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. 2022 May 13;46(3):859–868. doi: 10.1007/s40995-022-01287-5

Global Dynamics of a Diffusive Two-Strain Epidemic Model with Non-Monotone Incidence Rate

Anupam Khatua 1,✉, Debprasad Pal 2, Tapan Kumar Kar 1
PMCID: PMC9103621  PMID: 35601604

Abstract

In this article, we investigate a diffusive two-strain epidemic model with non-monotone incidence rate and virus mutation. The positivity, existence and uniform boundedness of the solutions of the model system are studied. It is found that the system has three equilibrium points, namely the infection-free equilibrium point, the strain-2 endemic equilibrium point and both the strain-1 and strain-2 endemic equilibrium points. The global asymptotic stability analysis of the diffusive model system near all the equilibrium points is carried out by constructing appropriate Lyapunov functional. It is found that the system has no strain-1 endemic equilibrium point possibly due to the virus mutation. So, in this type of diseases, the infection due to strain-1 cannot be persistent in the community.

Keywords: Two-strain epidemic model, Reaction–diffusion equation, Non-monotone incidence rate, Virus mutation, Global dynamics.

Introduction

Mathematical modeling has been extensively used in last few decades for studying the dynamics of the infectious diseases. After the pioneering work of Kermack and McKendrick (1927), different kinds of mathematical models have been proposed in order to achieve a better understanding of the transmission pattern of the infectious diseases (see Dubey et al. (2016a), Dubey et al. (2016b), Hattaf et al. (2012), Khatua and Kar (2020a), Khatua and Kar (2020b), Khatua et al. (2021), Mandal et al. (2020), Mandal et al. (2020) ). The proper choice of the incidence function is of great practical importance in studying the disease dynamics. There are several nonlinear incidence functions in literature for describing the disease transmission rate, for example bi-linear incidence rate (Martcheva (2015)), nonlinear incidence rate (Korobeinikov and Maini (2004)), saturated incidence rate (Zhang and Liu (2008)), non-monotone incidence rate (Xiao and Ruan (2007)), and general incidence rate (Ávila-Vales et al. (2017)). However, from a practical point of view, out of these, the non-monotone incidence is most important as it is capable to incorporate the behavioral changes of the susceptible population when the infected population is very large. Xiao and Ruan (2007) studied the global behavior of an epidemic system with non-monotonic incidence rate, while Muroya et al. (2011) investigated a delayed SIRS type epidemic model with a non-monotonic incidence rate. By using the monotone iterative techniques, they established the sufficient conditions for the global asymptotic stability of endemic equilibrium under the condition R0>1. Baba and Hincal (2017) investigated the dynamics of a two strain epidemic model with bi-linear and non-monotone incidence rate. They have shown that any strain with highest basic reproduction ratio will automatically outperform the other strain. Meskaf et al. (2020) studied the two-strain SEIR type model with non-monotone incidence rates. Very recently, Kumar (2021) studied the effects of non-monotonic functional response on a disease transmission model. Some other model-based research works using non-monotone incidence rate can be found in Feng and Qiu (2018), Li and Teng (2018), Kar and Batabyal (2010) and the references cited therein.

Also, there are many diseases in which more than one pathogen strains are observed due to the process of virus mutation, for example influenza, dengue, COVID-19, and some sexually transmitted diseases. So, it is better to use the multi-strain models as they can describe those diseases more accurately in comparison with the single strain models. Baba et al. (2018) studied an epidemic model consisting of two strains with vaccine for each strain. They concluded that if both the basic reproduction numbers are less than unity, then the disease dies out, and if one of the ratios is less than unity, then epidemic occurs with respect to the other. While Baba and Hincal (2018) proposed and analyzed an epidemic model for influenza with three strains and they studied the effects of vaccination and awareness, Nandi et al. (2019) studied the complex dynamical behavior of an epidemic model with two diseases, and also they pointed out the optimal control strategy. Similar kind of research articles on multi-strain models can be found in Li et al. (2013), Liu et al. (2018), Meskaf et al. (2020), and the references cited in those articles.

Moreover, spatial heterogeneity of the populations plays an important role in the spread of infectious diseases. Ignoring spatial diffusion in model is to ignore the reality. In this regard, reaction–diffusion equations are used to include the spatial movement of the populations into the models. Wang et al. (2012) investigated the complex dynamics of a reaction–diffusion epidemic model. Their results indicate that the spread of the epidemic is strongly influenced by the diffusion. Li and Bie (2019) studied the dynamics of a diffusive SIRS type epidemic system in spatially heterogeneous environment. They concluded that the spontaneous infection enhances the persistence of disease. Han and Lei (2019) studied the global dynamics of a diffusive SEIR epidemic model with nonlinear incidence. There are many research works investigating the role of spatial diffusion on the dynamics of the diseases, for example Holmes et al. (1994), Lotfi et al. (2014), Kuniya and Wang (2018), and the references cited therein. However, to our best knowledge no attempt has been made to study the dynamics of a two-strain reaction–diffusion epidemic model with non-monotone incidence rate for both the strains and virus mutation. In this present study, we will study the dynamical behavior of a diffusive two-strain epidemic model incorporating non-monotonic incidence rate.

The rest of this article is organized as follows: In Sect. 2, we formulate the two-strain epidemic model considering the spatial diffusion and virus mutation. Then, the existence, positivity and uniform boundedness of the solutions of the model system are studied in Sect. 3. All the possible equilibrium points of the system and their respective global stability analysis are investigated in the Sect. 4. Finally, in Sect. 5, some conclusions are provided.

Model Formulation

Here, we develop a two-strain diffusive epidemic model with virus mutation and non-monotone incidence rate. We assume that the total population is divided into four classes, namely susceptible class S(t), infected class with strain-1 I1(t), infected class with strain-2 I2(t) and recovered class R(t). Further we consider the following assumptions to construct the model.

∙ The recruitment rate to the susceptible class is taken as Λ.

∙ The susceptible individuals can become infected by strain-1 or strain-2 and move to the infected compartments I1 and I2 at a rate α1 and α2 respectively.

∙ Following Xiao and Ruan (2007), non-monotonic incidence rate kSI1+αI2 is considered. The incidence function is increasing when I is small and decreasing when I is large. This type of incidence is considered to interpret the psychological effect: for a very large number of infective individuals the infection force may decrease as the number of infective individuals increases, because in the presence of large number of infectives the population may tend to reduce the number of contacts per unit time.

  • The infected individuals with one of the strain cannot be infected with the other, i.e., there is no super-infection. However, it is considered that the strain-1 mutate into strain-2 at a rate ξ.

  • The infected individuals of I1 and I2 compartments recover at a rate ρ1 and ρ2 respectively.

  • The natural mortality rate for each classes is taken as d and the disease induced mortality rate for due to strain-1 and strain-2 is taken as μ1 and μ2 respectively.

  • Moreover, the spatial diffusion is taken into consideration, i.e., the population move randomly described as Brownian random motion.

Based on the above assumptions, our reaction–diffusion model takes the following form:

∂S∂t=Λ-α1SI11+γ1I12-α2SI21+γ2I22-dS+d1∇2S,x∈Ω,t>0,∂I1∂t=α1SI11+γ1I12-d+μ1+ρ1I1-ξI1+d2∇2I1,x∈Ω,t>0,∂I2∂t=α2SI21+γ2I22-d+μ2+ρ2I2+ξI1+d3∇2I2,x∈Ω,t>0,∂R∂t=ρ1I1+ρ2I2-dR+d4∇2R,x∈Ω,t>0, 1

with homogeneous Neumann boundary conditions

∂S∂ν=0,∂I1∂ν=0,∂I2∂ν=0,∂R∂ν=0,x∈∂Ω,t>0 2

and initial conditions

S(x,0)=S0(x)≥0,I1(x,0)=I10(x)≥0,I2(x,0)=I20(x)≥0,R(x,0)=R0(x)≥0. 3

Here, Ω is a bounded domain in Rn with smooth boundary ∂Ω, and ∂S∂ν, ∂I1∂ν, ∂I2∂ν, and ∂R∂ν are, respectively, the normal derivatives of S,I1,I2 and R on ∂Ω.

In the above, S(x,t),I1(x,t),I2(x,t),R(x,t), respectively, stand for the density of susceptible, infected with strain-1, infected with strain-2 and recovered populations at location x and time t. The positive constants d1,d2,d3,d4 are used to measure their respective migration (movement) mobility.

Global Existence, Positivity, and Boundedness

Proposition 1

The system (1) has a unique solution defined on [0,∞) and this solution remains non-negative for all t≥0.

Proof

The system (1) can be written abstractly in the Banach space X=C(Ω¯)×C(Ω¯) of the following form:

u′(t)=Au(t)+F(u(t)),t>0,u(0)=x0∈X.

where u=Col(S,I1,I2,R), A(u(t))=Col(d1∇2S,d2∇2I1,d3∇2I2,d4∇2R) and

F(u(t))=Λ-α1SI11+γ1I12-α2SI21+γ2I22-dSα1SI11+γ1I12-d+μ1+ρ1I1-ξI1α2SI21+γ2I22-d+μ2+ρ2I2+ξI1ρ1I1+ρ2I2-dR.

However, F is locally Lipschitz in X. Therefore, it can be concluded from Pazy (1983) that the system (1) admits a local solution on [0,Tmax], where Tmax is the maximum time for which the solution of the system (1) exist.

In addition, the system (1) can be written as:

∂S∂t-d1∇2S=Λ-α1SI11+γ1I12-α2SI21+γ2I22-dS=F1(S,I1,I2,R),∂I1∂t-d2∇2I1=α1SI11+γ1I12-d+μ1+ρ1I1-ξI1=F2(S,I1,I2,R),∂I2∂t-d3∇2I2=α2SI21+γ2I22-d+μ2+ρ2I2+ξI1=F3(S,I1,I2,R),∂R∂t-d4∇2R=ρ1I1+ρ2I2-dR=F4(S,I1,I2,R). 4

Here the functions Fi(S,I1,I2,R),i=1,2,3,4 are continuously differentiable functions and also

F1(0,I1,I2,R)=Λ>0,F2(S,0,I2,R)=0≥0,F3(S,I1,0,R)=ξ1I1≥0,F4(S,I1,I2,0)=ρ1I1+ρ2I2≥0.

Since the initial data of the system (1) are non-negative, all the solutions of the system (1) remain positive. □

Proposition 2

There exists a positive constant K1 independent of initial data such that the solution (S,I1,I2,R) of the system (1) satisfies

∣∣S(.,t)∣∣L∞(Ω)+∣∣I1(.,t)∣∣L∞(Ω)+∣∣I2(.,t)∣∣L∞(Ω)+∣∣R(.,t)∣∣L∞(Ω)≤K1,∀t≥T0,

for some large time T0>0.

Proof

First adding the equations of the system (1), we obtain

∂∂tS+I1+I2+R-d1∇2S-d2∇2I1-d3∇2I2-d4∇2R=Λ-dS+I1+I2+R-μ1I1-μ2I2,∀t∈(0,Tmax) 5

Now integrating both sides of Eq. (5) over Ω with respect to x by parts and using the zero Neumann boundary conditions, we then obtain

ddt∫ΩS+I1+I2+Rdx=∫ΩΛdx-∫ΩdS+I1+I2+Rdx-∫Ωμ1I1dx-∫Ωμ2I2dx≤∫ΩΛdx-∫ΩdS+I1+I2+Rdx 6
LetV(t)=∫ΩS+I1+I2+Rdx.

Then, from inequality (6), we have

dVdt≤∣Ω∣Λ-dVt

Now integrating the above inequality from 0 to t, we get

V(t)≤V(0)e-dt+∣Ω∣Λd1-e-dti.e.∫ΩS+I1+I2+Rdx≤e-dt∫ΩS0(x)+I10(x)+I20(x)+R(x)dx+∣Ω∣Λd1-e-dt∀t≥0

Thus, we obtain

limsupt→∞∫ΩS+I1+I2+Rdx≤∣Ω∣Λd. 7

Now in view of [Theorem 3.3 of Dung (1998) ], there exists a positive constant K1, which does not depend on initial data such that

∣∣S(.,t)∣∣L∞(Ω)+∣∣I1(.,t)∣∣L∞(Ω)+∣∣I2(.,t)∣∣L∞(Ω)+∣∣R(.,t)∣∣L∞(Ω)≤K1,∀t≥T0.

for some large time T0>0. Hence, the result follows. □

Note that R does not appear in the first three equations, so it is equivalent to study the following sub-system:

∂S∂t=Λ-α1SI11+γ1I12-α2SI21+γ2I22-dS+d1∇2S,∂I1∂t=α1SI11+γ1I12-d+μ1+ρ1I1-ξI1+d2∇2I1,∂I2∂t=α2SI21+γ2I22-d+μ2+ρ2I2+ξI1+d3∇2I2. 8

Model Analysis

In the absence of spatial movement, we find the basic reproduction number of the system (1) as:

R0=maxR01,R02,

where

R01=α1Λ(d+μ1+ρ1+ξ)dandR02=α2Λ(d+μ2+ρ2)d.

Here, R01(R02) is the number of secondary infection cases generated by infection of the first (second) strain, called the reproduction number of the first (second) strain.

Also, we define two invasion reproduction numbers. By definition, the invasion reproduction number of the strain-1 R12 is given by

R12=R01R02=α1(d+μ2+ρ2)α2(d+μ1+ρ1+ξ),

which gives the number of secondary infections that an individual infected by the strain-1 will generate in a population in which the strain-2 is at equilibrium.

Similar to R12, the invasion reproduction number of the strain-2 R21 is given by

R21=R02R01=α2(d+μ1+ρ1+ξ)α1(d+μ2+ρ2).

Existence of Equilibria

There may be at most four equilibria for the non-spatial system corresponding to the spatial system (8), and they are given below

(i) Disease-free equilibrium:

The disease-free equilibrium point is E0=S0,I1,0,I2,0, where S0=Λd,I1,0=I2,0=0

(ii) Strain-1 endemic equilibrium:

To derive the strain-1 endemic equilibrium point E1=S1,I1,1,I2,1, we consider I2,0=0 and we note that I2,0=0⇒I1,0=0 and Λ-dS1=0. Thus, no strain-1 endemic equilibrium can exist.

(iii) Strain-2 endemic equilibrium:

The strain-2 endemic equilibrium is E2=S2,I1,2,I2,2, where

I1,2=0, S2=Λd+α2I2,21+γ2I2,22=1+γ2I2,22Λd1+γ2I2,22+α2I2,2 and I2,2 is the positive root of the following equation

dγ2I2,22+α2I2,2-Λα2C-d=0 9

and it is given by I2,2=-α2+α22+4dγ2Λα2C-d2dγ2.

Again, for the positivity of I2,2, we have Λα2-Cd>0i.e.Λα2-d(d+μ2+ρ2)>0. i.e. R02>1.

(iv) Strain-1 and strain-2 endemic equilibrium:

Let us choose A=d+μ1+ρ1+ξ1, B=d+μ1+ρ1, C=d+μ2+ρ2.

Then, the endemic equilibrium point E3=(S3,I1,3,I2,3) is given by

I1,3=α2S31+γ2I2,32-CI2,3-ξ1S3=Λξ1-BCI2,3-Cξ1I2,3dξ1-Bα2I2,31+γ2I2,32=Λξ1-ACI2,3(1+γ2I2,32)ξ1(d+α2I2,3+dγ2I2,32)-Aα2I2,3

and I2,3 is obtained from the following equation:

a0I2,36+a1I2,35+a2I2,34+a3I2,33+a4I2,32+a5I2,3+a6=0 10

where

a0=AC2d2γ1γ22>0,a1=ACdγ2(2Cα2γ1+α1γ2ξ1)>0,a2=-A2Cα1α2γ2-dα1γ22Λξ12+A(C2γ1(α22+2d2γ2)+d2γ22ξ12+Cα2γ2(-2dγ1Λ+α1ξ1)),a3=-2A2dα2γ2ξ1-α1α2γ2Λξ12+A(2C2dα2γ1+α2γ2ξ1(α1Λ+2dξ1)+C(-2α22γ1Λ+2dα1γ2ξ1)),a4=A3α22-2dα1γ2Λξ12-A2α2(Cα1+2α2ξ1)+A(C2d2γ1+2d2γ2ξ12+C(-2dα2γ1Λ+α1α2ξ1)+α22(γ1Λ2+ξ12)),a5=ξ1(-2A2dα2-α1α2Λξ1+A(Cdα1+α1α2Λ+2dα2ξ1)),a6=d(Ad-α1Λ)ξ12=d2ξ12(d+μ1+ρ1+ξ1)(1-R01).

Now, we note that under the conditions R01>1, R02>1, Bα1γ2>Cα2γ1, Bα2>Cα1, Ad>Bα2 and ABα2(Bα2-Cα1)+2dγ2ξ12(Ad-Λα1)+Aγ1(Λα2-Cd)2<0, we have a0>0,a1>0,a2<0,a3<0,a4<0,a5<0,a6<0. Hence, using Descartes' rule of sign we conclude that Eq. (10) has a unique root and we write the following proposition.

Proposition 3

If the conditions R01>1, R02>1, Bα1γ2>Cα2γ1, Bα2>Cα1, Ad>Bα2 and ABα2(Bα2-Cα1)+2dγ2ξ12(Ad-Λα1)+Aγ1(Λα2-Cd)2<0, are satisfied, then there is a unique positive solution of Eq. (10).

So, for this unique I2,3, we have a I1,3 and hence a S3. Thus, the endemic E3=(S3,I1,3,I2,3) is unique under Proposition 3.

Global Stability Analysis

In this section, we investigate the global asymptotic stability of the model system (8) around all the possible equilibrium points. Here, we follow the technique as described by Hattaf and Yousfi (2013) to establish the global stability of the diffusive system. The Lyapunov functional are constructed based upon the Proposition 2.1. of Hattaf and Yousfi (2013). In fact, first we formulate the Lyapunov functional for the non-diffusive system, i.e., for the following ordinary differential equations system

dSdt=Λ-α1SI11+γ1I12-α2SI21+γ2I22-dS,dI1dt=α1SI11+γ1I12-d+μ1+ρ1I1-ξI1,dI2dt=α2SI21+γ2I22-d+μ2+ρ2I2+ξI1. 11

Then, we construct the Lyapunov functional for the diffusive system (8).

Theorem 1

The infection-free equilibrium point of the system (8) is globally asymptotically stable if R02<1 and Λα1<d(d+μ1+ρ1).

Proof

Following Hattaf and Yousfi (2013), we first construct the Lyapunov functional for system (11) as:

L1=S-S0-S0lnSS0+I1+I2. 12

Now calculating the time derivative of Eq. (12) along the solutions of the system (11), we get

dL1dt=1-S0SdSdt+dI1dt+dI2dt=1-S0SΛ-α1SI11+γ1I12-α2SI21+γ2I22-dS+α1SI11+γ1I12-d+μ1+ρ1I1-ξI1+α2SI21+γ2I22-d+μ2+ρ2I2+ξI1=dS02-SS0-S0S+S0Sα1SI11+γ1I12+α2SI21+γ2I22-d+μ1+ρ1I1-d+μ2+ρ2I2≤dS02-SS0-S0S+S0Sα1SI1+α2SI2-d+μ1+ρ1I1-d+μ2+ρ2I2=dS02-SS0-S0S+Λα1d-(d+μ1+ρ1)I1+Λα2d-(d+μ2+ρ2)I2=dS02-SS0-S0S+Λα1d-(d+μ1+ρ1)I1+(R02-1)(d+μ2+ρ2)I2 13

Now, by applying A.M.≥G.M., we have 2-SS0-S0S≤0. In addition, under the conditions R02<1 and Λα1<d(d+μ1+ρ1), we observe that dL1dt≤0.

Now we construct the Lyapunov functional for the diffusive system (8), at the disease-free state E0 as follows:

W1=∫ΩL1(S(x,t),I(x,t),I2(x,t))dx

Calculating the time derivative of W1 along the solutions of the system (8), we get

dW1dt≤∫ΩdS02-SS0-S0S+Λα1d-(d+μ1+ρ1)I1+(R02-1)(d+μ2+ρ2)I2-d1S0∫Ω|∇S|2S2dx 14

Now, under the conditions R02<1 and Λα1<d(d+μ1+ρ1), we have dW1dt≤0. Also, the largest set in Θ1=(S,I1,I2):dW1dt=0 is the singleton E0. Hence, from the LaSalle invariance principle (La Salle 1976), we conclude that the infection-free equilibrium point E0 is globally asymptotically stable under the stated conditions. Hence the theorem is proved. □

Theorem 2

The strain-2 endemic equilibrium point E2(S2,0,I2,2) is globally asymptotically stable if R02>1, S2<mind+μ1+ρ1α1,d+μ2+ρ2α2 and ξI1+α1SI21+γ2I22>2(d+μ2+ρ2)I2.

Proof

As earlier, following Hattaf and Yousfi (2013), we first construct the Lyapunov functional for system (11) as

L2=S-S2-S2lnSS2+I1+I2-I2,2-I2,2lnI2I2,2. 15

Now calculating the time derivative of the equation (15) along the solutions of the system (11), we get

dL2dt=1-S2SdSdt+dI1dt+1-I2,2I2dI2dt=1-S2SΛ-α1SI11+γ1I12-α2SI21+γ2I22-dS+α1SI11+γ1I12-d+μ1+ρ1I1-ξI1+1-I2,2I2α2SI21+γ2I22-d+μ2+ρ2I2+ξI1=dS22-SS2-S2S+α2S2I2,21+γ2I2,22-S2Sα2S2I2,21+γ2I2,22-α1SI11+γ1I12-α2SI21+γ2I22-(d+μ1+ρ1)I1-(d+μ2+ρ2)I2-α2SI2,21+γ2I22+(d+μ2+ρ2)I2,2-ξI1I2,2I2≤dS22-SS2-S2S+α2S2I2,21+γ2I2,22+α1S2I11+γ1I12+α2S2I21+γ2I22-(d+μ1+ρ1)I1-(d+μ2+ρ2)I2-α2SI2,21+γ2I22+(d+μ2+ρ2)I2,2-ξI1I2,2I2≤dS22-SS2-S2S+α2S2I2,21+γ2I2,22+α1S2I1+α2S2I2-(d+μ1+ρ1)I1-(d+μ2+ρ2)I2-α2SI2,21+γ2I22+(d+μ2+ρ2)I2,2-ξI1I2,2I2=dS22-SS2-S2S+α1S2-(d+μ1+ρ1)I1+α2S2-(d+μ2+ρ2)I2-I2,2I2α2SI21+γ2I22+ξI1-2(d+μ2+ρ2)I2 16

Now, by applying A.M.≥G.M., we have 2-SS2-S2S≤0. Further, under the conditions S2<mind+μ1+ρ1α1,d+μ2+ρ2α2 and ξI1+α1SI21+γ2I22>2(d+μ2+ρ2)I2, we note that dL2dt≤0.

Now we construct the Lyapunov functional for the diffusive system (8), at the strain-2 endemic steady state E2 as follows:

W2=∫ΩL2(S(x,t),I1(x,t),I2(x,t))dx

Calculating the time derivative of W2 along the solutions of the system (8), we get

dW2dt≤∫ΩdS22-SS2-S2S+α1S2-(d+μ1+ρ1)I1+α2S2-(d+μ2+ρ2)I2-I2,2I2α2SI21+γ2I22+ξI1-2(d+μ2+ρ2)I2dx-d1S2∫Ω|∇S|2S2dx-d2I2,2∫Ω|∇I2|2I22dx

Now, under the conditions as stated earlier, we have dW2dt≤0. Also, the largest set in Θ2=(S,I1,I2):dW2dt=0 is the singleton E2. Hence, from the LaSalle invariance principle (La Salle 1976), we conclude that the strain-2 endemic equilibrium point E2 is globally asymptotically stable under the stated conditions. Hence, the theorem follows. □

Theorem 3

The strain-1 and strain-2 endemic equilibrium point E3(S3,I1,3,I2,3) is globally asymptotically stable under the conditions R01>1, R02>1 and either I2I2,3≤1≤I1I1,3, I2I2,3≤SS3≤I1I1,3 or I1I1,3≤1≤I2I2,3, I1I1,3≤SS3≤I2I2,3.

Proof

As earlier, following Hattaf and Yousfi (2013), we first construct the Lyapunov functional for system (11) as:

L3=S-S3-S3lnSS3+I1-I1,3-I1,3lnI1I1,3+I2-I2,3-I2,3lnI2I2,3. 17

Now calculating the time derivative of the equation (17) along the solutions of the system (11), we get

dL3dt=1-S3SdSdt+1-I1,3I1dI1dt+1-I2,3I2dI2dt=S-S3S˙S+I1-I1,3I1˙I1+I2-I2,3I2˙I2 18

Now for clarity, we calculate the terms S˙S, I1˙I1 and I2˙I2 separately.

S˙S=ΛS-α1I11+γ1I12-α2I21+γ2I22-d=ΛS-α1I11+γ1I12-α2I21+γ2I22-d-ΛS3-α1I1,31+γ1I1,32-α2I2,31+γ2I2,32-d=ΛS3-SSS3-α1I11+γ1I12-I1,31+γ1I1,32-α2I21+γ2I22-I2,31+γ2I2,32=ΛS3-SSS3-α1I11+γ1I12-I1,31+γ1I12+I1,31+γ1I12-I1,31+γ1I1,32-α2I21+γ2I22-I2,31+γ2I22+I2,31+γ2I22-I2,31+γ2I2,32=ΛS3-SSS3-α1I1-I1,3(1+γ1I12)-γ1I1,3(I12-I1,32)(1+γ1I12)(1+γ1I1,32)-α2I2-I2,3(1+γ2I22)-γ2I2,3(I22-I2,32)(1+γ2I22)(1+γ2I2,32)
I1˙I1=α1S1+γ1I12-d+μ1+ρ1+ξ=α1S1+γ1I12-α1S31+γ1I1,32=α1S1+γ1I12-S31+γ1I12+S31+γ1I12-S31+γ1I1,32=α1S-S3(1+γ1I12)-γ1S3(I12-I1,32)(1+γ1I12)(1+γ1I1,32)
I2˙I2=α2S1+γ2I22-d+μ2+ρ2+ξI1I2=α2S1+γ2I22-d+μ2+ρ2+ξI1I2-α2S31+γ2I2,32-d+μ2+ρ2+ξI1,3I2,3=α2S1+γ2I22-S31+γ2I2,32+ξI1I2-I1,3I2,3=α2S1+γ2I22-S31+γ2I22+S31+γ2I22-S31+γ2I2,32+ξI1I2-I1,3I2,3-I1,3I2+I1,3I2=α2S-S3(1+γ2I22)+γ2S3(I2,32-I22)(1+γ2I22)(1+γ2I2,32)+ξI1-I1,3I2-I1,3(I2-I2,3)I2I2,3

Now substituting the values of S˙S, I1˙I1 and I2˙I2 in the equation (18), we get

dL3dt=(S-S3)ΛS3-SSS3-α1I1-I1,3(1+γ1I12)-γ1I1,3(I12-I1,32)(1+γ1I12)(1+γ1I1,32)-α2I2-I2,3(1+γ2I22)-γ2I2,3(I22-I2,32)(1+γ2I22)(1+γ2I2,32)+(I1-I1,3)α1S-S3(1+γ1I12)-γ1S3(I12-I1,32)(1+γ1I12)(1+γ1I1,32)+(I2-I2,3)α2S-S3(1+γ2I22)+γ2S3(I2,32-I22)(1+γ2I22)(1+γ2I2,32)+ξI1-I1,3I2-I1,3(I2-I2,3)I2I2,3

After some simplifications, we finally obtain

dL3dt=-Λ(S-S3)2SS3-ξI1,3(I2-I2,3)2I2I2,3+ξ(I1-I1,3)(I2-I2,3)I2+α1γ1(I1-I1,3)(I1+I1,3)(SI1,3-S3I1)(1+γ1I12)(1+γ1I1,32)+α2γ2(I2-I2,3)(I2+I2,3)(SI2,3-S3I2)(1+γ2I22)(1+γ2I2,32) 19

Now we note that if either I2I2,3≤1≤I1I1,3, I2I2,3≤SS3≤I1I1,3 or I1I1,3≤1≤I2I2,3, I1I1,3≤SS3≤I2I2,3, then dL3dt≤0.

Now we construct the Lyapunov functional for the diffusive system (8), at the strain-1 and strain-2 endemic steady state E3 as follows:

W3=∫ΩL3(S(x,t),I1(x,t),I2(x,t))dx

Calculating the time derivative of W3 along the solutions of the system (8), we get

dW3dt=∫Ω-Λ(S-S3)2SS3-ξI1,3(I2-I2,3)2I2I2,3+ξ(I1-I1,3)(I2-I2,3)I2+α1γ1(I1-I1,3)(I1+I1,3)(SI1,3-S3I1)(1+γ1I12)(1+γ1I1,32)+α2γ2(I2-I2,3)(I2+I2,3)(SI2,3-S3I2)(1+γ2I22)(1+γ2I2,32)dx-d1S3∫Ω|∇S|2S2dx-d2I1,3∫Ω|∇I2|2I22dx-d3I2,3∫Ω|∇I3|2I32dx

Therefore, under the conditions as stated earlier, we get dW3dt≤0. Also, the largest set in Θ3=(S,I1,I2):dW3dt=0 is the singleton E3. Hence, from the LaSalle invariance principle (La Salle 1976), it follows that the strain-1 and strain-2 endemic equilibrium point E3 is globally asymptotically stable under the stated conditions. Hence, the theorem follows. □

Conclusions

In this paper, we have proposed and analyzed a diffusive epidemic model with two strains and non-monotonic incidence rates for both the strains. These types of incidence rate are considered to interpret the psychological effects. The recent pandemic outbreak due to SARS-CoV-2 has such psychological effects on the common people; also several strains of the virus are found. So, this work can be applied to study transmission mechanisms of the corona virus disease. The biological feasibility conditions of the solutions of the system are studied. All the possible equilibrium points of the system are obtained and their global asymptotic stability are investigated. The parametric conditions are derived for the long-term occurrence of the disease-free steady state and the strain-1 and strain-2 endemic equilibrium point. It is observed that the model system has no strain-1 endemic steady state. This scenario occurs possibly due to the presence of the virus mutation. It indicates that the disease due to strain-1 do not stay permanently in the community.

An epidemic model becomes more useful from a practical point of view when it is calibrated with the real world data. Also it is quite important to visualize the obtained theoretical results in graphical way. We would like to address these issues in our future research which requires more advanced computational skills. However, this theoretical study may be very useful to explain the dynamical characteristics of a diffusive two strain epidemic model with virus mutation and non-monotonic incidence rate.

Acknowledgements

We are extremely grateful to the anonymous reviewers and the Editor-in-Chief Dr. Gholam Hossein Esslamzadeh, for their constructive suggestions which have helped us greatly to improve the quality of the manuscript.

Funding

Research of Anupam Khatua is financially supported by Department of Science and Technology-INSPIRE, Government of India (No. DST/INSPIRE Fellowship/2016/IF160667, dated: 21st September, 2016).

Data Availability Statement

No data are used in the manuscript.

Declarations

Conflict of interest

There is no conflict of interest.

Contributor Information

Anupam Khatua, Email: anupam.rs2016@math.iiests.ac.in, Email: akhatua06@gmail.com.

Debprasad Pal, Email: debprasadpal@gmail.com.

Tapan Kumar Kar, Email: tkar1117@gmail.com.

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Data Availability Statement

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