
In this paper, a novel one dimensional chaotic map K(x)=μx(1−x)1+x, x∈[0,1],μ>0 is proposed. Some dynamical properties including fixed points, attracting points, repelling points, stability and chaotic behavior of this map are analyzed. To prove the main result, various dynamical techniques like cobweb representation, bifurcation diagrams, maximal Lyapunov exponent, and time series analysis are adopted. Further, the entropy and probability distribution of this newly introduced map are computed which are compared with traditional one-dimensional chaotic logistic map. Moreover, with the help of bifurcation diagrams, we prove that the range of stability and chaos of this map is larger than that of existing one dimensional logistic map. Therefore, this map might be used to achieve better results in all the fields where logistic map has been used so far.
Citation: Amit Kumar, Jehad Alzabut, Sudesh Kumari, Mamta Rani, Renu Chugh. Dynamical properties of a novel one dimensional chaotic map[J]. Mathematical Biosciences and Engineering, 2022, 19(3): 2489-2505. doi: 10.3934/mbe.2022115
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In this paper, a novel one dimensional chaotic map K(x)=μx(1−x)1+x, x∈[0,1],μ>0 is proposed. Some dynamical properties including fixed points, attracting points, repelling points, stability and chaotic behavior of this map are analyzed. To prove the main result, various dynamical techniques like cobweb representation, bifurcation diagrams, maximal Lyapunov exponent, and time series analysis are adopted. Further, the entropy and probability distribution of this newly introduced map are computed which are compared with traditional one-dimensional chaotic logistic map. Moreover, with the help of bifurcation diagrams, we prove that the range of stability and chaos of this map is larger than that of existing one dimensional logistic map. Therefore, this map might be used to achieve better results in all the fields where logistic map has been used so far.
In the past few decades, there has been a lot of interest in mathematical models of viral dynamics and epidemic dynamics. Since viruses can directly reproduce inside of their hosts, a suitable model can shed light on the dynamics of the viral load population in vivo. In fact, by attacking infected cells, cytotoxic T lymphocytes (CTLs) play a crucial part in antiviral defense in the majority of virus infections. As a result, recent years have seen an enormous quantity of research into the population dynamics of viral infection with CTL response (see [1,2,3,4]). On the other hand, Bartholdy et al. [3] and Wodarz et al. [4] found that the turnover of free virus is much faster than that of infected cells, which allowed them to make a quasi-steady-state assumption, that is, the amount of free virus is simply proportional to the number of infected cells. In addition, the most basic models only consider the source of uninfected cells but ignore proliferation of the target cells. Therefore, a reasonable model for the population dynamics of target cells should take logistic proliferation term into consideration. Furthermore, in many biological models, time delay cannot be disregarded. A length of time τ may be required for antigenic stimulation to produce CTLs, and the CTL response at time t may rely on the antigen population at time t−τ. Xie et al. [4] present a model of delayed viral infection with immune response
{x′(t)=λ−dx(x)−βx(t)y(t),y′(t)=βx(t)y(t)−ay(t)−py(t)z(t),z′(t)=cy(t−τ)z(t−τ)−bz(t), | (1.1) |
where x(t),y(t) and z(t) represent the number of susceptible host cells, viral population and CTLs, respectively. At a rate of λ, susceptible host cells are generated, die at a rate of dx and become infected by the virus at a rate of βxy. According to the lytic effector mechanisms of the CTL response, infected cells die at a rate of ay and are killed by the CTL response at a rate of pyz. The CTL response occurs proportionally to the number of infected cells at a given time cy(t−z)(t−z) and exponentially decays according to its level of activity bz. Additionally, the CTL response time delay is τ.
The dynamical behavior of infectious diseases model with distributed delay has been studied by many researchers (see [5,6,7,8]) . Similar to [5] , in this paper, we will mainly consider the following viral infection model with general distribution delay
{dxdt=λ−dx(t)−βx(t)y(t),dydt=βx(t)y(t)−ay(t)−py(t)z(t),dzdt=c∫t−∞F(t−τ)y(τ)z(τ)dτ−bz(t). |
The delay kernel F:[0,∞)→[0,∞) takes the form F(s)=snαn+1e−αsn! for constant α>0 and integer n≥0. The kernel with n=0, i.e., F(s)=αe−αs is called the weak kernel which is the case to be considered in this paper.
However, in the real world, many unavoidable factors will affect the viral infection model. As a result, some authors added white noise to deterministic systems to demonstrate how environmental noise affects infectious disease population dynamics (see [9,10,11,12]). Linear perturbation, which is the simplest and most common assumption to introduce stochastic noise into deterministic models, is extensively used for species interactions and disease transmission. Here, we establish the stochastic infection model with distributed delay by taking into consideration the two factors mentioned above.
{dx(t)=[λ−dx(t)−βx(t)y(t)]dt+σ1x(t)dB1(t),dy(t)=[βx(t)y(t)−ay(t)−py(t)z(t)]dt+σ2y(t)dB2(t),dz(t)=[c∫t−∞F(t−τ)y(τ)z(τ)dτ−bz(t)]dt+σ3z(t)dB3(t). | (1.2) |
In our literature, we will consider weight function is weak kernel form. Let
w(t)=∫t−∞αe−α(t−τ)y(τ)z(τ)dτ. |
Based on the linear chain technique, the equations for system (1.2) are transformed as follows
{dx(t)=[λ−dx(t)−βx(t)y(t)]d(t)+σ1x(t)dB1(t),dy(t)=[βx(t)y(t)−ay(t)−py(t)z(t)]dt+σ2y(t)dB2(t),dz(t)=[cw(t)−bz(t)]dt+σ3z(t)dB3(t),dw(t)=[αy(t)z(t)−αw(t)]dt. | (1.3) |
For the purpose of later analysis and comparison, we need to introduce the corresponding deterministic system of model (1.3), namely,
{dx(t)=[λ−dx(t)−βx(t)y(t)]dt,dy(t)=[βx(t)y(t)−ay(t)−py(t)z(t)]dt,dz(t)=[cw(t)−bz(t)]dt,dw(t)=[αy(t)z(t)−αw(t)]dt. | (1.4) |
Using the similar method of Ma [13], the basic reproduction of system (1.4) can be expressed as R0=λβ/ad. If R0≤1, system (1.4) has an infection-free equilibrium E0=(λd,0,0,0) and is globally asymptotically stable. If 1<R0≤1+bβ/cd, in addition to the infection-free equilibrium E0, then system (1.4) has another unique equilibrium E1=(ˉx,ˉy,ˉz,ˉw)=(aβ,βλ−adaβ,0,0) and is globally asymptotically stable. If R0>1+bβcd, in addition E0 and E1, then system (1.4) still has another unique infected equilibrium E2=(x+,y+,z+,w+)=(cλcd+bβ,bc,cβλ−acd−abβcdp+bpβ,b(cβλ−acd−abβ)c(cdp+bpβ)).
We shall focus on the existence and uniqueness of a stable distribution of the positive solutions to model (1.3) in this paper. The stability of positive equilibrium state plays a key role in the study of the dynamical behavior of infectious disease systems. Compared with model (1.4), stochastic one (1.3) has no positive equilibrium to investigate its stability. Since stationary distribution means weak stability in stochastic sense, we focus on the existence of stationary distribution for model (1.3). The main effort is to construct the suitable Lyapunov function. As far as we comprehend, it is very challenging to create the proper Lyapunov function for system (1.3). This encourages us to work in this area. The remainder of this essay is structured as follows. The existence and uniqueness of a global beneficial solution to the system (1.3) are demonstrated in Section 2. In Section 3, several suitable Lyapunov functions are constructed to illustrate that the global solution of system (1.3) is stationary.
Theorem 2.1: For any initial value (x(0),y(0),z(0),w(0))∈R4+, there is a unique solution (x(t),y(t),z(t),w(t)) of system (1.3) on t≥0 and the solution will remain in R4+ with probability 1, i.e., (x(t),y(t),z(t),w(t))∈R4+ for t≥0 almost surely (a.s.).
Proof. In light of the similarity with [14], the beginning of the proof is omitted. We only present the key stochastic Lyapunov function.
Define a C2-function Q(x,y,z,w) by
Q(x,y,z,w)=x−c1−c1lnxc1+y−c2−c2lnyc2+z−1−lnz+c3w−1−lnc3w. |
where c1,c2,c3 are positive constant to be determined later. The nonnegativity of this function can be seen from
u−1−lnu≥0for anyu>0. |
Using Itô's formula, we get
dQ=LQdt+σ1(x−c1)dB1+σ2(y−c2)dB2+σ3(z−1)dB3, |
where
LQ=(1−c1x)(λ−dx−βxy)+(1−c2y)(βxy−ay−pyz)+(1−1z)(cw−bz)+(c3−1w)(αyz−αw)+12c1σ21+12c2σ22+12σ23=λ−dx−βxy+c1(−λx+d+βy+12σ21)+βxy−ay−pyz+c2(−βx+a+pz+12σ22)+cw−bz−cwz+b+12σ23+c3(αyz−αw)−αyzw+α≤λ+c1d+c112σ21+c2a+12c2σ22+b+12σ23+α+(c1β−a)y+(c2p−b)z+(c3α−p)yz+(c−c3α)w. |
Let c1=aβ,c2=bp, 0<c3≤min{pα,cα} such that c1β−a=0, c2p−b=0, c3α−p≤0, c−c3α≤0. Then,
LQ≤λ+c1d+c112σ21+c2a+12c2σ22+b+12σ23+α:=k0. |
Obviously, k0 is a positive constant which is independent of x,y,zand w. Hence, we omit the rest of the proof of Theorem 2.1 since it is mostly similar to Wang [14]. This completes the proof.
We need the following lemma to prove our main result. Consider the integral equation:
dX(t)=X(t0)+∫tt0b(s,X(s))ds+m∑n=1∫tt0σn(s,X(s))dβn(s). | (3.1) |
Lemma 3.1([15]). Suppose that the coefficients of (3.1) are independent of t and satisfy the following conditions for some constant B:
|b(s,x)−b(s,y)|+m∑n=1|σn(s,x)−σn(s,y)|≤B|x−y|,|b(s,x)|+m∑n=1|σn(s,x)|≤B(1+|x|), | (3.2) |
in Dρ∈Rd+ for every ρ>0, and that there exists a nonnegative C2-function V(x) in Rd+ such that
LV≤−1outside some compact set. | (3.3) |
Then, system (3.1) has a solution, which is a stationary Markov process.
Here, we present a stationary distribution theorem. Define
Rs:=Λ2−8c2r2λ(d−σ21)(r−σ22)2[(1+(d−σ21)(r−σ22)2r2)σ21ˉx+ˉy2(aβ+(d−σ21)(r−σ22)ˉyr2)σ22], |
where Λ=cˉy−(b+σ232)>0, r=d∧a, and we denote a∧b=min{a,b},a∨b=max{a,b}.
Theorem 3.1. Assume Rs>0,d−σ21>0 and r−σ22>0. Then there exists a positive solution (x(t),y(t),z(t),w(t)) of system (1.3) which is a stationary Markov process.
Proof. We can substitute the global existence of the solutions of model (1.3) for condition (3.2) in Lemma 3.1, based on Remark 5 of Xu et al. [16]. We have established that system (1.3) has a global solution by Theorem 2.1. Thus condition (3.2) is satisfied. We simply need to confirm that condition (3.3) holds. This means that for any (x,y,z,w)∈R4+∖Dϵ, LV(x,y,z,w)≤−1, we only need to construct a nonnegative C2-function V and a closed set Dϵ. As a convenience, we define
V1(x,y,z,w)=−lnz−e1αlnw+l[(x−¯x)22+aβ(y−¯y−¯ylnyˉy)+(d−σ21)(r−σ22)2r2(x−ˉx+y−ˉy)22+apˉybβz+apˉycαbβw]:=Q1+l[U1+aβU2+(d−σ21)(r−σ22)2r2U3+Q3]:=Q1+l(Q2+Q3), |
where e1 is a positive constant to be determined later, l=8r2c2(d−σ21)(r−σ22)Λ, U1=(x−ˉx)22, U2=y−ˉy−ˉylnyˉy, U3=(x−ˉx+y−ˉy)22, Q1=−lnz−e1αlnw, Q2=U1+aβU2+(d−σ21)(r−σ22)2r2U3, Q3=apˉybβz+apˉycαβbw.
Since λ−dˉx=βˉx¯y=aˉy, we apply Itô's formula to obtain
LU1=(x−ˉx)[λ−dx−βxy]+12σ21x2=(x−ˉx)[−d(x−ˉx)+β(ˉxˉy−xy)]+12σ21(x−¯x+ˉx)2=(x−ˉx)[−d(x−ˉx)+β(ˉxˉy−ˉxy+ˉxy−xy)]+12σ21(x−ˉx+ˉx)2≤−d(x−ˉx)2−β(x−ˉx)2y−β(x−ˉx)(y−ˉy)ˉx+σ21ˉx2+σ21(x−ˉx)2≤−d(x−ˉx)2−a(x−ˉx)(y−ˉy)+σ21(x−ˉx)2+σ21ˉx2=−(d−σ21)(x−ˉx)2−a(x−ˉx)(y−ˉy)+σ21ˉx2, | (3.4) |
LU2=(1−ˉyy)(βxy−ay−pyz)+12ˉyσ22=(y−ˉy)(βx−a−pz)+12σ22ˉy=(y−ˉy)(βx−βˉx+βˉx−a−pz)+12σ22ˉy=(y−¯y)(β(x−ˉx)−pz)+12σ22ˉy=β(x−ˉx)(y−¯y)−p(y−¯y)z+12σ22ˉy≤β(x−ˉx)(y−ˉy)+pˉyz+ˉy2σ22, | (3.5) |
and
LU3=(x−ˉx+y−ˉy)(λ−dx−ay−pyz)+12σ21x2+12σ22y2=(x−ˉx+y−ˉy)(λ−dx+dˉx−dˉx−ay−pyz)+12σ21x2+12σ22y2=(x−ˉx+y−ˉy)(−d(x−ˉx)−a(y−ˉy)−pyz)+12σ21(x−ˉx+ˉx)2+σ222(y−ˉy+ˉy)2≤−(d∧a)(x−ˉx+y−ˉy)2−p(x−ˉx+y−ˉy)yz+σ21(x−ˉx)2+σ21ˉx2+σ22(y−ˉy)2+σ22ˉy2=−(d∧a)(x−ˉx)2−(d∧a)(y−ˉy)2−2(d∧a)(x−ˉx)(y−ˉy)+p(ˉx+ˉy)yz+σ21(x−ˉx)2+σ21ˉx2+σ22(y−ˉy)2+σ22ˉy2=−(r−σ21)(x−ˉx)2−(r−σ22)(y−ˉy)2−2r(x−ˉx)(y−ˉy)+p(a2+βλ−ad)aβyz+σ21ˉx2+σ22ˉy2≤−(r−σ22)(y−ˉy)2+(r−σ22)2(y−ˉy)2+2r2r−σ22(x−ˉx)2+p(a2+βλ−ad)aβyz+σ21ˉx2+σ22ˉy2=−(r−σ22)2(y−ˉy)2+2r2r−σ22(x−ˉx)2+p(a2+βλ−ad)aβyz+σ21ˉx2+σ22ˉy2, | (3.6) |
where r=d∧a, we also use the basic inequality (a+b)2≤2(a2+b2) and Young inequality. It follows from (3.4)–(3.6) that
LQ2≤−(d−σ21)(r−σ22)4r2(y−ˉy)2+(d−σ21)(r−σ22)2r2p(a2+βλ−ad)aβyz+apˉyβz+(1+(d−σ21)(r−σ22)2r2)σ21ˉx2+(aβ+(d−σ21)(r−σ22)ˉyr2)σ22ˉy2, |
Making use of Itô's formula to Q3 yields
LQ3=apˉybβ(cw−bz)+apˉycαbβ(αyz−αw)=−apˉyβz+apˉycbβyz. |
Therefore,
L(Q2+Q3)≤−(d−σ21)(r−σ22)4r2(y−ˉy)2+pβ(acˉyb+(d−σ21)(r−σ22)(a2+βλ−ad)2r2a)yz+(1+(d−σ21)(r−σ22)2r2)σ21ˉx2+(aβ+(d−σ21)(r−σ22)ˉyr2)σ22ˉy2. | (3.7) |
In addition,
LQ1=−cwz−e1yzw+e1+b+12σ23≤−2√yce1+e1+b+12σ23=−2√ˉyce1+e1+b+12σ23−2√ce1(√y−√ˉy). |
Letting e1=c⋅ˉy, by virtue of Young inequality, one gets
LQ1≤−cˉy+b+12σ23+2c√ˉy|y−ˉy|√y+√ˉy≤−Λ+2c|y−ˉy|≤−Λ2+2c2Λ(y−ˉy)2. |
Together with (3.7), this results in
LV1≤−Rs+(2r2acˉyb(d−σ21)(r−σ22)+a2+βλ−ada)4c2p(r−σ22)λβyz=−Rs+qyz, | (3.8) |
where
q=(2r2acˉyb(d−σ21)(r−σ22)+a2+βλ−ada)4c2p(r−σ22)λβ. |
Define
V2(x)=−lnx,V3(w)=−lnw. |
Then, we obtain
LV2=−λx+d+βy+12σ21, |
and
LV3=−yzw+α. | (3.9) |
Define
V4(x,y,z,w)=1θ+2(x+y+p2cz+pαw)θ+2, |
where θ is a constant satisfying 0<θ<min{d−σ212d+σ212,a−σ222a+σ222,b−σ232b+σ232}. Then,
LV4=(x+y+p2cz+pαw)θ+1(λ−dx−ay−pb2cz−p2w) |
LV4=(x+y+p2cz+pαw)θ+1(λ−dx−ay−pb2cz−p2w)+θ+12(x+y+p2cz+pαw)θ(σ21x2+σ22y2+(p2c)2σ23z2)≤λ(x+y+p2cz+pαw)θ+1−dxθ+2−ayθ+2−b(p2c)θ+2zθ+2−12pθ+2αθ+1wθ+2+θ+12(x+y+p2cz+pαw)θ(σ21x2+σ22y2+(p2c)2σ23z2)≤F1−dθxθ+2−aθyθ+2−bθ(p2c)θ+2zθ+2−14pθ+2αθ+1wθ+2, | (3.10) |
in which
F1=sup(x,y,z,w)∈R4+{λ(x+y+p2cz+pαw)θ+1−d(1−θ)xθ+2−a(1−θ)yθ+2−b(1−θ)(p2c)θ+2zθ+2−14pθ+2αθ+1wθ+2+θ+12(x+y+p2cz+pαw)θ(σ21x2+σ22y2+(p2c)2σ23z2)}<∞. |
Construct
G(x,y,z,w)=MV1(x,y,z,w)+V2(x)+V3(w)+V4(x,y,z,w), |
where M>0, satisfies
−MRs+F2≤−2, |
and
F2=supy∈R+{βy−aθ2yθ+2+d+α+12σ21+F1}. | (3.11) |
Note that G is a continuous function and lim infn→∞,(x,y,z,w)∈R4+∖QnG(x,y,z,w)=+∞, where Qn=(1n,n)×(1n,n)×(1n,n)×(1n,n). Thus, G(x,y,z,w) has a minimum point (x0,y0,z0,w0) in the interior of R4+. Define a nonnegative C2 -function by
V(x,y,z,w)=G(x,y,z,w)−G(x0,y0,z0,w0) |
In view of (3.8)–(3.10) and (3.11), we get
LV≤−MRs+Mqyz−λx−yzw−dθxθ+2−aθ2yθ+2−bθ(p2c)θ+2zθ+2−14pθ+2αθ+1wθ+2+F2, | (3.12) |
One can easily see from (3.12) that, if y→0+orz→0+, then
LV≤−MRs+F2≤−2; |
if x→0+ or w→0+ or x→+∞ or y→+∞ or\, z→+∞ or w→+∞, then
LV≤−∞. |
In other words,
LV≤−1for any (x,y,z,w)∈R4+∖Dϵ, |
where Dϵ={(x,y,z,w)∈R4+:ϵ≤x≤1ϵ,ϵ≤y<1ϵ,ϵ≤z≤1ϵ,ϵ3≤w≤1ϵ3} and ϵ is a sufficiently small constant. The proof is completed.
Remark 3.1. In the proof of above theorem, the construction of V1 is one of the difficulties. The term Q3 in V1 is is constructed to eliminate apˉyβz in LQ2. The item l(Q2+Q3) is used to eliminate 2c2Λ(y−ˉy)2 in LQ1.
Remark 3.2. From the expression of Rs, we can see that if there is no white noise, Rs>0 is equivalent to R1>1+bβcd.
Using the well-known numerical method of Milstein [17], we get the discretization equation for system (1.3)
{xk+1=xk+(λ−dxk−βxkyk)△t+σ1xk√△tη1,k+σ21xk2(η21,k−1)△t,yk+1=yk+(βxkyk−ayk−pykzk)△t+σ2yk√△tη2,k+σ22yk2(η22,k−1)△t,zk+1=zk+(cwk−bzk)△t+σ3zk√△tη3,k+σ23zk2(η23,k−1)△t,wk+1=wk+(αykzk−αwk)△t. |
where the time increment △t>0 and ηi,k(i=1,2,3) are three independent Gaussian random variables which follow the distribution N(0,1), equivalently, they come from the three independent from each other components of a three dimensional Wiener process with zero mean and variance △t, for k=1,2,⋯. According to Xie et al. [4], the corresponding biological parameters of system (1.3) are assumed: λ=255,α=1,d=0.1,β=0.002,a=5,p=0.1,c=0.2,b=0.1,r=d∧a=0.1, σ1=σ2=σ3=0.0001. The initial condition is (x0,y0,z0,w0)=(2600,0.5,0.5,0.25). Then, we calculate that Rs=0.05>0. Based on Theorems 2.1 and 3.1, we can conclude that system (1.3) admits a global positive stationary solution on R4+, see the left-hand figures of Figure 1 and the corresponding histograms of each population can be seen in right-hand column.
In this paper, we consider a special kernel function F(t)=αe−αt to investigate the continuous delay effect on the population of stochastic viral infection systems. We derived the sufficient conditions for the existence of stationary distribution by constructing a suitable stochastic Lyapunov function. In addition, we only consider the effect of white noise on the dynamics of the viral infection system with distributed delays. It is interesting to consider the effect of Lévy jumps. Some researchers [18,19] studied the persistence and extinction of the stochastic systems with Lévy jumps. Furthermore, it should be noted that the system may be analytically solved by using the Lie algebra method [20,21]. In our further research, we will study the existence of a unique stationary distribution of the stochastic systems with distributed delay and Lévy jumps. Also, it may be possible to solve the stochastic model via the Lie algebra method.
The authors declare they have not used Artificial Intelligence (AI) tools in the creation of this article.
This work is supported by Hainan Provincial Natural Science Foundation of China (No.121RC554,122RC679) and Talent Program of Hainan Medical University (No. XRC2020030).
No potential conflict of interest.
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