<?xml version="1.0" encoding="UTF-8"?><!DOCTYPE article  PUBLIC "-//NLM//DTD Journal Publishing DTD v3.0 20080202//EN" "http://dtd.nlm.nih.gov/publishing/3.0/journalpublishing3.dtd"><article xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink" dtd-version="3.0" xml:lang="en" article-type="research article"><front><journal-meta><journal-id journal-id-type="publisher-id">JAMP</journal-id><journal-title-group><journal-title>Journal of Applied Mathematics and Physics</journal-title></journal-title-group><issn pub-type="epub">2327-4352</issn><publisher><publisher-name>Scientific Research Publishing</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.4236/jamp.2017.512188</article-id><article-id pub-id-type="publisher-id">JAMP-80899</article-id><article-categories><subj-group subj-group-type="heading"><subject>Articles</subject></subj-group><subj-group subj-group-type="Discipline-v2"><subject>Physics&amp;Mathematics</subject></subj-group></article-categories><title-group><article-title>
 
 
  Global Analysis of an SEIR Epidemic Model with a Ratio-Dependent Nonlinear Incidence Rate
 
</article-title></title-group><contrib-group><contrib contrib-type="author" xlink:type="simple"><name name-style="western"><surname>Xiaomei</surname><given-names>Ren</given-names></name><xref ref-type="aff" rid="aff1"><sup>1</sup></xref></contrib><contrib contrib-type="author" xlink:type="simple"><name name-style="western"><surname>Tiansi</surname><given-names>Zhang</given-names></name><xref ref-type="aff" rid="aff1"><sup>1</sup></xref></contrib></contrib-group><aff id="aff1"><addr-line>College of Science, University of Shanghai for Science and Technology, Shanghai, China</addr-line></aff><pub-date pub-type="epub"><day>06</day><month>12</month><year>2017</year></pub-date><volume>05</volume><issue>12</issue><fpage>2311</fpage><lpage>2319</lpage><history><date date-type="received"><day>10,</day>	<month>October</month>	<year>2017</year></date><date date-type="rev-recd"><day>4,</day>	<month>December</month>	<year>2017</year>	</date><date date-type="accepted"><day>7,</day>	<month>December</month>	<year>2017</year></date></history><permissions><copyright-statement>&#169; Copyright  2014 by authors and Scientific Research Publishing Inc. </copyright-statement><copyright-year>2014</copyright-year><license><license-p>This work is licensed under the Creative Commons Attribution International License (CC BY). http://creativecommons.org/licenses/by/4.0/</license-p></license></permissions><abstract><p><html>
 <head></head>
 
  In this paper, a SEIR model with ratio-dependent transmission rate in the form 
  <img alt="" src="Edit_1394ac5d-61e4-40f9-a333-ba792f7f66f5.bmp" /> is studied and the basic reproduction number which determines the disease’s extinction or continued existence is obtained. By constructing the proper Lyapunov function, we prove that if 
  R
  <sub>0</sub> ≤ 1, the disease-free equilibrium point of the model is globally asymptotically stable and the disease always dies out; if 
  R
  <sub>0</sub> &gt; 1, the endemic equilibrium point is globally asymptotically stable and the disease persists.
 
</html></p></abstract><kwd-group><kwd>SEIR Model</kwd><kwd> the Ratio-Dependent Transmission Rate</kwd><kwd> Basic Reproduction Number</kwd><kwd> Equilibrium</kwd><kwd> Global Stability</kwd></kwd-group></article-meta></front><body><sec id="s1"><title>1. Introduction</title><p>As we all know, infectious diseases are enemies of human health. For a long time, people have been fighting various infectious disease; and many methods have been used to study the spread of infectious diseases, so as to control and eliminate infectious diseases, see [<xref ref-type="bibr" rid="scirp.80899-ref1">1</xref>] . Amongst them, mathematical model has become an important tool to analyze the epidemiological characteristics of infectious diseases since the pioneer work of Kermack and McKendrick [<xref ref-type="bibr" rid="scirp.80899-ref2">2</xref>] [<xref ref-type="bibr" rid="scirp.80899-ref3">3</xref>] , which provides us useful control measures in [<xref ref-type="bibr" rid="scirp.80899-ref4">4</xref>] . In standard epidemiological models, the incidence rate (the rate of new infections) is bilinear in the infective and susceptible individuals, see [<xref ref-type="bibr" rid="scirp.80899-ref5">5</xref>] [<xref ref-type="bibr" rid="scirp.80899-ref6">6</xref>] [<xref ref-type="bibr" rid="scirp.80899-ref7">7</xref>] . It has been suggested that the diseases transmission process may have a nonlinear incidence rate, see [<xref ref-type="bibr" rid="scirp.80899-ref8">8</xref>] [<xref ref-type="bibr" rid="scirp.80899-ref9">9</xref>] [<xref ref-type="bibr" rid="scirp.80899-ref10">10</xref>] .</p><p>In real life, epidemics tend to have an incubation period, as susceptible to infection after contacting with infected people. First of all, carrying virus, the virus is not immediately, but after a period of time, to onset and into the herd of infected people. In the paper, on the basis of the work of Yuan and Li in [<xref ref-type="bibr" rid="scirp.80899-ref11">11</xref>] an SEIR (Susceptible-Exposed-Infected-Removed) epidemic model is considered with a ratio-dependent nonlinear incident rate g ( S , I ) .</p><p>The transmission function g ( S , I ) plays a key role in determining disease dynamics, see [<xref ref-type="bibr" rid="scirp.80899-ref12">12</xref>] [<xref ref-type="bibr" rid="scirp.80899-ref13">13</xref>] . Traditionally, the density-dependent transmission (or the bilinear incidence rate, g ( S , I ) = k S I , k the proportionality constant) and the frequency-dependent transmission (or the standard incidence rate,</p><p>g ( S , I ) = k S I S + I ) are two extreme forms of disease transmission, which have</p><p>been frequently used in well-know epidemic models [<xref ref-type="bibr" rid="scirp.80899-ref14">14</xref>] [<xref ref-type="bibr" rid="scirp.80899-ref15">15</xref>] . For example, Capasso and Serio [<xref ref-type="bibr" rid="scirp.80899-ref16">16</xref>] introduced a saturated transmission rate g ( S , I ) = f ( I ) S , where the infectious force f ( I ) is a function of infectious individuals which has been used in many classic disease model. Especially, Yuan and Li [<xref ref-type="bibr" rid="scirp.80899-ref11">11</xref>] studied a rate-dependent nonlinear incident rate with the following form</p><p>g ( S , I ) = f ( I S ) S = k ( I S ) l S 1 + α ( I S ) h = k S h − l + 1 I l S h + α I h , (1)</p><p>where α is a parameter which measures the psychological or inhibitory effect. It should be noted that if α = 1 and h = l = 1 , (1) becomes the well-known</p><p>frequency-dependent transmission rate k S I S + I .</p><p>In the case of l = 1 , we can obtain the rate-dependent transmission rate g ( S , I ) as the following form:</p><p>g ( S , I ) = f ( I S ) S = k I 1 + α ( I S ) h = k S h I S h + α I h , (2)</p><p>which indicates that the transmission rate of disease is approximately governed</p><p>by k I if I S is small (e.g., at the beginning of disease’s spreading) or it is approximately governed by k α ( S I ) h − 1 S if I S is large (e.g., in the endemic when</p><p>almost everyone is infected). Therefore, the ratio-dependent transmission rate (2) indeed takes accounts of the crowding effects and behavior changes during epidemics. In this paper, we mainly focus on a SEIR epidemic model with the ratio-dependent incidence rate (2).</p><p>We consider the global properties of this SEIR model and show that if the basic reproduction number R 0 ≤ 1 , the disease-free equilibrium point is globally asymptotically stable, while if R 0 &gt; 1 , the disease-free equilibrium point is unstable and the unique endemic equilibrium point is globally asymptotically stable.</p><p>The organization of this paper is as follows: in the next section, we present the model and derive the disease-free equilibrium point and the endemic equilibrium point. In Section 3 we analyze the global stability of the equilibrium point. A brief discussion and summarize are given in Section 4.</p></sec><sec id="s2"><title>2. Model Formulation</title><p>The whole population N ( t ) is divided into four subclasses based on disease status: the susceptible population, the exposed population, the infected population and removed population, denoted by S ( t ) , E ( t ) , I ( t ) , R ( t ) , respectively, and N ( t ) = S ( t ) + E ( t ) + I ( t ) + R ( t ) . We assume that infectious disease can cause additional mortality, then the SEIR model can be modeled by the following set of nonlinear differential Equations (3) deterministically:</p><p>{ d S d t = A − k S h I S h + α I h − μ S , d E d t = k S h I S h + α I h − ( μ + q ) E , d I d t = q E − ( μ + δ + γ ) I , d R d t = γ I − μ R , (3)</p><p>where A is the recruitment rate of the population, μ is the natural death rate, q is the constant rate such that the exposed individuals become infective, γ is the constant rate for recovery, δ is the disease inducing death. Since R does not appear in the first three equations of system (3), thus (3) reduces to the following three-dimensional system (4)</p><p>{ d S d t = A − k S h I S h + α I h − μ S , d E d t = k S h I S h + α I h − ( μ + q ) E , d I d t = q E − ( μ + δ + γ ) I . (4)</p><p>Because d S d t | S = 0 = A &gt; 0 , d E d t | E = 0 = k S h I S h + α I h ≥ 0 , d I d t | I = 0 = q E ≥ 0 , the</p><p>non-negativity of the initial value of system (4) in R + 3 is guaranteed, where</p><p>R + 3 = { ( S , E , I ) : S &gt; 0 , E &gt; 0 , I &gt; 0 } , (5)</p><p>It follows from system (4) that:</p><p>d ( S + E + I ) d t = A − μ S − ( μ + q ) E + q E − ( μ + δ + γ ) I = A − μ S − μ E − ( μ + δ + γ ) I = A − μ ( S + E + I ) − ( δ + γ ) I ≤ A − μ ( S + E + I ) . (6)</p><p>Since lim t → + ∞ sup ( S + E + I ) ≤ A μ , the feasible region for system (4) is thus a</p><p>bounded set Γ :</p><p>Γ = { ( S , E , I ) : S + E + I ≤ A μ , S &gt; 0 , E ≥ 0 , I ≥ 0 } . (7)</p><p>The region Γ is positively invariant with respect to systems (4). So, the only solution with the associated initial conditions will be considered inside the region Γ , where the uniqueness of solutions, usual existence, and continuation results are satisfied. Hence, system (4) is considered mathematically and epidemiologically well posed in Γ . Notice that model (4) has a disease-free equilibrium</p><p>point P 0 = ( A μ , 0 , 0 ) for all parameter values. Let X = ( E , I , S ) T , system (4) can</p><p>be written as (see [<xref ref-type="bibr" rid="scirp.80899-ref17">17</xref>] )</p><p>d X d t = F ( X ) − V ( X ) . (8)</p><p>And</p><p>F ( X ) = ( k S h I S h + α I h 0 0 ) , (9)</p><p>V ( X ) = ( ( μ + q ) E − q E + ( μ + δ + γ ) I − A + k S h I S h + α I h + μ S ) . (10)</p><p>The jacobian matrices of F ( X ) and V ( X ) at the disease-free equilibrium point P 0 are, respectively,</p><p>D F ( P 0 ) = ( F 0 0 0 ) , (11)</p><p>D V ( P 0 ) = ( V 0 J 1 J 2 ) , (12)</p><p>where</p><p>F = ( 0 k 0 0 ) , (13)</p><p>V = ( μ + q 0 − q μ + δ + γ ) . (14)</p><p>So the regeneration matrix of system (4) is</p><p>Q = F V − 1 = ( k q ( μ + q ) ( μ + δ + γ ) k μ + δ + γ 0 0 ) , (15)</p><p>the spectral radius of F V − 1 is</p><p>ρ ( F V − 1 ) = k q ( μ + q ) ( μ + δ + γ ) . (16)</p><p>Hence the basic reproduction number R 0 (see [<xref ref-type="bibr" rid="scirp.80899-ref18">18</xref>] ) is</p><p>R 0 = k q ( μ + q ) ( μ + δ + γ ) . (17)</p><p>Without difficulty we can get unique endemic equilibrium point state P * = ( S * , E * , I * ) of model (4) with</p><p>{ S * = A μ − ( μ + q ) ( μ + δ + γ ) I * μ q , E * = ( μ + δ + γ ) I * q , I * = ( k S * h q α ( μ + q ) ( μ + δ + γ ) − S * h α ) 1 h , (18)</p><p>and the endemic equilibrium point is written in the following form:</p><p>{ S * = A R 0 R 0 μ + k ( R 0 − 1 α ) 1 h , E * = k A ( R 0 − 1 α ) 1 h ( μ + q ) [ R 0 μ + k ( R 0 − 1 α ) 1 h ] , I * = A R 0 ( R 0 − 1 α ) 1 h R 0 μ + k ( R 0 − 1 α ) 1 h , (19)</p><p>if R 0 &gt; 1 .</p><p>Through the above analysis, system (4) has no endemic equilibrium point for R 0 ≤ 1 , and from (19) we know that system (4) has a unique endemic equilibrium point if R 0 &gt; 1 .</p></sec><sec id="s3"><title>3. Global Stability of the Equilibrium Point</title><p>In this section, we first consider the global stability of model (4) at the disease-free equilibrium point P 0 .</p><p>Theorem 1: If R 0 ≤ 1 , the disease-free equilibrium point P 0 is globally asymptotically stable; if R 0 &gt; 1 , P 0 is unstable.</p><p>Proof. The characteristic equation of system (4) at P 0 is give by</p><p>( λ + μ ) [ λ 2 + ( 2 μ + q + δ + γ ) λ + ( μ + q ) ( μ + δ + γ ) − k q ] = 0. (20)</p><p>It is clear that λ = − μ is one root of (20). The other roots of (20) are determined by the following equation</p><p>λ 2 + ( 2 μ + q + δ + γ ) λ + ( μ + q ) ( μ + δ + γ ) − k q = 0. (21)</p><p>If R 0 &lt; 1 , ( μ + q ) ( μ + δ + γ ) − k q &gt; 0 , thus (21) has two roots with negative real parts, therefore, the disease-free equilibrium point P 0 is locally asymptotically stable.</p><p>To complete the proof, we construct the following Lyapunov function</p><p>L 1 = q E + ( μ + q ) I . (22)</p><p>The time derivative of L 1 along the solution of (4) is</p><p>d L 1 d t = q d E d t + ( μ + q ) d I d t = q k S h I S h + α I h − ( μ + q ) q E + ( μ + q ) q E − ( μ + q ) ( μ + δ + γ ) I = q k S h I S h + α I h − ( μ + q ) ( μ + δ + γ ) I ≤ k q I − ( μ + q ) ( μ + δ + γ ) I = [ k q − ( μ + q ) ( μ + δ + γ ) ] I . (23)</p><p>When R 0 ≤ 1 , we have d L 1 d t ≤ 0 . By the LaSalle’s invariance principle, see</p><p>[<xref ref-type="bibr" rid="scirp.80899-ref19">19</xref>] , we conclude that P 0 is globally asymptotically stable if R 0 ≤ 1 .</p><p>When R 0 &gt; 1 , the Jacobian matrix of model (4) evaluated at P 0 is</p><p>J ( P 0 ) = ( − μ 0 − k 0 − ( μ + q ) k 0 q − ( μ + δ + γ ) ) , (24)</p><p>which has an eigenvalue − μ &lt; 0 . Denoted by</p><p>B = ( − ( μ + q ) k q − ( μ + δ + γ ) ) , (25)</p><p>we find that t r B &lt; 0 ( t r B represents the trace of matrix B, which is the sum of the elements of the main diagonal of the matrix B). When R 0 &gt; 1 , and d e t B &lt; 0 ( d e t B is the determinant of matrix B), the matrix B must have a positive eigenvalue, thus the disease-free equilibrium point P 0 is unstable whenever R 0 &gt; 1 . This completes the proof.</p><p>For the stability of endemic equilibrium point P * = ( S * , E * , I * ) of model (4), we have the following theorem:</p><p>Theorem 2: If R 0 &gt; 1 , the unique endemic equilibrium point P * = ( S * , E * , I * ) of model (4) is globally asymptotically stable.</p><p>Proof. Suppose that ( S , E , I ) is any positive solution to system (4). Define a Lyapunov function</p><p>L 2 ( S , E , I ) = | S − S * | + | E − E * | + | I − I * | . (26)</p><p>Obviously L 2 ( P * ) = 0 and when P ≠ P * , L 2 ( P ) ≠ 0 . Remember that P * is the solution to the system (4), the upper right derivative of L 2 can be estimated:</p><p>D + L 2 = s g n ( S − S * ) ( S ′ − ( S * ) ′ ) + s g n ( E − E * ) ( E ′ − ( E * ) ′ )     + s g n ( I − I * ) ( I ′ − ( I * ) ′ ) = s g n ( S − S * ) [ A − k S h I S h + α I h − μ S − ( A − k S * h I * S * h + α I * h − μ S * ) ]     + s g n ( E − E * ) [ k S h I S h + α I h − ( μ + q ) E − ( k S * h I * S * h + α I * h − ( μ + q ) E * ) ]     + s g n ( I − I * ) [ q E − ( μ + δ + λ ) I − ( q E * − ( μ + δ + λ ) I * ) ] . (27)</p><p>and we all know that when x &gt; 0 , s g n ( x ) = 1 ; x = 0 , s g n ( x ) = 0 ; x &lt; 0 , s g n ( x ) = − 1 .</p><p>In (27), there are 8 kinds of situation for the size of S and S * , E and E * , I and I * , it is enough to analyze the situation of S &gt; S * , E &gt; E * , I &gt; I * , while for the other situations, the discussion is similar.</p><p>Firstly there is</p><p>D + L 2 ≤ − μ | S − S * | − μ | E − E * | − ( μ + δ + λ ) | I − I * | ≤ − μ | S − S * | − μ | E − E * | − μ | I − I * | ≤ − μ L 2 . (28)</p><p>Integrate from t 0 to t on both sides of (28), we have</p><p>L 2 ( t ) + μ ∫ t 0 t L 2 ( x ) d x ≤ L 2 ( t 0 ) &lt; + ∞ . (29)</p><p>Since the front set Γ has a boundary, S , E and I must have boundaries, and their derivatives are bounded. It means that L 2 is uniformly continuous.</p><p>By Barbalat Lemma in [<xref ref-type="bibr" rid="scirp.80899-ref20">20</xref>] , there is</p><p>lim t → + ∞ L 2 ( t ) = 0 , (30)</p><p>and the unique endemic equilibrium point P * of model (4) is globally asymptotically stable. This completes the proof.</p></sec><sec id="s4"><title>4. Brief Summary</title><p>In this paper, we consider the SEIR epidemic model which is different from the classical nonlinear incident rate. We assume that the infectious force is a function of a number ratio of the infective to that of the susceptible which takes the</p><p>form k S h I S h + α I h , and the regeneration matrix is used to obtain the basic reproductive number R 0 ; the existence of equilibrium is obtained by direct calculation.</p><p>By constructing the proper Lyapunov functions, we prove that if R 0 ≤ 1 , there exists only the disease-free equilibrium point which is globally asymptotically stable, and if R 0 &gt; 1 , there is a unique endemic equilibrium point and this endemic equilibrium point is globally asymptotically stable.</p><p>In the future work, we can further consider adding pulse condition to the model studied in this paper.</p></sec><sec id="s5"><title>Cite this paper</title><p>Ren, X.M. and Zhang, T.S. (2017) Global Analysis of an SEIR Epidemic Model with a Ratio-Dependent Nonlinear Incidence Rate. 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