Research article Topical Sections

Impact of COVID-19 on tourism sector: a case study of Rajasthan, India

  • Background 

    SARS-CoV-2 or Severe Acute Respiratory Syndrome, is a virus that causes severe respiratory illness, also known as COVID-19, is a global pandemic caused by a novel coronavirus, firstly reported China (Wuhan City) on Dec, 2019. In India, Kerala is the first state in which the COVID-19 first case has registered which has raised to three cases by 3 Feb, 2020.

    Purpose 

    The aim of this research is to map the impact and assessment of the COVID 19 pandemic situation using geospatial technology in Rajasthan and suggest various measures to control the pandemic situation.

    Objectives 

    (a) Assessing and mapping the affected parts of Rajasthan and evaluating the risk of the pandemic on tourism, and (b) Initially tracking and forecasting the cases of COVID-19 in the study area.

    Methodology 

    The methodology consists of four main phases. In the first phase understanding the risk of the pandemic situation at three primary levels i.e. risk analysis, risk evaluation, risk management after that, second step is to identify the target risk zones of COVID-19 cases using geospatial technology based on bulk screening. Assessment and mapping of pandemic risk is the third phase. In the fourth phase, treatment of the risk and evaluation of future occurrence possibilities.

    Result 

    COVID 19 pandemic is the greatest threat globally. Geospatial technology provides valuable support in assessing and mapping the risk of COVID 19 cases in Rajasthan at the initial level.

    Conclusion 

    This study shows that the geospatial technique contributes very significantly in detecting pre and post COVID 19 pandemic conditions and helps in proper decision-making, not only in Rajasthan but also in the entire world.

    Citation: Rajeev Singh Chandel, Shruti Kanga, Suraj Kumar Singh. Impact of COVID-19 on tourism sector: a case study of Rajasthan, India[J]. AIMS Geosciences, 2021, 7(2): 224-243. doi: 10.3934/geosci.2021014

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  • Background 

    SARS-CoV-2 or Severe Acute Respiratory Syndrome, is a virus that causes severe respiratory illness, also known as COVID-19, is a global pandemic caused by a novel coronavirus, firstly reported China (Wuhan City) on Dec, 2019. In India, Kerala is the first state in which the COVID-19 first case has registered which has raised to three cases by 3 Feb, 2020.

    Purpose 

    The aim of this research is to map the impact and assessment of the COVID 19 pandemic situation using geospatial technology in Rajasthan and suggest various measures to control the pandemic situation.

    Objectives 

    (a) Assessing and mapping the affected parts of Rajasthan and evaluating the risk of the pandemic on tourism, and (b) Initially tracking and forecasting the cases of COVID-19 in the study area.

    Methodology 

    The methodology consists of four main phases. In the first phase understanding the risk of the pandemic situation at three primary levels i.e. risk analysis, risk evaluation, risk management after that, second step is to identify the target risk zones of COVID-19 cases using geospatial technology based on bulk screening. Assessment and mapping of pandemic risk is the third phase. In the fourth phase, treatment of the risk and evaluation of future occurrence possibilities.

    Result 

    COVID 19 pandemic is the greatest threat globally. Geospatial technology provides valuable support in assessing and mapping the risk of COVID 19 cases in Rajasthan at the initial level.

    Conclusion 

    This study shows that the geospatial technique contributes very significantly in detecting pre and post COVID 19 pandemic conditions and helps in proper decision-making, not only in Rajasthan but also in the entire world.



    Deterministic continuum models for the growth of cell populations have been increasingly used as theoretical tools to support empirical research regarding a broad spectrum of aspects of the development of solid tumours and living tissues. These models comprise partial differential equations (PDEs) that describe the evolution of cellular densities (or cell volume fractions) in response to pressure gradients that are generated by population growth, which can be mechanically-regulated [1], [2], nutrient-limited [3], pressure-dependent [4][6] or regulated by a combination of these mechanisms [7][11]. These models are amenable not only to numerical simulations but also to analytical approaches, which enable a complete exploration of the model parameter space. This permits a precise identification of the validity domain of the results obtained and ensures higher robustness and precision of the conclusions drawn therefrom, which ultimately provides a more in-depth theoretical understanding of the underlying cellular dynamics [12], [13].

    Ideally, instead of defining such PDE models on the basis of population-scale phenomenological assumptions, one wants to derive them from first principles, that is, as the deterministic continuum limits of stochastic discrete models, i.e. individual-based (IB) models, which track the dynamics of single cells [14], [15]. This is to ensure that the terms comprised in the model equations provide a faithful mean-field representation of the underlying cellular dynamics. In fact, although being computationally intensive to simulate for large cell numbers and, to a wider extent, inaccessible to analytical techniques, IB models permit the representation of the finer details of cell-scale mechanisms and capture stochastic intercellular variability in the spatial and evolutionary trajectories of single cells. These aspects, which cannot be directly incorporated into phenomenological deterministic continuum models, become especially important in scenarios where cell numbers and densities are low (e.g. in the early stages of embryonic development and tissue regeneration, during the formation of distant metastases upon cancer cell extravasation, and when tumour size is severely reduced after therapy), due to the stronger impact that single-cell processes and demographic stochasticity are expected to have on the dynamics of cell populations. For this reason, a range of asymptotic techniques, probabilistic methods and limiting procedures have been developed and used in previous studies to systematically derive PDE models for the growth of cell populations from their individual-based counterparts [13]. For example, reaction-diffusion and nonlinear diffusion equations have been derived from their underlying random walks [16][21], from systems of discrete equations of motion [22][24], from discrete lattice-based exclusion processes [25][28] and from cellular automata [29][31]. However, these previous studies have mainly been focused on homogeneous populations in which all cells have the same phenotypic characteristics. Such homogeneity is rarely present in cellular systems, where significant intercellular phenotypic variability is commonly observed. In light of these considerations, we develop here an IB model for the growth of phenotypically heterogeneous cell populations. In this model, every cell is viewed as an individual agent whose phenotypic state is described by a structuring variable that captures intercellular variability in cell proliferation and migration rates. Cells undergo directional movement in response to pressure differentials [32][35], pressure-dependent proliferation [2], [36][38], and heritable phenotypic changes [39][41] according to a set of rules that correspond to a discrete-time branching random walk on the physical space and the space of phenotypic states [19], [42], [43]. We formally show that the deterministic continuum limit of this model is given by a non-local PDE for the cell population density function, which generalises earlier models [34], [38], [44] to the case of phenotypically heterogeneous cell populations. We then carry out numerical simulations of the IB model and compare the results obtained with the results of formal travelling-wave analysis and numerical simulations of the PDE model.

    The paper is organised as follows. In Section 2, we introduce the IB model. In Section 3, we present its PDE counterpart (a formal derivation is provided in Section S1 of the Supplementary Material). In Section 4, in order to obtain results with broad structural stability under parameter changes, we first carry out formal travelling-wave analysis of the PDE model and then integrate the results obtained with numerical simulations of the IB model and numerical solutions of the PDE model. In Section 5, we summarise the main findings of our study and outline directions for future research.

    We model the dynamics of a phenotypically heterogeneous growing cell population. Cells within the population have the potential to undergo:

  • directional movement in response to pressure differentials – i.e. cells move down pressure gradients towards regions where they feel less compressed [32], [34], [37];
  • spontaneous, heritable phenotypic changes, which lead cells to randomly transition from one phenotypic state into another [39][41];
  • pressure-dependent proliferation – i.e. cells stop dividing, and can thus only die or remain quiescent, when the pressure that they experience overcomes a critical threshold, which is known as homeostatic pressure [34], [38], [45].
  • Focusing on a one-dimensional spatial domain scenario, the position of every cell at time t ∈ ℝ+ is described by the variable x ∈ ℝ. Moreover, the phenotypic state of each cell is characterised by a structuring variable y ∈ [0,Y] ⊂ ℝ+, with Y > 0, which takes into account intercellular variability in cell proliferation and migration rates. Here, the variable y could represent the level of expression of a gene that regulates both cell division and cell migration, such as those involved in the epithelial-to-mesenchymal transition promoting tumour invasion [46][48]. More specifically, the overexpression of some cancer-promoting genes has been shown to inhibit cell proliferation and promote cell migration in cancer cells, for example, FBXL10 expession in ovarian cancer cell lines [49] and EphB2 expression in glioblastomas [50]. Similarily, the downregulation of miR-451 observed in glioblastomas has been shown to reduce the proliferation rate and increase the migration potential of the cells [51].

    Therefore in the model, without loss of generality, we consider the case where larger values of y correlate with a higher cell migration rate but a lower proliferation rate due to proliferation-migration tradeoffs [47], [48], [52][59].

    We discretise the time, space and phenotype variables via

    tk=kτ+,  xi=iχ and yj=jη[0,Y] with k,j0,i,τ,χ,η+*.
    Here τ, χ and η are the time-, space- and phenotype-step, respectively. We represent every single cell as an agent that occupies a position on the lattice {xi}i×{yj}j0, and we introduce the dependent variable Nki,j0 to model the number of cells in the phenotypic state yj at position xi at time tk. The cell population density and the corresponding cell density are defined, respectively, as follows
    nki,jn(tk,xi,yj):=Nki,jχη and ρkiρ(tk,xi):=ηjnki,j.
    We further define the pressure experienced by the cells (i.e. the cell pressure) as a function of the cell density through the following barotropic relation
    pkip(tk,xi)=Π(ρki),
    where the function Π satisfies the following assumptions [34], [44], [60]
    Π(0)=0,ddρΠ(ρ)0 for ρ+*.

    As summarised by the schematics in Figure 1, between time-steps k and k + 1, each cell in phenotypic state yj ∈ (0,Y) at position xi ∈ ℝ can first move, next undergo phenotypic changes and then die or divide according to the rules described in the following subsections.

    Figure 1.  Schematics summarising the rules that govern the spatial evolutionary dynamics of single cells in the IB model. Between time-steps k and k + 1, each cell in phenotypic state yj ∈ (0,Y) at position xi ∈ ℝ may: a. move to either of the positions xi−1 and xi+1 with probabilities 𝒫kLi,j and 𝒫kRi,j defined via (2.12) and (2.13); b. undergo a phenotypic change and thus enter into either of the phenotypic states yj−1 and yj+1 with probabilities λ/2; c. die or divide with probabilities 𝒫kDi,j and 𝒫kBi,j defined via (2.4) and (2.5).

    To incorporate the effects of cell proliferation, we assume that a dividing cell is instantly replaced by two identical cells that inherit the phenotypic state of the parent cell (i.e. the progenies are placed on the same lattice site as their parent), while a dying cell is instantly removed from the population. We model pressure-dependent proliferation by letting the cells divide, die or remain quiescent with probabilities that depend on their phenotypic states and the pressure that they experience.

    In particular, to define the probabilities of cell division and death, we introduce the function R(yj,pki), which describes the net growth rate of the cell population density at position xi at time tk, and assume that between time-steps k and k + 1 a cell in phenotypic state yj at position xi may die with probability

    𝒫kDi,j:=τR(yj,pki) where R(yj,pki)=min(0,R(yj,pki)),
    divide with probability
    𝒫kBi,j:=τR(yj,pki)+ where R(yj,pki)+=max(0,R(yj,pki))
    or remain quiescent (i.e. do not divide nor die) with probability
    𝒫kQi,j:=1𝒫kBi,j𝒫kDi,j.
    Note that we are implicitly assuming the time-step τ to be sufficiently small that 0<𝒫kBi,j+𝒫kDi,j<1 for all values of i, j and k.

    In order to capture the fact that, as mentioned earlier, larger values of yj correlate with a lower cell proliferation rate, along with the fact that cells will stop dividing if the pressure at their current position becomes larger than the homeostatic pressure, which we model by means of the parameter pM>0, we make the following assumptions

    R(Y,0)=0,R(0,pM)=0,pR(y,p)<0 and yR(y,p)<0 for(y,p)(0,Y)×+.
    In particular, we will focus on the case where
    R(y,p):=r(y)ppM with r(Y)=0,  r(0)=1,  ddyr(y)<0 for y(0,Y).
    Remark 1. Under assumptions (2.7), definitions (2.5)(2.6) ensure that if pkipM then every cell at position xi can only die or remain quiescent between time-steps k and k + 1. Hence, in the remainder of the paper we will let the following condition hold
    maxip0ipM
    so that
    pkipM for all (k,i)0×.

    We take into account heritable phenotypic changes by allowing cells to update their phenotypic states according to a random walk along the phenotypic dimension. More precisely, between time-steps k and k + 1, every cell either enters a new phenotypic state, with probability λ ∈ [0,1], or remains in its current phenotypic state, with probability 1-λ. Since, as mentioned earlier, we consider only spontaneous phenotypic changes that occur randomly due to non-genetic instability, we assume that a cell in phenotypic state yj that undergoes a phenotypic change enters into either of the phenotypic states yj±1 = yj ± η with probabilities λ/2. No-flux boundary conditions are implemented by aborting any attempted phenotypic variation of a cell if it requires moving into a phenotypic state outside the interval [0,Y].

    We model directional cell movement in response to pressure differentials as a biased random walk along the spatial dimension, whereby the movement probabilities depend on the difference between the pressure at the position occupied by a cell and the pressure at the neighbouring positions. As mentioned earlier, we consider the case where larger values of yj correlate with a higher cell migration rate. Hence, we modulate the probabilities of cell movement by the function μ(yj), which provides a measure of the mobility of cells in phenotypic state yj and thus satisfies the following assumptions

    μ(0)>0,ddyμ(y)>0 for y(0,Y].
    Then we assume that between time-steps k and k + 1 a cell in phenotypic state yj at position xi may move to the position xi−1 = xiχ (i.e. move left) with probability
    𝒫kLi,j=νμ(yj)(pkipki1)+2pM where (pkipki1)+=max(0,pkipki1),
    move to the position xi+1 = xi+χ (i.e. move right) with probability
    𝒫kRi,j=νμ(yj)(pkipki+1)+2pM where (pkipki+1)+=max(0,pkipki+1)
    or remain stationary (i.e. do not move left nor right) with probability
    𝒫kSi,j=1𝒫kLi,j𝒫kRi,j.
    Here, the parameter v > 0 is a scaling factor, which we implicitly assume to be sufficiently small that 0 < (yj) < 1 for all yj ∈ [0,Y]. Under condition (2.9), this assumption on v along with the a priori estimate (2.10) implies that definitions (2.12) and (2.13) are such that 0<𝒫kLi,j+𝒫kRi,j<1 for all values of i, j and k.

    Remark 2. Definitions (2.12) and (2.13) ensure that cells will move down pressure gradients so as to reach regions where they feel less compressed.

    Through a method analogous to those that we previously employed in [19], [61][64], letting the time-step τ → 0, the space-step χ → 0 and the phenotype-step η → 0 in such a way that

    νχ22τα+* and λη22τβ+*,
    one can formally show (see Section S1 of the Supplementary Material) that the deterministic continuum counterpart of the stochastic discrete model presented in Section 2 is given by the following non-local PDE for the cell population density function n(t,x,y)
    (tnαˆμ(y)x(nxp)=R(y,p)n+β2yyn,(x,y)×(0,Y)p=Π(ρ),ρ:=Y0n(t,x,y) dy,
    where ˆμ(y):=μ(y)pM. The non-local PDE (3.2) is subject to zero Neumann (i.e. no-flux) boundary conditions at y = 0 and y = Y, as well as to an initial condition such that the continuum analogue of condition (2.9) holds, that is,
    maxxp(0,x)pM.

    The mathematical model defined by complementing (3.2) with assumptions (2.3), (2.7) and (2.11) generalises earlier models of pressure-dependent cell population growth [34], [38], [44] to the case of phenotypically heterogeneous cell populations.

    In this section, we first present the result of formal travelling-wave analysis of the PDE model (Subsection 4.1) and then integrate these results with numerical simulations of the IB model and numerical solutions of the PDE model (Subsection 4.2).

    We focus on a biological scenario in which cell movement occurs on a slower timescale compared to cell division and death, while spontaneous, heritable phenotypic changes occur on a slower timescale compared to cell movement [41], [65]. To this end, we introduce a small parameter ϵ > 0 and let

    α:=ϵ,β:=ϵ2.
    Moreover, in order to explore the long-time behaviour of the cell population (i.e. the behaviour of the population over many cell generations), we use the time scaling ttϵ in (3.2). Taken together, this gives the following non-local PDE for the cell population density function nϵ(t,x,y)=n(tϵ,x,y)
    (ϵtnϵϵˆμ(y)x(nϵxpϵ)=R(y,pϵ)nϵ+ϵ22yynϵ,(x,y)×(0,Y)pϵ=Π(ρϵ),ρϵ:=Y0nϵ(t,x,y) dy.
    Using a method analogous to those that we have previously employed in [66], [67], denoting by δ(·)(y) the Dirac delta centred at y = (·), one can formally show (see Section S2 of the Supplementary Material) that, under assumptions (2.3), (2.8) and (2.11), as ϵ → 0, the non-local PDE (4.2) admits travelling-wave solutions of the form
    nϵ(z,y)ρ(z)δˉy(z)(y),z=xct,c+*,
    where y(z) is the unique maximum point of the solution to the following equation
    (c+ˆμ(y)p)zu=(r(y)ppM)+(yu)2,uu(z,y),(z,y)×(0,Y)
    and the cell density ρ(z) is such that the pressure p(z) = Π(ρ(z)) satisfies the following relation
    p(z)=pMr(ˉy(z))zSupp(p),
    provided that the wave speed c satisfies the following necessary condition
    csupzSupp(r(ˉy))2|ddyr(ˉy(z))|μ(ˉy(z))|2yyu(z,ˉy(z))|.
    Moreover,
    Supp(p)=(,) with  such that ˉy()=Y
    and
    limzˉy(z)=0,limzp(z)=pM,ˉy(z)>0 and p(z)<0z(,).

    From a biological point of view, y(z) represents the dominant phenotype of cells at a certain position along the invading wave p(z). Since larger values of y correlate with a lower proliferation rate and a higher migration rate, the fact that y(z) increases monotonically from 0 to Y while p(z) decreases monotonically from pM to 0 (cf. the results given by (4.6) and (4.7)) provides a mathematical formalisation of the idea that spatial sorting causes cells with a more mobile/less proliferative phenotype to become concentrated towards the front of the invading wave, which is thus a sparsely populated region, whereas phenotypic selection leads cells with a less mobile/more proliferative phenotype to dominate at the rear, which is then a densely populated region.

    In order to carry out numerical simulations, we consider the time interval [0,T], with T = 8, we restrict the physical domain to the closed interval [0,X], with X = 25, and choose Y = 1. In order to facilitate the integration between numerical simulations and the results of formal travelling-wave analysis presented in Subsection 4.1, we solve numerically the rescaled PDE model (4.2), with ϵ = 0.01, and we carry out numerical simulations of the scaled IB model obtained by introducing the time scaling tktkϵ=kτϵ and reformulating the governing rules of cell dynamics that are detailed in Section 2 in terms of

    pkϵipϵ(tk,xi)=p(tkϵ,xi)=Π(ρkϵi),
    with
    ρkϵiρϵ(tk,xi)=ρ(tkϵ,xi):=ηjnkϵi,j and nkϵi,jnϵ(tk,xi,yj)=n(tkϵ,xi,yj):=Nkϵi,jχη.
    Moreover, we choose τ = 5 × 10−5, χ = 0.01 and η = 0.02, and then set ν=2τχ2ϵ and λ=2τη2ϵ2 in order to ensure that conditions (3.1) and (4.1) are simultaneously satisfied.

    We consider a biological scenario in which, initially, the cell population is localised along the x = 0 boundary and most of the cells are in the phenotypic state y = y0 at every position. Specifically, we implement the following initial cell distribution for the IB model

    N0ϵi,j=int(Fϵ(xi,yj)) with Fϵ(x,y)=A0Cex2e(yˉy0)2ϵ,
    where int(·) is the integer part of (·)and C is a normalisation constant such that
    CY0e(yˉy0)2ϵ dy=1.
    Unless otherwise specified, we choose A0 = 10 and y0 = 0.2, that is, the initially dominant phenotype of the cell population is y = 0.2. The initial cell density and pressure are then calculated via (2.1) and (2.2). The initial cell population density function nϵ(0,x,y)=n0ϵ(x,y), is defined as a suitable continuum analogue of the cell population density n0ϵi,j:=N0ϵi,jχη, with N0ϵi,j given by (4.8). Specifically, we set
    n0ϵ(x,y):=(Fϵ(x,y)χη1.5χη)+,
    where Fϵ(x,y) is defined via (4.8) and (·)+is the positive part of (·).

    We define R(y, pϵ) via (2.8) and, having chosen Y = 1, we further define

    r(y):=1y2 and μ(y):=0.01+y2
    so as to ensure that assumptions (2.7), (2.8) and (2.11) are satisfied. Moreover, we investigate the following three definitions of the barotropic relation for the cell pressure, all satisfying assumptions (2.3):
    pϵ=Π(ρϵ):=(ρϵ(Case 1)Kγ(ρϵ)γ   with Kγ>0,γ>1(Case 2)κ(ρϵρ*)+ with κ,ρ*>0(Case 3).

    The definition given by Case 1 corresponds to the simplified scenario in which the cell pressure is a linear function of the cell density. In the definition given by Case 2, which was proposed in [44], the parameter Kγ is a scaling factor and the parameter γ provides a measure of the stiffness of the barotropic relation (i.e. the limit γ → ∞ corresponds to the scenario in which cells behave like an incompressible fluid). In the definition given by Case 3, which is such that the cell pressure is zero for ρρ* and is a monotonically increasing function of the cell density for ρ > ρ*, the parameter κ is a scaling factor and ρ* is the density below which the force that the cells exert upon one another is negligible [38], [60]. Unless otherwise specified: when the cell pressure is defined via Case 1 we choose pM = 4.95 × 104; when the cell pressure is defined via Case 2 we choose pM = 3.675 × 109, γ = 2 and Kγ=32; when the cell pressure is defined via Case 3 we choose pM = 4.94 × 105, κ = 10 and ρ* = 102.

    Remark 3. The initial conditions and the values of pM that are considered here are such that conditions (2.9) and (3.3) are satisfied.

    All simulations are performed in Matlab. At each time-step, each cell undergoes a three-phase process: (i) cell movement, according to the probabilities defined via (2.12)(2.14); (ii) phenotypic changes, with probabilities λ/2; (iii) division and death, according to the probabilities defined via (2.5) and (2.6). For each cell, during each phase, a random number is drawn from the standard uniform distribution on the interval (0,1) using the built-in Matlab function rand. It is then evaluated whether this number is lower than the probability of the event occurring and if so the event occurs. Since xi ∈ [0,X], the attempted movement of a cell is aborted if it requires moving out of the spatial domain.

    Full details of the methods used to solve numerically the non-local PDE (4.2) posed on (0,T]×(0,X)×(0,Y) and subject to suitable initial and boundary conditions are given in Section S3 of the Supplementary Material.

    Formation of complex spatial patterns of population growth. The plots in the top lines of Figures 24 summarise the results of numerical simulations of the IB model for the barotropic relations given by Cases 1–3 in (4.9). We plot in the left panels the scaled cell population density, nϵ/ρϵ, and in the right panels (solid blue lines) the scaled cell pressure, pϵ/pM, at progressive times.

    The results of numerical simulations under all three cases display very similar dynamics, both with respect to the cell population density and the cell pressure, where we observe evolution to travelling-wave profiles of almost identical shapes and speeds (see also Remark 4). The incorporation of proliferation-migration tradeoffs lead cells to be non-uniformly distributed across both physical and phenotype space. More precisely, we observe a relatively small subpopulation of highly-mobile but minimally-proliferative cells (i.e. cells in phenotypic states yY) that becomes concentrated towards the front of the invading wave, while rapidly-proliferating but minimally-mobile cells (i.e. cells in phenotypic states y ≈ 0) make up the bulk of the population in the rear. This is due to a dynamic interplay between spatial sorting and phenotypic selection. In fact, a more efficient response to pressure differentials by more-mobile cells leads to their positioning at the front of the wave, where the pressure is lower, before being overcome by the more-proliferative cells encroaching from the rear of the wave, which are ultimately selected due to their higher proliferative potential.

    Quantitative agreement between the IB model and its PDE counterpart. The plots in the bottom lines of Figures 24 summarise the corresponding numerical solutions of the PDE model (4.2). Comparing these plots with those in the top lines, we can see that there is an excellent quantitative agreement between the results of numerical simulations of the IB model and the numerical solutions of its PDE counterpart, both with respect to the cell population density and the cell pressure, for each of the barotropic relations given by Cases 1–3 in (4.9).

    All these plots indicate that, in agreement with the results presented in Subsection 4.1 (cf. the results given by (4.3)), when ϵ is sufficiently small, the scaled cell population density nϵ/ρϵ is concentrated as a sharp Gaussian with maximum at a single point yϵ(t,x) for all xSupp(pϵ). The maximum point yϵ(t,x) corresponds to the dominant phenotype within the cell population at position x and time t. Again in agreement with the results presented in Subsection 4.1 (cf. the results given by (4.6) and (4.7)), the cell pressure pϵ behaves like a one-sided compactly supported and monotonically decreasing travelling front that connects pM to 0, while the dominant phenotype yϵ increases monotonically from y = 0 to y = Y across the support of the invading wave. Moreover, we find an excellent quantitative agreement between pϵ(t,x)/pM and r(yϵ(t,x)) (cf. the solid blue and dashed cyan lines in the right panels of Figures 24). This indicates that, when ϵ is sufficiently small, relation (4.4) is satisfied as well.

    In order to measure the speed of these travelling waves, we track the dynamics of the points xϵ1(t), xϵ2(t) and xϵ3(t) such that

    pϵ(t,xϵ1(t))=0.2pM,pϵ(t,xϵ2(t))=0.5pM,pϵ(t,xϵ3(t))=0.8pM.
    Notably, we observe the evolution of xϵ1(t), xϵ2(t) and xϵ3(t) towards straight lines of approximatively the same slope ≈ 2.5 (see the insets of the right panels in Figures 24). Moreover, an equivalent tracking of ˜xϵ1(t), ˜xϵ2(t) and ˜xϵ3(t) such that ˉyϵ(t,˜xϵ1(t))=0.2, ˉyϵ(t,˜xϵ2(t))=0.5 and ˉyϵ(t,˜xϵ3(t))=0.8, with
    ˉyϵ(t,x):=argmaxy[0,Y]nϵ(t,x,y),
    yields quasi-identical results (results not shown). This supports the idea that pϵ behaves like a travelling front of speed c ≈ 2.5. Such a value of the speed is coherent with the condition on the minimal wave speed given by (4.5). In fact, inserting into (4.5) the numerical values of yϵ(8,x) in place of y(z) and the numerical values of 2yyuϵ(8,x,ˉyϵ(8,x)) with uϵ = ϵlog(nϵ) in place of 2yyu(z,ˉy(z)) gives c ⪆ 2.5.

    Possible discrepancies between the IB model and its PDE counterpart. In the cases discussed so far, we have observed excellent quantitative agreement between averaged results of numerical simulations of the IB model and numerical solutions of the corresponding PDE model. However, we hypothesise that possible differences between the two models can emerge when cell dynamics are strongly impacted by demographic stochasticity, which cannot be captured by the PDE model.

    In general, we expect demographic stochasticity to have a stronger impact on cell dynamics in the presence of smaller values of the homeostatic pressure pM, since smaller values of pM correlate with smaller cell numbers. Moreover, in the case where cells are initially distributed across both physical and phenotype space according to (4.8), we expect demographic stochasticity to escalate during the early stages of cell dynamics if sufficiently small values of the parameter A0 and sufficiently large values of the parameter y0 (i.e. values of y0 sufficiently far from 0 and sufficiently close to Y) are considered. In fact, smaller values of A0 correlate with lower initial cell numbers. Moreover, since cells in phenotypic states y ≈ 0 will ultimately be selected in the rear of the invading wave (cf. the plots in the left panels of Figures 24), bottleneck effects leading to a temporary drastic reduction in the size of the cell population may occur if y0 is sufficiently far from 0.

    Remark 4. The robustness of the results of numerical simulations of the IB model presented so far is supported by the fact that there is an excellent quantitative agreement between them and the results of numerical simulations and formal travelling-wave analysis of the corresponding PDE model. In fact, in the light of this agreement, independently of the specific definitions of the model functions Π, R and μ, provided that assumptions (2.3), (2.7) and (2.11) are satisfied, and sufficiently large cell numbers are considered, in the asymptotic regime ϵ → 0, one can expect the rules governing the spatial evolutionary dynamics of single cells considered here to bring about patterns of population growth that will ultimately be qualitatively similar to those of Figures 24.

    Hence, to test the aforementioned hypothesis, we carry out numerical simulations of the two models for decreasing values of A0 and increasing values of y0 in the initial cell distribution (4.8). Furthermore, we define the cell pressure through the barotropic relation given by Case 1 in (4.9) and set pM:=maxx[0,X]Π(ρϵ(0,x)), so that smaller values of A0 correspond to smaller value of pM as well.

    Figure 2.  Numerical simulation results of the IB model (top row) and the PDE model (4.2) (bottom row) in the case where the cell pressure is defined through the barotropic relation given by Case 1 in (4.9). Plots display the scaled cell population density nϵ/ρϵ (left panels) and the scaled cell pressure pϵ/pM (right panels, solid blue lines) at three successive time instants (i.e. t = 4, t = 6 and t = 8) for both modelling approaches. The dashed cyan lines in the right panels highlight the corresponding values of r(yϵ), with yϵ defined via (4.11). The insets of the right panels display the plots of xϵ1(t) (blue squares), xϵ2(t) (red diamonds) and xϵ3(t) (black stars) defined via (4.10). The results from the IB model were obtained by averaging over 10 simulations.
    Figure 3.  Numerical simulation results of the IB model (top row) and the PDE model (4.2) (bottom row) in the case where the cell pressure is defined through the barotropic relation given by Case 2 in (4.9). Plots display the scaled cell population density nϵ/ρϵ (left panels) and the scaled cell pressure pϵ/pM (right panels, solid blue lines) at three successive time instants (i.e. t = 4, t = 6 and t = 8) for both modelling approaches. The dashed cyan lines in the right panels highlight the corresponding values of r(yϵ), with yϵ defined via (4.11). The insets of the right-hand panels display the plots of xϵ1(t) (blue squares), xϵ2(t) (red diamonds) and xϵ3(t) (black stars) defined via (4.10). The results from the IB model were obtained by averaging over 10 simulations.
    Figure 4.  Numerical simulation results of the IB model (top row) and the PDE model (4.2) (bottom row) in the case where the cell pressure is defined through the barotropic relation given by Case 3 in (4.9). Plots display the scaled cell population density nϵ/ρϵ (left panels) and the scaled cell pressure pϵ/pM (right panels, solid blue lines) at three successive time instants (i.e. t = 4, t = 6 and t = 8) for both modelling approaches. The dashed cyan lines in the right panels highlight the corresponding values of r(yϵ), with yϵ defined via (4.11). The insets of the right-hand panels display the plots of xϵ1(t) (blue squares), xϵ2(t) (red diamonds) and xϵ3(t) (black stars) defined via (4.10). The results from the IB model were obtained by averaging over 10 simulations.

    The results obtained for the IB model are summarised by the plots in Figure 5, which display typical dynamics of the scaled cell pressure pϵ/pM, while the corresponding results for the PDE model (4.2) are summarised by the plots in Figure 6. These results corroborate our hypothesis by demonstrating that the quantitative agreement between the IB model and its PDE counterpart deteriorates when smaller values of A0 and larger values of y0 are considered (cf. the plots in the bottom-line panels of Figures 5 and 6).

    Figure 5.  Numerical simulation results of the IB model for different values of the parameters A0 and y0 in the initial cell distribution (4.8)i.e. y0 = 0.2 (left column) or y0 = 0.8 (right column) and A0 = 10 (top row) or A0 = 1 (central row) or A0 = 0.27 (bottom row). The solid blue lines highlight the values of the scaled cell pressure pϵ/pM at three successive time instants (i.e. t = 3, t = 5 and t = 7). The dashed cyan lines highlight the corresponding values of r(yϵ), with yϵ defined via (4.11). These results were obtained by averaging over 10 simulations.
    Figure 6.  Numerical simulation results of the PDE model (4.2) for different values of the parameters A0 and y0 in the initial cell distribution (4.8)i.e. y0 = 0.2 (left column) or y0 = 0.8 (right column) and A0 = 10 (top row) or A0 = 1 (central row) or A0 = 0.27 (bottom row). The solid blue lines highlight the values of the scaled cell pressure pϵ/pM at three successive time instants (i.e. t = 3, t = 5 and t = 7). The dashed cyan lines highlight the corresponding values of r(yϵ), with yϵ defined via (4.11).

    In line with our expectations, this is due to the fact that stronger stochastic effects associated with small population levels in the initial phase of cell dynamics create the potential for population extinction to occur in some simulations of the IB model – i.e. under the exact same parameter setting, we can observe extinction or survival of the population in the IB model due to demographic stochasticity (cf. the single simulation results displayed in Figures 7 and 8). On the other hand, the cell population will always persist according to the PDE model. This ultimately results in discrepancies between the average behaviour of the IB model and the behaviour of the PDE model (cf. the plots in the bottom-line panels of Figures 5 and 6).

    Figure 7.  Numerical results of a single simulation of the IB model with A0 = 0.27 and y0 = 0.8 in the initial cell distribution (4.8)i.e. 1 out of the 10 simulations that are used to produce the average results displayed in the right-column, bottom-line panel of Figure 5. Plots display the scaled cell population density nϵ/ρϵ (top panels) and the scaled cell pressure pϵ/pM (bottom panels, solid blue lines) at five successive time instants (i.e. t = 0, t = 1, t = 2, t = 3 and t = 4). The dashed cyan lines in the bottom panels highlight the corresponding values of r(yϵ), with yϵ defined via (4.11). In this simulation, the cell population does not go extinct.
    Figure 8.  Numerical results of a single simulation of the IB model with A0 = 0.27 and y0 = 0.8 in the initial cell distribution (4.8)i.e. 1 out of the 10 simulations that are used to produce the average results displayed in the right-column, bottom-line panel of Figure 5. Plots display the scaled cell population density nϵ/ρϵ (top panels) and the scaled cell pressure pϵ/pM (bottom panels, solid blue lines) at five successive time instants (i.e. t = 0, t = 1, t = 2, t = 3 and t = 4). The dashed cyan lines in the bottom panels highlight the corresponding values of r(yϵ), with yϵ defined via (4.11). In this simulation, the cell population goes extinct rapidly.

    We developed an IB model for the dynamics of phenotypically heterogeneous growing cell populations, which captures intercellular variability in cell proliferation and migration rates. We concentrated on a proliferation-migration tradeoff scenario, where the cell phenotypes span a spectrum of states from minimally-mobile but highly-proliferative to highly-mobile but minimally-proliferative. In the context of cancer invasion, such a tradeoff is the tenet of the “go-or-grow” hypothesis, which was conceived following observations of glioma cell behaviour [56] and has stimulated much empirical and theoretical research – see, for instance, [53], [56], [57], [59], [68][72] and references therein.

    We reported on the results of numerical simulations of the IB model which illustrate how proliferation-migration tradeoffs shaping the evolutionary dynamics of single cells can lead, at the population level, to the generation of travelling waves whereby phenotypes are structured across the support of the wave, with highly-mobile cells being found at the invasive front and more-proliferative cells dominating at the rear. Similar patterns of cell population growth have been observed in gliomas, where cells within the interior of the tumour exhibit higher proliferation and lower migration rates, while cells on the tumour border are instead characterised by lower proliferation and higher migration rates [48], [50], [56], [73], [74].

    We formally derived the deterministic continuum counterpart of the IB model, which comprises a non-local PDE for the cell population density function, and carried out a comparative study between numerical simulations of the IB model and both numerical solutions and formal travelling-wave analysis of the PDE model. We demonstrated that there is an excellent quantitative agreement between the results of numerical simulations of the IB model and the results of numerical simulations and travelling-wave analysis of the corresponding PDE model, when sufficiently large cell numbers are considered. This testifies to the robustness of the results of numerical simulations of the IB model presented here (see Remark 4).

    In general, agreement between IB models and their continuum counterparts arises in regions of the model parameter space that correspond to sufficiently large cell numbers [75][77], while discrepancies may arise when the number of cells becomes low – e.g. if the rate of cell death is sufficiently large [78] – leading to possible extinction of the population in the IB model. We have provided numerical evidence of situations such as these in which the predictions of the two models can differ due to demographic stochasticity, which cannot be captured by the PDE model. This indicates the importance of integrating individual-based and continuum approaches when modelling the growth of phenotypically heterogeneous cell populations.

    Although in this work we focused on a one-dimensional spatial domain scenario, the IB model presented here, and the formal limiting procedure to derive the corresponding continuum model, could easily be adapted to higher spatial dimensions. Furthermore, while we represented the spatial domain of the IB model as a regular lattice, it would certainly be interesting to generalise the underlying modelling approach, as well as the formal method to derive the continuum counterpart of the model, to cases where cells are distributed over irregular lattices and also to cases where off-latice representations of the spatial domain are adopted. The present IB model could also be extended further to include the effects of chemical species (e.g. nutrients, growth factors, chemoattractants, chemorepulsants) and how the cells interact with and respond to these chemicals. To include and implement chemical species in the current model, we could use a hybrid modelling approach whereby the probabilistic rules governing the dynamics of single cells would be coupled with balance equations for the chemical concentrations. Hybrid modelling approaches of this type have been utilised in the context of modelling various aspects of cancer growth and development – see, for instance, [11], [62], [79][82].

    The generality of our assumptions makes the IB modelling framework presented here applicable to a broad range of biological processes that are driven by the growth of phenotypically heterogeneous cell populations, including tumour invasion and tissue remodelling and repair. It would thus be interesting to focus on particular cellular systems, and consequently define specific models, which could then be more accurately parameterised using precise biological data. This would offer the opportunity to dissect out the role played by different spatiotemporal evolutionary processes at the single-cell level in the formation of complex spatial patterns of population growth.



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