance, denoted μs and σs2, respectively, of the distribution pIs(I) are obtained as

μs=N(A¯+1)eC¯/2C¯A¯/2WhittakerW1A¯2,1+A¯2(C¯)=(A¯+1)NC¯A¯+1eC¯Γ(1A¯,C¯),σs2=(A¯+1)(A¯+2)N2C¯A¯+1U(3+A¯;2+A¯;C¯)[(A¯+1)NC¯A¯+1eC¯Γ(1A¯,C¯)]2,

where Γ(a,z)=zta1etdt is the upper incomplete gamma function and U(a;b;z) is the Kummer/confluent hypergeometric function [46]. We see later in (3.40) that these results correspond to the limiting mean and variance of the distribution pI(I|t,I0). It follows from (3.35) that the median is the number m^ that satisfies the equation

1Γ(A¯+1)γ(A¯+1,C¯m^Nm^)=1/2.

The following theorem shows interval where the stationary density function is decreasing and increasing.

Theorem 4

Define

s±=N4[(2A¯C¯)±(2A¯C¯)2+8A¯]. (3.36)
  • (i)

    IfA¯0,thens0,s+>0and the probability stationary distributionpIs(I)is increasing and decreasing on the interval(0,s+)and(s+,N),respectively, with maximum value attained ats+.

  • (ii)

    If1<A¯<0and(2A¯C¯)2+8A¯>0,thenpIs(I)is increasing and decreasing on the interval(s,s+)and(0,N)[s,s+],respectively. In this case,pIs(I)has local maximum ats+but no absolute maximum value on[0,N].

  • (iii)

    If(2A¯C¯)2+8A¯<0,thenpIs(I)is decreasing on the interval(0,N).

Proof

We note that dpIs(I)dI>0 on (s,s+) and dpIs(I)dI<0 on (0,N)(s,s+). If A¯0, then s0, s+>0. Hence, pIs(I) attains its maximum value at s+ and (i) follows. Likewise, if 1<A¯<0 and (2A¯C¯)2+8A¯>0, then 0<s<s+ and (ii) follows. Finally, if (2A¯C¯)2+8A¯<0, then dpIs(I)dI<0 on (0,N) and (iii) follows. □

3.1.1. Special case where R0=1

The condition R0=1 is equivalent to A¯=0. For this case, pIs(I) reduces to

pIs(I)=NC¯(NI)2eC¯INI,0<I<N.

If {I1,I2,,IM} are samples of M independent identically distributed random variables, the maximum likelihood estimate C¯^ of C¯ is

C¯^=(1Mj=1MIjNIj)1.

3.2. Properties of the density function pI(I|t,I0)

The jth moment, denoted μI(j)(t), of the distribution pI(I|t,I0) at time t is obtained as

μI(j)(t)=0IjpI(I|t,I0)dI,=Njn=0Merntn!αnΓ(αn+n+1)(C¯I0NI0)nLnαn(C¯I0NI0)Q1(j,n)+Njπ2(C¯I0NI0)1A¯20er(η)tηsinh(2πη)Γ(qη)Γ(q¯η)e12C¯I0NI0WhittakerW1+A¯2,iη(C¯I0NI0)Q2(j,η)dη, (3.37)

where

Q1(j,n)=0zj+A¯n(z+C¯)jezLnαn(z)dz,Q2(j,η)=0zj1+A¯2(z+C¯)jez/2WhittakerW1+A¯2,iη(z)dz, (3.38)

qη=A¯+12+iη and q¯η=A¯+12iη, with

Q1(1,n)=(1)nΓ(A¯+2n)eC¯/2C¯A¯/2WhittakerW1A¯2,αn/2(C¯),Q2(1,η)=|Γ(3+A¯2+iη)|2eC¯/2C¯A¯/2WhittakerW1A¯2,iη(C¯),

using identities (13.14.5), (13.6.19) and (13.16.6) in [46]. The mean μI(1)(t), variance σI2(t)=μI(2)(t)(μI(1)(t))2, skewness skI(t)=E[(IμI(1)(t))3]/σI3(t), and kurtosis KurtI(t)=E[(IμI(1)(t))4]/σI4(t), of the distribution pI(I|t,I0) can easily be calculated from (3.37). The limiting jth moment, limtμI(j)(t), is obtained as

limtμI(j)(t)=NjC¯A¯+1Γ(j+1+A¯)Γ(α0)U(1+A¯+j;2+A¯;C¯), (3.39)

where α0 is defined in (3.21) and U(a;b;z) is the Kummer/Congruent Hypergeometric function[46]. It follows immediately from (3.39) that

limtμI(1)(t)=(A¯+1)C¯A¯+1NU(2+A¯;2+A¯;C¯)=N(A¯+1)C¯A¯+1eC¯Γ(1A¯,C¯),limtσI2(t)=(A¯+1)(A¯+2)C¯A¯+1N2U(3+A¯;2+A¯;C¯)[(A¯+1)C¯A¯+1eC¯NΓ(1A¯,C¯)]2,limtskI(t)=limtμI(3)(t)3limtμI(1)(t)limtμI(2)(t)+2(limtμI(1)(t))3(limtσI2(t))3/2,limtKurtI(t)=limtμI(4)(t)4limtμI(1)(t)limtμI(3)(t)+6(limtμI(1)(t))2limtμI(2)(t)3(limtμI(1)(t))4(limtσI2(t))2, (3.40)

where Γ(a,z)=zta1etdt is the incomplete gamma function. The values obtained in (3.40) are the mean, variance, skewness, and kurtosis, respectively, of the stationary density function pIs(I) in (3.30). This is confirmed numerically in Section 4.

3.3. Special cases

In this section, we briefly discuss few interesting cases of the expression for pI(I|t,I0) given in (3.30) involving particular values for the parameters μ, γ, β, and σ.

3.3.1. Case for small μ+γ,C¯0

If C¯0, then pI(I|t,I0) is approximately

pI(I|t,I0)NI(NI)σ2πtexp((ln(I(NI)(NI0)I0)βt)22tσ2),0<I<N, (3.41)

with pIs(I)0.

3.3.2. Case for large μ+γ

The constant E=μ+γ is called the harvesting effort of the system (2.4). It follows from (3.11) that 0<μ+γ<βσ2/2. For large E=μ+γ so that μ+γβσ2/2, it follows from (2.8) that I(t)0. That is, large value of μ+γ leads the infected population to extinct. Also, this condition is equivalent to A¯0 so that pIs(I)NC¯(NI)2eC¯INI and the probability density function pI(I|t,I0) reduces to that in (3.30). This is verified numerically in Section 4.

3.3.3. Case for large noise intensity σ

As the noise intensity in the transmission rate of disease increases (that is, as σ), we see that A¯1, C¯0 and the probability distribution P(I|t,I0) converges to as I0+ and IN. This effect is shown numerically in Section 4.

4. Numerical simulation

In this section, numerical simulation is carried out to verify our claim. First, we use published and assumed COVID-19 epidemiological parameters in Subsection 4.1 to confirm our results. The properties of the distribution are investigated numerically in Subsection 4.2. In Subsection 4.3, the obtained time-dependent and stationary probability density function are used to analyze the distribution of aggregate number of COVID-19 infection cases in the United States.

4.1. Analysis using published data

We apply the distribution using published and assumed parameters. According to recent survey conducted by CDC1 on people with mild COVID-19 cases, one-third did not return to normal health within two to three weeks of testing positive, and recovery takes six weeks or more for those with severe cases. For this reason, we set γ to be in the range [1/30,1/2] for our analysis. The CIA World Factbook2 reported that the current population of the United States as at July 2020 is 332,639,102. So, we set N=1 unit representing 332,639,102 individuals. The total number of infected cases3 as of November 30, 2020 is 13386251. So I0 is about 13,386,251332,639,1020.04 and increasing. For this reason, we suggest I0[0.04,0.05]. Also, the annual U.S. birth rates for the year 2020 is 12.4 births per 1000 population, while the death rate is 8.3 death per 1000 population and life expectancy is 80.3 years4 . Therefore, we set μ to be in the range [833650000,180.3×365]. The parameters used are associated with COVID-19 data and are given in Table 1 below. A MATHEMATICA program that evaluates the Whittaker and Laguarre functions and performs the integration in (3.32) is available from the author upon request.

Table 1.

Parameter values associated with COVID-19 data.

Parameter Description Value Source
γ temporary recovery rate (day1) [1/30,1/2] CDC1
μ death rate (day1) [833650000,180.3×365] CIA4
Λ recruitment rate (day1) μ
β transmission rate (day1) [0.5,1.5],[0.1,2] [18], Assumed
σ noise intensity [0.01,8] Assumed
N population Size 1 CIA2
I0 initial infection cases [0.04,0.05] CDC3

4.1.1. Verification of the result obtained

We note from (3.1) that the time-dependent probability density function pI(I|t,I0) reduces to pI(I|t,I0) if the population size is converted to fractions, that is, if N=1. For the rest of the numerical analysis in this subsection, we set N=1.

In order to verify the correctness of the density function pI(I|t,I0) and the stationary density function pIs(I) obtained in (3.30), we first discretize the stochastic model (3.4) using the Milstein scheme [20] as follows:

Ij+1l=Ijl+(βIjl(1Ijl)(μ+γ)Ijl+σ22Ijl(1Ijl)(12Ijl))Δt+σIjl(1Ijl)ΔWj+1lΔt+σ22Ijl(1Ijl)(12Ijl)((ΔWj+1l)21)Δt, (4.1)

where Ijl=Il(tj), ΔWj+1l=Wl(tj+1)Wl(tj), are independent standard normal variable, tj=jΔt, Δt=1/10, j=1,2,,N, for sample size N, l=1,2,,L for L simulations. For large number of simulations L, the probability density function derived from the histogram of the random variable {I20l}l=1L is plotted and compared with the graph of the probability density function pI(I|t=2,I0) for t20=20Δt=2 in Fig. 1 (a) below. To check the correctness of the result for pIs(I), we simulate the probability density function derived from the histogram of the random variable {INl}l=1L for large N and large number of simulations L. The simulated density function is now compared with the graph of pIs(I) in Fig. 1(b) below

Fig. 1.

Fig. 1

Comparison of the exact density functions pI(I|t=2,I0) and pIs(I) with simulated distribution of {I20l}l=1L and {I1000l}l=1L, respectively.

The red and blue curves in Fig. 1(a) are the trajectories of the exact probability density function pI(I|t=2,I0) and simulated distribution of {I20l}l=1L, respectively, for L=30,000 simulations at time t=2, using the parameters β=0.5, γ=1/7, μ=1/(80×365), σ=0.2. The red and blue curves in Fig. 1(b) are the trajectories of the exact probability density function pIs(I) and simulated distribution of {I1000l}l=1L, respectively, for L=30,000 simulations, tN=t1000=1000Δt=100, using the same parameters above.

4.1.2. Behavior of the distribution of I as the transmission rate changes

In this section, we analyze numerically the behavior of the time-dependent distribution pI(I|t,I0=0.05) and pIs(I) as the transmission rate β increases.

Fig. 2 (a), (b) and (c) is the graph of the probability density function pI(I,t|I0=0.05) for the case where β=0.5, β=0.8, and β=1, respectively. Here, we use μ=180.3×365, γ=1/7 and σ=0.65. Fig. 2(d) shows the stationary probability distribution pIs(I), which is the limiting distribution limtpI(I|t,I0=0.05). We see here that the distributions for the three cases skewed left. This is evident in Figs. 9(b) and 10(b) as we can see there that the skewness plot is negative. We see from Fig. 2(d) that pI(I|t,I0=0.05)pIs(I) as t. Also, we observe that as β increases, the stationary density function shifts concentration to the right. The concentration moves closer to I*=N=1 as β grows larger. This is because as the transmission rate increases, we expect the number of infection to increase until everyone in the population becomes infected. This can be confirmed analytically using (3.30).

Fig. 2.

Fig. 2

Graphs of the probability density function pI(I,t|I0=0.05) and pIs(I) as β increases.

Fig. 9.

Fig. 9

Graphs of the mean, variance, skewness, kurtosis function with time.

Fig. 10.

Fig. 10

Graphs of the mean, variance, skewness, kurtosis function with time.

4.1.3. Behavior of the distribution of I as R01+ and R01+.

As shown in Theorem 1, the disease will die out on the long run if R01 (implying R01 also). Fig. 3(a) and (b) show the behavior of the distribution as disease dies out in the population using parameters μ=180.3×365,γ=1/7, σ=0.1 and varying β so that R01+ in 3(a) and R01+ in 3(b). The result shows that on the long run, the density function of I converges to the Dirac delta function δ(I) as R01+.

Fig. 3.

Fig. 3

Stationary density function pI(I,) for the case where R01+ and R01+, respectively.

4.1.4. Effect of change in temporary recovery rate

It follows from condition (3.11) that 0<γ<βμ.

Fig. 4 (a) and (b) shows the effect of increase in the parameter γ on the stationary density function pIs(I) using parameters μ=180.3×365, β=0.5, with σ=0.1 in Fig. 4(a), and σ=0.3 in Fig. 4(b), respectively. We see here that as γ increases to βμ from the left, the distribution shifts concentration to the left until it concentrates entirely on 0. This shows that the disease dies out as γβμ. We also see the effect of large noise in the system as γ increases. We see that the distribution becomes taller and narrower in the presence of small noise, and flatter and wider in the presence of large noise. In Fig. 4(c), we see that the stationary distribution pIs(I) concentrates more on the final size of the epidemic as the recovery rate decreases to zero. This analysis shows that the disease dies out as the recovery rate γ reaches the threshold βμ. The number of infected reaches maximum as the number of those who recovered declines to zero.

Fig. 4.

Fig. 4

Effect of changing γ on the stationary density function pIs(I).

4.1.5. Distribution for the case where A0.

Fig. 5 (a) and (b) show the probability and stationary density functions pI(I|t,I0=0.05) and pI(I), respectively, for the case where β(μ+γ)σ2/20, or equivalently, A¯0 using parameters in Table 1 with β=0.5, σ=0.65. We see here that as I1, the stationary distribution pIs(I). This follows directly from (3.30).

Fig. 5.

Fig. 5

Probability and stationary density functions pI(I|t,I0=0.05) and pIs(I), respectively, for the case where A¯0.

4.1.6. Distribution for the case where μ+γ0.

Fig. 6 shows the probability density function pI(I|t,I0=0.05) for the case where E=μ+γ=0 using parameters in Table 1 with β=0.5, σ=0.7. The analysis also shows that if the number of infection is not harvested in any way (in this case, by recovering), then pI(I|t,I0) as IN for some T>0 with t<T. Also, we see that pIs(I)=0. This is true because if E=0, pI(I|t,I0)=NI(NI)σ2πtexp((ln(I(NI)(NI0)I0)βt)22tσ2)0 if 0<I<N as t→∞

Fig. 6.

Fig. 6

Probability density function pI(I|t,I0=0.05) for the case where E=μ+γ0.

4.1.7. Effect of noise in the system

Fig. 7 shows the effect of noise intensity σ on the stationary density function pIs(I) using μ=180.3×365, β=0.5, γ=1/7 and varying σ. Fig. 7(a) shows the distribution as σ0 while Fig. 7(b) shows the distribution as σ. We see from Fig. 7(a) that the stationary density function concentrates entirely on the number I*=(11R0)N as σ0. This is because the solution

I(t)=(11R0)N1+(11R0)NI0I0e(β(μ+γ))t

of the deterministic equivalent of (3.4) where σ=0 converges to I*=(11R0)N if R0>1. The number I*=(11R0)N is the endemic equilibrium of the deterministic equivalent of (3.4) where σ=0. Endemic persists in the deterministic system if R0>1. This is confirmed in Fig. 7(a). The graph shows that pIs(I)δ(II*), the Dirac delta function, as σ0+. This is not the case for large σ. In fact, as σ, the stationary density function pIs(I) as I0+ and as I1.

Fig. 7.

Fig. 7

Effect of noise intensity σ on the stationary density function pIs(I).

4.2. Plot of the mean, variance, skewness, and kurtosis function using published parameters

Fig. 8 (a), (b), (c) and (d) is the graph of the mean, variance, skewness, and kurtosis, respectively, of the distribution pI(I|t,I0=0.04) at time t using parameters in Table 1 with μ=180.3×365, β=0.2, γ=1/7 and σ=0.1. The dashed line is the horizontal line representing the limits limtμI(t), limtσI2(t), limtskI(t), limtKurtI(t) of the mean, variance, skewness, and kurtosis functions, respectively, of the distribution pIs(I), given in (3.40). Fig. 8(a) shows that if the transmission rate is β=0.2 and the temporary recovery rate is as low as γ=1/7, the average number of infection cases will rise to 28% on the long run if proper care and prevention is not taken. The variance function converges to 0.0039 on the long run. This shows the magnitude of the spread of the data away from the mean is small. The skewness function is a positive function, suggesting that the distribution of the data is skewed right.

Fig. 8.

Fig. 8

Graphs of the mean, variance, skewness, kurtosis function with time.

Fig. 9 (a), (b), (c) and (d) is the graph of the mean, variance, skewness, and kurtosis, respectively, of the distribution pI(I|t,I0=0.05) at time t using parameters in Table 1 with μ=180.3×365, β=0.8, γ=1/7 and σ=0.65. The dashed line is as described in Fig. 8. Fig. 9(a) shows that if the transmission rate is β=0.8 and the temporary recovery rate is as low as γ=1/7, the average number of infection cases will rise to 77.9% on the long run if proper care and prevention is not taken. The variance function converges to 0.012 on the long run. The skewness function is a negative function, suggesting that the distribution is left skewed.

Fig. 10 (a), (b), (c) and (d) is the graph of the mean, variance, skewness, and kurtosis, respectively, of the distribution pI(I|t,I0=0.05) at time t using parameters in Table 1 with μ=180.3×365, β=1, γ=1/7 and σ=0.65. The dashed line is as described in Fig. 8. Fig. 10(a) shows that if the transmission rate is β=1 and the temporary recovery rate is as low as γ=1/7, the average number of infection cases will rise to 82.8% on the long run if proper care and prevention is not taken. The variance function converges to 0.0064 on the long run. The skewness function is a negative function. By comparing the results derived in Figs. 9 and 10, it follows that the average number of cases increases and the variance decreases on the long run as the transmission rate increases.

4.3. Probability distribution of aggregate number of COVID-19 infections in the United States

Several epidemiological models [1], [10], [23], [38], [43], [44], [49], [51], [57] have been developed to study the transmission of the COVID-19 virus. As it is well known, the generalized logistic equation is widely used in interpreting the aggregate number of COVID-19 infection trajectories in several countries [49], [50], [57]. We see in our work that model (2.2) is a logistic differential equation. In the case of modeling the aggregate number of infected cases, β is referred to as the aggregate infection growth rate, N is the aggregate infection carrying capacity, and (μ+γ) serves as the aggregate infection harvesting effort. In this section, we study the trajectory and the distribution of the aggregate counts of COVID-19 cases reported by the Centers for Disease Control and Prevention (CDC)5 for some states in the United States using model (2.6) and the time-dependent density function (3.30), respectively. We assume the aggregate number of infection follows the model (2.6), where I(t) in this case represents the aggregate infection cases at time t. The advantage of using model (2.6) over most models available in literature is that it considers presence of external perturbations/disturbances in the contact rate of the disease that can be caused by many factors such as pneumonia seasonality, mobility, testing rates, mask use per capital weather [27], social behavior, strain-specific factors [42], and public health intervention [34]. Also, in the presence of this noise, the harvesting function is not constant as widely assumed, but non-linear.

Figs. 11, 12, and 13 shows the plot of the aggregate infection counts of COVID-19 cases for the states and territories: AK, AR, AZ, CA, CO, CT, DC, DE, GA, GU, HI, IA, ID, IL, IN, KS, KY, LA, MD, ME, MI, MN, MO, MP, MS, MT, NC, ND, NE, NH, NJ, NM, NV, OH, OK, OR, PA, RI, SC, SD, TN, TX, UT, VA, VT, WI, WV, WY, in the United States for the period 01/22/2020 to 03/23/2021 using model (2.6), and the parameters in the model estimated for the deterministic version of the model case using the Non-linear Least Squares estimation scheme [15], [36]. We also estimated the initial point I0 for better fit.

Fig. 11.

Fig. 11

Real and simulated aggregate counts of COVID-19 infection for the states and territories: AK, AR, AZ, CA, CO, CT, DC, DE, GA, GU, HI, IA, ID, IL, IN, KS in the United States.

Fig. 12.

Fig. 12

Real and simulated aggregate counts of COVID-19 infection for the states and territories: KY, LA, MD, ME, MI, MN, MO, MP, MS, MT, NC, ND, NE, NH, NJ, NM in the United States.

Fig. 13.

Fig. 13

Real and simulated aggregate counts of COVID-19 infection for the states and territories: NV, OH, OK, OR, PA, RI, SC, SD, TN, TX, UT, VA, VT, WI, WV, WY in the United States.

The parameter estimates N^, β^, γ^, and I^0 of the aggregate infection carrying capacity N, the infection growth rate β, the infection recovery rate γ, and the initial population size I0 are estimated along with the root mean square error (RMSE) of the estimation and reported in Table 2 . T is the number of non-zero aggregate infection days from January 22, 2020 to March 23, 2021. The trajectory of the aggregate infection counts, together with the estimated trajectory for each of the 48 states and territories studied are reported in Fig. 11, Fig. 12, and 13. The red and blue curves are the trajectory for the real and simulated COVID-19 aggregate count data, respectively. The estimated parameter N^ here represents the carrying capacity of the aggregate infection count for each states. We show in later section that as the aggregate harvesting effort μ+γ reduces, or as the aggregate infection growth rate increases due to no proper public health intervention, the aggregate COVID-19 count estimate converges to N^.

Table 2.

Parameter estimates and the RMSE for the period of Jan 22, 2020-March 23, 2021.

State N^ β^ γ^ I0 T RMSE
AK 116955 0.06495 0.03196 11.7 373 1169.2
AR 1387119 0.05572 0.03857 3073.4 374 8295.1
AZ 6207611 0.05191 0.03901 10109.9 419 42953.8
CA 18525258 0.04999 0.03442 18040.2 419 180570.9
CO 1287227 0.06487 0.04007 528.3 381 17744.6
CT 4265220 0.05993 0.04875 8086.5 377 16566.6
DC 1139045 0.06526 0.05747 3.501.3 379 1926.8
DE 993497 0.06256 0.05049 2217.8 375 3.887.0
GA 7996680 0.06166 0.04890 23805.8 386 38483.0
GU 14309 0.06804 0.03079 2.4421 371 152.2
HI 88343 0.066541 0.045843 231.96 381 1164.9
IA 1047217 0.058366 0.037049 1664.8 378 10774
ID 490785 0.055512 0.033361 688.45 372 4195.1
IL 4441504 0.053073 0.035285 5387.3 422 47364
IN 1783274 0.057553 0.033006 898.27 380 24196
KS 868640 0.058924 0.035784 615.67 378 7801
KY 1386548 0.06343 0.041157 797.04 379 7928.9
LA 3399215 0.063446 0.051774 19790 377 17743
MD 4032036 0.062989 0.0521 16646 381 15558
ME 152787 0.0656 0.040101 24.428 374 2044
MI 2316851 0.057358 0.037583 3746.3 376 32390
MN 1243941 0.061734 0.035266 555.81 380 20819
MO 1580962 0.056665 0.033793 1439.2 379 10266
MP 857 0.066576 0.053355 10.391 358 2.8125
MS 1939174 0.063662 0.049823 7495.3 374 9953.3
MT 188925 0.064356 0.029378 14.373 375 1290
NC 4994376 0.056624 0.041666 10277 384 26445
ND 174226 0.064338 0.026613 14.732 374 2473.8
NE 655227 0.062605 0.040601 714.66 380 7454
NH 232013 0.065474 0.038755 24.024 384 3291.7
NJ 21306864 0.064247 0.055493 45087 381 44812
NM 511161 0.062123 0.036503 208.01 375 7326.1
NV 1387057 0.065965 0.048652 2906.5 381 11652
OH 2680011 0.060963 0.035346 871.78 376 35223
OK 1386379 0.056107 0.035141 1358.7 379 10747
OR 655383 0.063132 0.043888 674.69 386 4765.3
PA 3720047 0.06246 0.041921 2585.5 380 44433
RI 559165 0.051781 0.035041 975.64 384 6601.1
SC 4294273 0.060356 0.047188 10037 381 20568
SD 245266 0.067793 0.035468 43.639 376 3069.5
TN 3173919 0.05427 0.036698 6150.5 381 26324
TX 17156629 0.05962 0.045363 43642 381 78597
UT 1095558 0.054204 0.03238 1074.7 378 9331.2
VA 5879402 0.056827 0.044575 13170 378 19814
VT 132684 0.076231 0.058152 46.712 378 607.51
WI 1372907 0.058849 0.030678 477.69 383 13913
WV 327686 0.064602 0.034811 36.89 369 3243.5
WY 99777 0.070869 0.031364 2.2229 374 1245.1

4.3.1. Distribution of the aggregate infection count in the United States for March 23, 2021

Here, we study the effect of small disturbances in the system by setting σ=0.08 and plot the distribution of the aggregate number of infection that occurred on March 23, 2021 for the state of AK, ID, KY, ND, SD, WI, WV, WY. Let T be the number of non-zero days from January 22, 2020 (first day CDC started recording data) to March 23, 2021. We plot the curve for the distribution pI(I|t=T,I^0), together with the density function obtained from the histogram of the random variable {ITl}, l=1,2,,L, in (4.1) for L=10,000 simulations. The value of T for each of the states analyzed are reported in Table 3 . We confirm the result derived in Fig. 7(a), that is, the probability density function pI(I|t=T,I^0) of the aggregate count of COVID-19 for March 23, 2021 concentrates entirely on the number N¯=(11R0)N for small σ. This result is shown in Fig. 14 . The analysis shows that the aggregate count of COVID-19 for the states analyzed converges to N¯ asymptotically on the day March 23, 2021. This number is estimated and reported in Table 3.

Table 3.

Parameter estimate N¯ for the day March 23, 2021.

State AK ID KY ND SD WI WV WY
N¯ 59355 195541 486138 102066 116825 656407 150941 55572
Fig. 14.

Fig. 14

Probability distribution of aggregate number of counts that occurred on March 23, 2021.

4.3.2. Distribution of the final size of the aggregate infection count in the United States

In this section, we study and analyze the distribution of the final size of the aggregate infection count in the United States by studying how the distribution pI(I|t,I^0) behaves as t. According to (3.34), we know that

limtpI(I|t,I^0)=pIs(I).

We verify this by plotting, for large t, say, t=100,000, the distribution pI(I|t,I^0) together with pIs(I). The verification plot is shown in Fig. 15 . For this reason, we analyze the distribution of the final size of the aggregate infection count using the stationary probability density function pIs(I).

Fig. 15.

Fig. 15

Comparison of the probability density function pIs(I) and limtpI(I|t,I0).

Fig. 15 shows the comparison of the stationary density function pIs(I) (in red color) and the limiting distribution limtpI(I|t,I0) (in blue color).

As evidenced in Fig. 2(d), we see that the stationary probability density function pIs(I) concentrates more on the final size of the epidemic N^ as the infection growth rate β increases. We also see a similar behavior in Figs. 4(c) and 7 (b) as the aggregate harvesting effort μ+γ reduces and as the noise intensity σ increases, respectively. For this reason, we study the effect of high infection growth rate β, low recovery rate (low aggregate harvesting effort μ+γ), and effect of large noise on the distribution of the aggregate COVID-19 counts in the United States in the following subsections. This is done by plotting the stationary probability density function pIs(I) of the final size of the aggregate infection count for large, small, and large β, γ, and σ, respectively. We see that the graph of pIs(I) concentrates on the estimate N^ (obtained in Table 2), which is the aggregate carrying capacity of the COVID-19 count in the United States as public health intervention reduced.

Fig. 16 shows the distribution of the final size of the aggregate infection count as the infection growth rate β increases using the estimated parameters in Table 2 with large noise intensity σ=0.2 and varying infection growth rates β=0.06 (blue curve), β=0.15 (black curve), and β=0.3 (red curve) for each states analyzed. The figure shows that if proper intervention is not taken (resulting in increase in infection growth rate β and constant recovery rate γ), the aggregate count of COVID-19 infection will rise to the estimated aggregate carrying capacity value N^ in Table 2 for each respective states and territories. The analysis was done for the 48 states and territories mentioned in Table 2 and similar results obtained for each states and territories. For this reason and in order to minimize space, we only report the plots for the state of AK, ID, KY, ND, SD, WI, WV, WY.

Fig. 16.

Fig. 16

Distribution pIs(I) of the final size of the aggregate infection as the infection growth rate β increases for the states: AK, ID, KY, ND, SD, WI, WV, WY in the United States.

Fig. 17 shows the distribution of the final size of the aggregate infection count as the aggregate harvesting effort decreases using the estimated parameters in Table 2 with large noise intensity σ=0.2 and varying recovery rate γ=0.02 (blue curve), γ=0.015 (black curve), and γ=0.01 (red curve) for each states analyzed. The figure shows that if proper intervention is not taken (resulting in decline in recovery rate γ and constant aggregate growth rate β), the aggregate count of COVID-19 infection will rise to the estimated aggregate carrying capacity value N^ in Table 2 for each respective states and territories. The analysis was done for the 48 states and territories mentioned in Table 2 and similar results obtained for each states and territories. We only report the plots for the state of AK, ID, KY, ND, SD, WI, WV, WY here.

Fig. 17.

Fig. 17

Distribution pIs(I) of the final size of the aggregate infection as the aggregate harvesting rate μ+γ reduces with large noise σ for the states: AK, ID, KY, ND, SD, WI, WV, WY in the United States.

5. Results, conclusion and discussion

By assuming the contact rate β of certain diseases is affected by environmental perturbations, we convert the general deterministic SIS epidemic model with vital dynamics and constant population to a stochastic SIS model and used this model to study the dynamics of some infectious diseases. The study in this work involves analyzing the distribution of numbers of infections whose dynamic follows the SIS stochastic model (2.6). To do this, we derive the closed-form time-dependent probability density function pI(I|t,I0) of the number of infection I at time t given the initial point I0. The stationary probability density function pIs(I) of the process is also derived and analyzed and our studies show that pI(I|t,I0) converges to pIs(I) on the long run. We showed that these distibutions exist if the average number, R0, of individuals infected by an infectious individual in a completely susceptible population is more than one. Also, we showed that the disease will die out if R01. Using the Milstein scheme, the stochastic model (2.6) is discretized for N sample size and L simulations and the correctness of the obtained probability density functions pI(I|t=2,I0) and pIs(I) are verified in Section 4.1.1 by comparing them to the probability density function derived from the histogram of the discretized processes I20l and INl (for large N), respectively, in (4.1), for 1jN, 1lL, and Δt=1/10 using published epidemiological data. The effect of changes in the transmission rate and temporary recovery rate on the distribution pI(I|t,I0) and pIs(I) is studied. It was shown that as R0 approaches 1 (from above), the distribution pIs(I) approaches the Dirac delta function δ(I) and concentrates entirely on zero. That is, on the long run, the number of infection declines and the disease eventually dies out as the reproduction number R0 approaches 1 (from above). Also, as the recovery rate decreases to zero, the distribution of the number of infection shifts concentration to the right until it concentrates entirely on the infection carrying capacity N. That is, the infected population converges to the infection carrying capacity N as the recovery rate reduces significantly. A similar analysis done on the transmission rate β shows that the infected population converges to the infection carrying capacity N as β increases. The effect of noise on the system is also analyzed. It was shown that on the long run, the probability density function pI(I|t,I0) shifts concentration on the disease endemic equilibrium point (11R0)N as the noise intensity σ approaches zero. This is because (2.2) has an endemic equilibrium (11R0)N that is globally stable if R0>1. Some properties of the time-dependent probability density function, namely the mean, variance, skewness, and Kurtosis functions are derived and analyzed as a function of time.

Similar analysis described above is done using the real aggregate counts of COVID-19 cases reported by the Centers for Disease Control and Prevention for the states: AK, AR, AZ, CA, CO, CT, DC, DE, GA, GU, HI, IA, ID, IL, IN, KS, KY, LA, MD, ME, MI, MN, MO, MP, MS, MT, NC, ND, NE, NH, NJ, NM, NV, OH, OK, OR, PA, RI, SC, SD, TN, TX, UT, VA, VT, WI, WV, WY in the United States. We study the trajectory and the distribution of the aggregate counts using the time-dependent density function pI(I|t,I0) and stationary distribution pIs(I) given in (3.30). The validity of the derived time-dependent density function pI(I|t,I0) is verified by comparing the distribution pI(I|t=T,I0) for the aggregate count of COVID-19 for the day March 23, 2021 with the histogram of the distribution of the random variable ITl, l=1,2,,L, for L=10,000 simulations, where T is the number of non-zero days from January 1, 2020 to March 23, 2021. We also show numerically using the real COVID-19 aggregate counts for AK, ID, KY, ND, SD, WI, WV, WY that on the long run, the time-dependent density function pI(I|t,I0) converges to the stationary density function pIs(I). We use the distribution to confirm the estimate of the aggregate count for the month of March 23, 2021 in Table 3 and compare the result with the real data. By studying the distribution of the final size of the aggregate infection counts, our analysis shows that on the long run, if proper intervention is not taken such that the harvesting effort decreases significantly to 0.01 (or less), the aggregate counts of COVID-19 cases for each states may increase to the value N^ reported in Table 2. A similar analysis shows that the aggregate counts of COVID-19 cases for each states may increase to the value N^ if the infection growth rate increases to 0.3 (or more). These studies are confirmed by showing that the distribution pIs(I) shifts concentration on the value N^ as the harvesting effort decreases or the infection growth rate increases. More studies are still ongoing on the distribution of the aggregate count of infection as data are being updated daily. Further extension of the result obtained in this work using fractional order cases as discussed in Jajarmi et al. [28], [29] is under investigation. For more readings on fractional derivatives, we direct readers to the papers [3], [4], [51], [56].

Availability of data and materials

The data used in the analysis can be found on the CDC5 website.

Funding

This research did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sectors.

CRediT authorship contribution statement

Olusegun Michael Otunuga: Conceptualization, Data curation, Formal analysis, Software, Writing - original draft, Writing - review & editing.

Declaration of Competing Interest

The author declares that there is no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

Footnotes

Appendix A. Supplementary materials

Supplementary Data S1

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Associated Data

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Supplementary Materials

Supplementary Data S1

Supplementary Raw Research Data. This is open data under the CC BY license http://creativecommons.org/licenses/by/4.0/

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Supplementary Data S2

Supplementary Raw Research Data. This is open data under the CC BY license http://creativecommons.org/licenses/by/4.0/

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Supplementary Raw Research Data. This is open data under the CC BY license http://creativecommons.org/licenses/by/4.0/

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Supplementary Raw Research Data. This is open data under the CC BY license http://creativecommons.org/licenses/by/4.0/

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Supplementary Raw Research Data. This is open data under the CC BY license http://creativecommons.org/licenses/by/4.0/

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Supplementary Data S6

Supplementary Raw Research Data. This is open data under the CC BY license http://creativecommons.org/licenses/by/4.0/

mmc6.fig (35.7KB, fig)
Supplementary Data S7

Supplementary Raw Research Data. This is open data under the CC BY license http://creativecommons.org/licenses/by/4.0/

mmc7.fig (35.8KB, fig)
Supplementary Data S8

Supplementary Raw Research Data. This is open data under the CC BY license http://creativecommons.org/licenses/by/4.0/

mmc8.fig (34.8KB, fig)
Supplementary Data S9

Supplementary Raw Research Data. This is open data under the CC BY license http://creativecommons.org/licenses/by/4.0/

mmc9.fig (35.4KB, fig)
Supplementary Data S10

Supplementary Raw Research Data. This is open data under the CC BY license http://creativecommons.org/licenses/by/4.0/

mmc10.fig (34.9KB, fig)
Supplementary Data S11

Supplementary Raw Research Data. This is open data under the CC BY license http://creativecommons.org/licenses/by/4.0/

mmc11.fig (41.8KB, fig)
Supplementary Data S12

Supplementary Raw Research Data. This is open data under the CC BY license http://creativecommons.org/licenses/by/4.0/

mmc12.fig (54.2KB, fig)
Supplementary Data S13

Supplementary Raw Research Data. This is open data under the CC BY license http://creativecommons.org/licenses/by/4.0/

mmc13.fig (64.3KB, fig)
Supplementary Data S14

Supplementary Raw Research Data. This is open data under the CC BY license http://creativecommons.org/licenses/by/4.0/

mmc14.fig (62.1KB, fig)
Supplementary Data S15

Supplementary Raw Research Data. This is open data under the CC BY license http://creativecommons.org/licenses/by/4.0/

mmc15.fig (52.2KB, fig)
Supplementary Data S16

Supplementary Raw Research Data. This is open data under the CC BY license http://creativecommons.org/licenses/by/4.0/

mmc16.fig (213.6KB, fig)
Supplementary Data S17

Supplementary Raw Research Data. This is open data under the CC BY license http://creativecommons.org/licenses/by/4.0/

mmc17.fig (211KB, fig)
Supplementary Data S18

Supplementary Raw Research Data. This is open data under the CC BY license http://creativecommons.org/licenses/by/4.0/

mmc18.fig (34.5KB, fig)
Supplementary Data S19

Supplementary Raw Research Data. This is open data under the CC BY license http://creativecommons.org/licenses/by/4.0/

mmc19.fig (34.4KB, fig)
Supplementary Data S20

Supplementary Raw Research Data. This is open data under the CC BY license http://creativecommons.org/licenses/by/4.0/

mmc20.fig (34.8KB, fig)
Supplementary Data S21

Supplementary Raw Research Data. This is open data under the CC BY license http://creativecommons.org/licenses/by/4.0/

mmc21.fig (33.1KB, fig)
Supplementary Data S22

Supplementary Raw Research Data. This is open data under the CC BY license http://creativecommons.org/licenses/by/4.0/

mmc22.fig (34.7KB, fig)
Supplementary Data S23

Supplementary Raw Research Data. This is open data under the CC BY license http://creativecommons.org/licenses/by/4.0/

mmc23.fig (33.8KB, fig)
Supplementary Data S24

Supplementary Raw Research Data. This is open data under the CC BY license http://creativecommons.org/licenses/by/4.0/

mmc24.fig (35.7KB, fig)
Supplementary Data S25

Supplementary Raw Research Data. This is open data under the CC BY license http://creativecommons.org/licenses/by/4.0/

mmc25.fig (35.9KB, fig)
Supplementary Data S26

Supplementary Raw Research Data. This is open data under the CC BY license http://creativecommons.org/licenses/by/4.0/

mmc26.fig (34.7KB, fig)
Supplementary Data S27

Supplementary Raw Research Data. This is open data under the CC BY license http://creativecommons.org/licenses/by/4.0/

mmc27.fig (34.3KB, fig)
Supplementary Data S28

Supplementary Raw Research Data. This is open data under the CC BY license http://creativecommons.org/licenses/by/4.0/

mmc28.fig (37.3KB, fig)
Supplementary Data S29

Supplementary Raw Research Data. This is open data under the CC BY license http://creativecommons.org/licenses/by/4.0/

mmc29.fig (35.6KB, fig)
Supplementary Data S30

Supplementary Raw Research Data. This is open data under the CC BY license http://creativecommons.org/licenses/by/4.0/

mmc30.fig (220.2KB, fig)
Supplementary Data S31

Supplementary Raw Research Data. This is open data under the CC BY license http://creativecommons.org/licenses/by/4.0/

mmc31.fig (221.3KB, fig)
Supplementary Data S32

Supplementary Raw Research Data. This is open data under the CC BY license http://creativecommons.org/licenses/by/4.0/

mmc32.fig (281.6KB, fig)
Supplementary Data S33

Supplementary Raw Research Data. This is open data under the CC BY license http://creativecommons.org/licenses/by/4.0/

mmc33.fig (282.7KB, fig)
Supplementary Data S34

Supplementary Raw Research Data. This is open data under the CC BY license http://creativecommons.org/licenses/by/4.0/

mmc34.fig (283.7KB, fig)
Supplementary Data S35

Supplementary Raw Research Data. This is open data under the CC BY license http://creativecommons.org/licenses/by/4.0/

mmc35.fig (280.5KB, fig)
Supplementary Data S36

Supplementary Raw Research Data. This is open data under the CC BY license http://creativecommons.org/licenses/by/4.0/

mmc36.fig (281KB, fig)
Supplementary Data S37

Supplementary Raw Research Data. This is open data under the CC BY license http://creativecommons.org/licenses/by/4.0/

mmc37.fig (283.9KB, fig)
Supplementary Data S38

Supplementary Raw Research Data. This is open data under the CC BY license http://creativecommons.org/licenses/by/4.0/

mmc38.fig (34.6KB, fig)

Data Availability Statement

The data used in the analysis can be found on the CDC5 website.


Articles from Chaos, Solitons, and Fractals are provided here courtesy of Elsevier

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