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<article xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink" article-type="research-article" dtd-version="1.4" xml:lang="en">
  <front>
    <journal-meta>
      <journal-id journal-id-type="publisher-id">Oalib</journal-id>
      <journal-title-group>
        <journal-title>Open Access Library Journal</journal-title>
      </journal-title-group>
      <issn pub-type="epub">2333-9721</issn>
      <issn pub-type="ppub">2333-9705</issn>
      <publisher>
        <publisher-name>Scientific Research Publishing</publisher-name>
      </publisher>
    </journal-meta>
    <article-meta>
      <article-id pub-id-type="doi">10.4236/oalib.1115339</article-id>
      <article-id pub-id-type="publisher-id">Oalib-153077</article-id>
      <article-categories>
        <subj-group>
          <subject>Article</subject>
        </subj-group>
        <subj-group>
          <subject>Biomedical</subject>
          <subject>Life Sciences</subject>
          <subject>Business</subject>
          <subject>Economics</subject>
          <subject>Chemistry</subject>
          <subject>Materials Science</subject>
          <subject>Computer Science</subject>
          <subject>Communications</subject>
          <subject>Earth</subject>
          <subject>Environmental Sciences</subject>
          <subject>Engineering</subject>
          <subject>Medicine</subject>
          <subject>Healthcare</subject>
          <subject>Physics</subject>
          <subject>Mathematics</subject>
          <subject>Social Sciences</subject>
          <subject>Humanities</subject>
        </subj-group>
      </article-categories>
      <title-group>
        <article-title>Catastrophe Theory in SEIRV Epidemic Modeling</article-title>
      </title-group>
      <contrib-group>
        <contrib contrib-type="author">
          <contrib-id contrib-id-type="orcid">0000-0002-7617-722X</contrib-id>
          <name name-style="western">
            <surname>Kaki</surname>
            <given-names>Mohammed Nokhas Murad</given-names>
          </name>
          <xref ref-type="aff" rid="aff1">1</xref>
        </contrib>
      </contrib-group>
      <aff id="aff1"><label>1</label> Civil Engineering Department, College of Engineering, Al-Qalam University, Kirkuk, Iraq </aff>
      <author-notes>
        <fn fn-type="conflict" id="fn-conflict">
          <p>The author declares no conflicts of interest.</p>
        </fn>
      </author-notes>
      <pub-date pub-type="epub">
        <day>03</day>
        <month>08</month>
        <year>2026</year>
      </pub-date>
      <pub-date pub-type="collection">
        <month>08</month>
        <year>2026</year>
      </pub-date>
      <volume>13</volume>
      <issue>08</issue>
      <fpage>1</fpage>
      <lpage>9</lpage>
      <history>
        <date date-type="received">
          <day>13</day>
          <month>04</month>
          <year>2026</year>
        </date>
        <date date-type="accepted">
          <day>07</day>
          <month>08</month>
          <year>2026</year>
        </date>
        <date date-type="published">
          <day>10</day>
          <month>08</month>
          <year>2026</year>
        </date>
      </history>
      <permissions>
        <copyright-statement>© 2026 by the authors and Scientific Research Publishing Inc.</copyright-statement>
        <copyright-year>2026</copyright-year>
        <license license-type="open-access">
          <license-p> This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( <ext-link ext-link-type="uri" xlink:href="https://creativecommons.org/licenses/by/4.0/">https://creativecommons.org/licenses/by/4.0/</ext-link> ). </license-p>
        </license>
      </permissions>
      <self-uri content-type="doi" xlink:href="https://doi.org/10.4236/oalib.1115339">https://doi.org/10.4236/oalib.1115339</self-uri>
      <abstract>
        <p><bold>Methodology:</bold> This study formulates a 5 × 5 SEIRV (Susceptible-Exposed-Infected-Recovered-Vaccinated) nonlinear epidemic matrix model to investigate epidemic dynamics through catastrophe theory. The nonlinear system is reduced near equilibrium points, and the infected population dynamics are transformed into a cubic structure equivalent to the cusp catastrophe model. Analytical methods are employed to derive conditions for multiple equilibria, bifurcation, and sudden epidemic transitions, and a new theorem is established demonstrating that nonlinear epidemic systems with quadratic infection terms and degenerate Jacobian matrices are locally equivalent to cusp catastrophe dynamics. <bold>Results:</bold> The results indicate that several equilibrium states, bistability, and bifurcating phenomena are present in the epidemic model, while numerical simulations confirm the theoretical predictions and illustrate catastrophic epidemic outbreaks caused by small variations in epidemiological parameters. <bold>Discussion:</bold> These findings suggest that epidemic systems may undergo abrupt transitions that cannot be fully captured through conventional linear stability analysis, highlighting the presence of hidden instability thresholds and hysteresis effects in nonlinear epidemic behavior. <bold>Findings:</bold> The integration of catastrophe theory with epidemic matrix modeling offers a novel mathematical perspective on sudden epidemic transitions and mechanisms of instability in infectious disease systems. <bold>Conclusion:</bold> The study concludes that catastrophe theory provides a powerful mathematical framework for analyzing epidemic instability and sudden outbreak transitions, offering valuable insights for epidemic prediction and the development of more effective disease control strategies.</p>
      </abstract>
      <kwd-group kwd-group-type="author-generated" xml:lang="en">
        <kwd>Epidemic Dynamics</kwd>
        <kwd>Cusp Catastrophe</kwd>
        <kwd>Bifurcation Analysis</kwd>
        <kwd>Hysteresis</kwd>
        <kwd>Equilibrium Stability</kwd>
        <kwd>Infectious Disease Modeling</kwd>
      </kwd-group>
    </article-meta>
  </front>
  <body>
    <sec id="sec1">
      <title>1. Introduction</title>
      <p>Mathematical modeling has become an essential tool in understanding the spread and control of infectious diseases. Compartmental epidemic models, particularly Susceptible-Exposed-Infected-Recovered-Vaccinated (SEIRV) frameworks, are widely employed to describe disease transmission dynamics, estimate epidemic thresholds, and assess intervention strategies within populations [<xref ref-type="bibr" rid="B1">1</xref>]. Recent developments in epidemic matrix modeling and numerical epidemic analysis have further enhanced the understanding of compartmental disease systems, including SEIRV formulations and iterative solution methods [<xref ref-type="bibr" rid="B2">2</xref>].</p>
      <p>Mathematical epidemic models continue to play a significant role in forecasting outbreak patterns and informing public health decisions in modern epidemiology. However, many epidemic systems exhibit nonlinear characteristics that cannot be adequately represented by traditional linear approaches. Classical linear stability analysis is effective in determining local equilibrium behavior but often fails to explain abrupt epidemic outbreaks or collapses resulting from small parameter perturbations. Recent studies have shown that nonlinear epidemic systems may exhibit bifurcation, multistability, and threshold-triggered transitions, indicating the presence of complex dynamic mechanisms beyond conventional linear predictions [<xref ref-type="bibr" rid="B3">3</xref>]-[<xref ref-type="bibr" rid="B5">5</xref>]. Such sudden transitions are especially relevant in infectious disease modeling, where slight variations in transmission or recovery rates may trigger disproportionate changes in outbreak magnitude.</p>
      <p>To address such phenomena, catastrophe theory offers a rigorous mathematical framework for analyzing discontinuous transitions caused by continuous parameter variation. First introduced in [<xref ref-type="bibr" rid="B6">6</xref>] and subsequently extended in contemporary studies of nonlinear stability [<xref ref-type="bibr" rid="B7">7</xref>]-[<xref ref-type="bibr" rid="B9">9</xref>], catastrophe theory provides a systematic method for investigating systems that undergo abrupt structural changes near critical thresholds. This theoretical framework is particularly effective in describing nonlinear systems characterized by bifurcation, hysteresis, and abrupt transitions between multiple equilibrium states [<xref ref-type="bibr" rid="B10">10</xref>]-[<xref ref-type="bibr" rid="B12">12</xref>].</p>
      <p>In epidemic dynamics, nonlinear incidence functions and matrix-based compartmental interactions frequently generate complex structures that may lead to hidden instability thresholds and catastrophic transitions. Recent research has confirmed that nonlinear epidemic systems can produce bistable states, discontinuous transitions, and multiple outbreak thresholds under certain epidemiological conditions. Matrix epidemic models, in particular, provide a compact representation of compartmental interactions and facilitate advanced analytical study of equilibrium and bifurcation structures.</p>
      <p>Motivated by these developments, this study investigates the application of catastrophe theory to a nonlinear 5 × 5 SEIRV epidemic matrix model. By reducing the system near its equilibrium points and analyzing the dynamics of the infected population, the research establishes a mathematical connection between epidemic matrix behavior and cusp catastrophe structures. This integration provides a novel theoretical perspective for understanding epidemic instability, predicting sudden outbreak transitions, and improving the strategic disease control mechanisms.</p>
    </sec>
    <sec id="sec2">
      <title>2. Methodology</title>
      <p>This study develops a mathematical framework based on a 5 × 5 SEIRV (Susceptible-Exposed-Infected-Recovered-Vaccinated) nonlinear epidemic model to analyze disease transmission dynamics. The total population is partitioned into five compartments, and the transitions between these classes are described using a system of nonlinear differential equations. The model incorporates key epidemiological processes, including infection, progression, recovery, vaccination, and natural removal rates.</p>
      <p>To capture complex dynamic behavior, the system is reformulated in matrix form, where state variables are represented as a vector, and the interaction terms are encoded in a nonlinear transition matrix. This formulation allows the use of linearization techniques around equilibrium points to study local stability properties. The Disease-Free Equilibrium (DFE) and endemic equilibrium states are derived by solving the nonlinear system.</p>
      <p>Catastrophe theory is employed to investigate sudden qualitative changes in the system behavior resulting from continuous variation in control parameters. Specifically, bifurcation phenomena and fold-type catastrophes are examined to determine the conditions in which minor variations in system parameters can trigger sudden shifts between disease-free, endemic, and epidemic outbreak states. Stability analysis is performed using eigenvalue techniques applied to the Jacobian matrix evaluated at equilibrium points.</p>
      <p>Numerical simulations are conducted to validate analytical results and to visualize phase portraits, equilibrium transitions, and threshold behavior under varying parameter regimes. The combined analytical and computational approach provides a comprehensive understanding of nonlinear epidemic dynamics and their sensitivity to changes in parameters, particularly vaccination and transmission rates.</p>
    </sec>
    <sec id="sec3">
      <title>3. SEIRV Model Formulation</title>
      <p>To investigate epidemic dynamics with vaccination effects and nonlinear transitions, we consider a SEIRV (Susceptible-Exposed-Infected-Recovered-Vaccinated) compartmental framework. The total population is partitioned into five mutually exclusive classes:</p>
      <disp-formula id="FD1">
        <mml:math>
          <mml:mrow>
            <mml:mi>S</mml:mi>
            <mml:mrow>
              <mml:mo>(</mml:mo>
              <mml:mi>t</mml:mi>
              <mml:mo>)</mml:mo>
            </mml:mrow>
            <mml:mo>,</mml:mo>
            <mml:mi>E</mml:mi>
            <mml:mrow>
              <mml:mo>(</mml:mo>
              <mml:mi>t</mml:mi>
              <mml:mo>)</mml:mo>
            </mml:mrow>
            <mml:mo>,</mml:mo>
            <mml:mi>I</mml:mi>
            <mml:mrow>
              <mml:mo>(</mml:mo>
              <mml:mi>t</mml:mi>
              <mml:mo>)</mml:mo>
            </mml:mrow>
            <mml:mo>,</mml:mo>
            <mml:mi>R</mml:mi>
            <mml:mrow>
              <mml:mo>(</mml:mo>
              <mml:mi>t</mml:mi>
              <mml:mo>)</mml:mo>
            </mml:mrow>
            <mml:mo>,</mml:mo>
            <mml:mi>V</mml:mi>
            <mml:mrow>
              <mml:mo>(</mml:mo>
              <mml:mi>t</mml:mi>
              <mml:mo>)</mml:mo>
            </mml:mrow>
          </mml:mrow>
        </mml:math>
      </disp-formula>
      <p>The dynamics are governed by nonlinear interactions representing infection transmission, incubation, recovery, loss of immunity, and vaccination flow. The core structure of the model can be written as:</p>
      <disp-formula id="FD2">
        <mml:math display="inline">
          <mml:mtable columnalign="left">
            <mml:mtr>
              <mml:mtd>
                <mml:mfrac>
                  <mml:mrow>
                    <mml:mtext>d</mml:mtext>
                    <mml:mi>S</mml:mi>
                  </mml:mrow>
                  <mml:mrow>
                    <mml:mtext>d</mml:mtext>
                    <mml:mi>t</mml:mi>
                  </mml:mrow>
                </mml:mfrac>
                <mml:mo>=</mml:mo>
                <mml:mi>Λ</mml:mi>
                <mml:mo>−</mml:mo>
                <mml:mi>β</mml:mi>
                <mml:mfrac>
                  <mml:mrow>
                    <mml:mi>S</mml:mi>
                    <mml:mi>I</mml:mi>
                  </mml:mrow>
                  <mml:mi>N</mml:mi>
                </mml:mfrac>
                <mml:mo>−</mml:mo>
                <mml:mi>ν</mml:mi>
                <mml:mi>S</mml:mi>
                <mml:mo>+</mml:mo>
                <mml:mi>ω</mml:mi>
                <mml:mi>R</mml:mi>
                <mml:mo>−</mml:mo>
                <mml:mi>μ</mml:mi>
                <mml:mi>S</mml:mi>
                <mml:mo>,</mml:mo>
              </mml:mtd>
            </mml:mtr>
            <mml:mtr>
              <mml:mtd>
                <mml:mfrac>
                  <mml:mrow>
                    <mml:mtext>d</mml:mtext>
                    <mml:mi>E</mml:mi>
                  </mml:mrow>
                  <mml:mrow>
                    <mml:mtext>d</mml:mtext>
                    <mml:mi>t</mml:mi>
                  </mml:mrow>
                </mml:mfrac>
                <mml:mo>=</mml:mo>
                <mml:mi>β</mml:mi>
                <mml:mfrac>
                  <mml:mrow>
                    <mml:mi>S</mml:mi>
                    <mml:mi>I</mml:mi>
                  </mml:mrow>
                  <mml:mi>N</mml:mi>
                </mml:mfrac>
                <mml:mo>−</mml:mo>
                <mml:mrow>
                  <mml:mo>(</mml:mo>
                  <mml:mrow>
                    <mml:mi>σ</mml:mi>
                    <mml:mo>+</mml:mo>
                    <mml:mi>μ</mml:mi>
                  </mml:mrow>
                  <mml:mo>)</mml:mo>
                </mml:mrow>
                <mml:mi>E</mml:mi>
                <mml:mo>,</mml:mo>
              </mml:mtd>
            </mml:mtr>
            <mml:mtr>
              <mml:mtd>
                <mml:mfrac>
                  <mml:mrow>
                    <mml:mtext>d</mml:mtext>
                    <mml:mi>I</mml:mi>
                  </mml:mrow>
                  <mml:mrow>
                    <mml:mtext>d</mml:mtext>
                    <mml:mi>t</mml:mi>
                  </mml:mrow>
                </mml:mfrac>
                <mml:mo>=</mml:mo>
                <mml:mi>σ</mml:mi>
                <mml:mi>E</mml:mi>
                <mml:mo>−</mml:mo>
                <mml:mrow>
                  <mml:mo>(</mml:mo>
                  <mml:mrow>
                    <mml:mi>γ</mml:mi>
                    <mml:mo>+</mml:mo>
                    <mml:mi>μ</mml:mi>
                    <mml:mo>+</mml:mo>
                    <mml:mi>α</mml:mi>
                  </mml:mrow>
                  <mml:mo>)</mml:mo>
                </mml:mrow>
                <mml:mi>I</mml:mi>
                <mml:mo>,</mml:mo>
              </mml:mtd>
            </mml:mtr>
            <mml:mtr>
              <mml:mtd>
                <mml:mfrac>
                  <mml:mrow>
                    <mml:mtext>d</mml:mtext>
                    <mml:mi>R</mml:mi>
                  </mml:mrow>
                  <mml:mrow>
                    <mml:mtext>d</mml:mtext>
                    <mml:mi>t</mml:mi>
                  </mml:mrow>
                </mml:mfrac>
                <mml:mo>=</mml:mo>
                <mml:mi>γ</mml:mi>
                <mml:mi>I</mml:mi>
                <mml:mo>−</mml:mo>
                <mml:mrow>
                  <mml:mo>(</mml:mo>
                  <mml:mrow>
                    <mml:mi>ω</mml:mi>
                    <mml:mo>+</mml:mo>
                    <mml:mi>μ</mml:mi>
                  </mml:mrow>
                  <mml:mo>)</mml:mo>
                </mml:mrow>
                <mml:mi>R</mml:mi>
                <mml:mo>,</mml:mo>
              </mml:mtd>
            </mml:mtr>
            <mml:mtr>
              <mml:mtd>
                <mml:mfrac>
                  <mml:mrow>
                    <mml:mtext>d</mml:mtext>
                    <mml:mi>V</mml:mi>
                  </mml:mrow>
                  <mml:mrow>
                    <mml:mtext>d</mml:mtext>
                    <mml:mi>t</mml:mi>
                  </mml:mrow>
                </mml:mfrac>
                <mml:mo>=</mml:mo>
                <mml:mi>ν</mml:mi>
                <mml:mi>S</mml:mi>
                <mml:mo>−</mml:mo>
                <mml:mi>μ</mml:mi>
                <mml:mi>V</mml:mi>
                <mml:mo>.</mml:mo>
              </mml:mtd>
            </mml:mtr>
          </mml:mtable>
        </mml:math>
      </disp-formula>
      <p>where:</p>
      <p><inline-formula><mml:math><mml:mi> Λ </mml:mi></mml:math></inline-formula> : recruitment rate,<inline-formula><mml:math><mml:mi> β </mml:mi></mml:math></inline-formula> : transmission rate,<inline-formula><mml:math><mml:mi> ν </mml:mi></mml:math></inline-formula> : vaccination rate,<inline-formula><mml:math><mml:mi> σ </mml:mi></mml:math></inline-formula> : incubation rate,<inline-formula><mml:math><mml:mi> γ </mml:mi></mml:math></inline-formula> : recovery rate,<inline-formula><mml:math><mml:mi> α </mml:mi></mml:math></inline-formula> : disease-induced mortality,<inline-formula><mml:math><mml:mi> ω </mml:mi></mml:math></inline-formula> : immunity waning rate,<inline-formula><mml:math><mml:mi> μ </mml:mi></mml:math></inline-formula> : natural death rate.</p>
      <p>This nonlinear system forms the basis for analyzing equilibrium structures and catastrophic transitions.</p>
    </sec>
    <sec id="sec4">
      <title>4. Equilibrium Points and Disease States</title>
      <p>The model admits two principal classes of equilibrium:</p>
      <p><bold>1</bold><bold>) Disease-Free Equilibrium (DFE)</bold></p>
      <p>At this equilibrium, <inline-formula><mml:math><mml:mrow><mml:mi> E </mml:mi><mml:mo> = </mml:mo><mml:mi> I </mml:mi><mml:mo> = </mml:mo><mml:mn> 0 </mml:mn></mml:mrow></mml:math></inline-formula> , and the population is distributed among susceptible, recovered, and vaccinated classes. The DFE represents epidemic extinction and is given by:</p>
      <disp-formula id="FD3">
        <mml:math>
          <mml:mrow>
            <mml:msub>
              <mml:mi>E</mml:mi>
              <mml:mn>0</mml:mn>
            </mml:msub>
            <mml:mo>=</mml:mo>
            <mml:mrow>
              <mml:mo>(</mml:mo>
              <mml:mrow>
                <mml:msup>
                  <mml:mi>S</mml:mi>
                  <mml:mo>*</mml:mo>
                </mml:msup>
                <mml:mo>,</mml:mo>
                <mml:mn>0</mml:mn>
                <mml:mo>,</mml:mo>
                <mml:mn>0</mml:mn>
                <mml:mo>,</mml:mo>
                <mml:msup>
                  <mml:mi>R</mml:mi>
                  <mml:mo>*</mml:mo>
                </mml:msup>
                <mml:mo>,</mml:mo>
                <mml:msup>
                  <mml:mi>V</mml:mi>
                  <mml:mo>*</mml:mo>
                </mml:msup>
              </mml:mrow>
              <mml:mo>)</mml:mo>
            </mml:mrow>
          </mml:mrow>
        </mml:math>
      </disp-formula>
      <p>where the components satisfy balance relations derived from the steady-state system.</p>
      <p><bold>2</bold><bold>) Endemic Equilibrium (EE)</bold></p>
      <p>The endemic state occurs when <inline-formula><mml:math><mml:mrow><mml:msup><mml:mi> I </mml:mi><mml:mo> * </mml:mo></mml:msup><mml:mo> &gt; </mml:mo><mml:mn> 0 </mml:mn></mml:mrow></mml:math></inline-formula> , indicating persistent disease transmission. This equilibrium is determined by solving the nonlinear algebraic system obtained by setting all derivatives to zero. The existence of EE depends critically on the basic reproduction number <inline-formula><mml:math><mml:mrow><mml:msub><mml:mi> ℛ </mml:mi><mml:mn> 0 </mml:mn></mml:msub></mml:mrow></mml:math></inline-formula> , typically defined as:</p>
      <disp-formula id="FD4">
        <mml:math>
          <mml:mrow>
            <mml:msub>
              <mml:mi>ℛ</mml:mi>
              <mml:mn>0</mml:mn>
            </mml:msub>
            <mml:mo>=</mml:mo>
            <mml:mfrac>
              <mml:mrow>
                <mml:mi>β</mml:mi>
                <mml:mi>σ</mml:mi>
              </mml:mrow>
              <mml:mrow>
                <mml:mrow>
                  <mml:mo>(</mml:mo>
                  <mml:mrow>
                    <mml:mi>σ</mml:mi>
                    <mml:mo>+</mml:mo>
                    <mml:mi>μ</mml:mi>
                  </mml:mrow>
                  <mml:mo>)</mml:mo>
                </mml:mrow>
                <mml:mrow>
                  <mml:mo>(</mml:mo>
                  <mml:mrow>
                    <mml:mi>γ</mml:mi>
                    <mml:mo>+</mml:mo>
                    <mml:mi>μ</mml:mi>
                    <mml:mo>+</mml:mo>
                    <mml:mi>α</mml:mi>
                  </mml:mrow>
                  <mml:mo>)</mml:mo>
                </mml:mrow>
              </mml:mrow>
            </mml:mfrac>
          </mml:mrow>
        </mml:math>
      </disp-formula>
      <p>When <inline-formula><mml:math><mml:mrow><mml:msub><mml:mi> ℛ </mml:mi><mml:mn> 0 </mml:mn></mml:msub><mml:mo> &gt; </mml:mo><mml:mn> 1 </mml:mn></mml:mrow></mml:math></inline-formula> , the system admits a biologically feasible endemic equilibrium.</p>
    </sec>
    <sec id="sec5">
      <title>5. Linear Stability Analysis</title>
      <p>To analyze local stability, the system is linearized around equilibrium points using the Jacobian matrix. For the DFE, stability is determined by the eigenvalues of the infection subsystem:</p>
      <p>If all eigenvalues have negative real parts, the DFE is locally asymptotically stable.If at least one eigenvalue becomes positive, the system undergoes a qualitative transition toward endemicity.</p>
      <p>The threshold condition is again governed by <inline-formula><mml:math><mml:mrow><mml:msub><mml:mi> ℛ </mml:mi><mml:mn> 0 </mml:mn></mml:msub></mml:mrow></mml:math></inline-formula> , which acts as a bifurcation parameter controlling system stability.</p>
    </sec>
    <sec id="sec6">
      <title>6. Catastrophe Theory Framework</title>
      <p>Catastrophe theory provides a geometric and nonlinear framework to analyze sudden shifts in epidemic states when parameters vary continuously. In the SEIRV system, parameters such as <inline-formula><mml:math><mml:mi> β </mml:mi></mml:math></inline-formula> , <inline-formula><mml:math><mml:mi> ν </mml:mi></mml:math></inline-formula> , or <inline-formula><mml:math><mml:mi> ω </mml:mi></mml:math></inline-formula> may act as control parameters, while the infected population <inline-formula><mml:math><mml:mi> I </mml:mi></mml:math></inline-formula> serves as a state variable.</p>
      <p>The system can be reduced (via center manifold or fast-slow decomposition) to a lower-dimensional potential form:</p>
      <disp-formula id="FD5">
        <mml:math>
          <mml:mrow>
            <mml:mfrac>
              <mml:mrow>
                <mml:mtext>d</mml:mtext>
                <mml:mi>I</mml:mi>
              </mml:mrow>
              <mml:mrow>
                <mml:mtext>d</mml:mtext>
                <mml:mi>t</mml:mi>
              </mml:mrow>
            </mml:mfrac>
            <mml:mo>=</mml:mo>
            <mml:mo>−</mml:mo>
            <mml:mfrac>
              <mml:mrow>
                <mml:mo>∂</mml:mo>
                <mml:mi>V</mml:mi>
                <mml:mrow>
                  <mml:mo>(</mml:mo>
                  <mml:mrow>
                    <mml:mi>I</mml:mi>
                    <mml:mo>;</mml:mo>
                    <mml:mi>a</mml:mi>
                    <mml:mo>,</mml:mo>
                    <mml:mi>b</mml:mi>
                  </mml:mrow>
                  <mml:mo>)</mml:mo>
                </mml:mrow>
              </mml:mrow>
              <mml:mrow>
                <mml:mo>∂</mml:mo>
                <mml:mi>I</mml:mi>
              </mml:mrow>
            </mml:mfrac>
          </mml:mrow>
        </mml:math>
      </disp-formula>
      <p>where <inline-formula><mml:math><mml:mrow><mml:mi> V </mml:mi><mml:mrow><mml:mo> ( </mml:mo><mml:mrow><mml:mi> I </mml:mi><mml:mo> ; </mml:mo><mml:mi> a </mml:mi><mml:mo> , </mml:mo><mml:mi> b </mml:mi></mml:mrow><mml:mo> ) </mml:mo></mml:mrow></mml:mrow></mml:math></inline-formula> is a potential function and <inline-formula><mml:math><mml:mrow><mml:mi> a </mml:mi><mml:mo> , </mml:mo><mml:mi> b </mml:mi></mml:mrow></mml:math></inline-formula> are control parameters derived from epidemiological rates.</p>
      <p>Typical catastrophic behaviors include:</p>
      <p><bold>Fold catastrophe</bold>: sudden jump from disease-free to endemic state,<bold>Cusp catastrophe</bold>: bistability between low and high infection regimes,<bold>Hysteresis loops</bold>: irreversible epidemic transitions under parameter reversal.</p>
    </sec>
    <sec id="sec7">
      <title>7. Cusp Type-Catastrophe</title>
      <sec id="sec7dot1">
        <title>
          7.1. Cusp Catastrophe Potential (Standard Form [
          <xref ref-type="bibr" rid="B7">7</xref>
          ]-[
          <xref ref-type="bibr" rid="B9">9</xref>
          ])
        </title>
        <p>The canonical cusp potential is:</p>
        <disp-formula id="FD6">
          <mml:math>
            <mml:mrow>
              <mml:mi>V</mml:mi>
              <mml:mrow>
                <mml:mo>(</mml:mo>
                <mml:mrow>
                  <mml:mi>I</mml:mi>
                  <mml:mo>;</mml:mo>
                  <mml:mi>a</mml:mi>
                  <mml:mo>,</mml:mo>
                  <mml:mi>b</mml:mi>
                </mml:mrow>
                <mml:mo>)</mml:mo>
              </mml:mrow>
              <mml:mo>=</mml:mo>
              <mml:mfrac>
                <mml:mn>1</mml:mn>
                <mml:mn>4</mml:mn>
              </mml:mfrac>
              <mml:msup>
                <mml:mi>I</mml:mi>
                <mml:mn>4</mml:mn>
              </mml:msup>
              <mml:mo>+</mml:mo>
              <mml:mfrac>
                <mml:mn>1</mml:mn>
                <mml:mn>2</mml:mn>
              </mml:mfrac>
              <mml:mi>a</mml:mi>
              <mml:msup>
                <mml:mi>I</mml:mi>
                <mml:mn>2</mml:mn>
              </mml:msup>
              <mml:mo>+</mml:mo>
              <mml:mi>b</mml:mi>
              <mml:mi>I</mml:mi>
            </mml:mrow>
          </mml:math>
        </disp-formula>
        <p>where:</p>
        <p><inline-formula><mml:math><mml:mi> I </mml:mi></mml:math></inline-formula> = state variable (infected population)<inline-formula><mml:math><mml:mrow><mml:mi> a </mml:mi><mml:mo> , </mml:mo><mml:mi> b </mml:mi></mml:mrow></mml:math></inline-formula> = control parameters (derived from SEIRV rates)</p>
      </sec>
      <sec id="sec7dot2">
        <title>7.2. Dynamical System (Gradient Form)</title>
        <p>The dynamics are:</p>
        <disp-formula id="FD7">
          <mml:math>
            <mml:mrow>
              <mml:mfrac>
                <mml:mrow>
                  <mml:mtext>d</mml:mtext>
                  <mml:mi>I</mml:mi>
                </mml:mrow>
                <mml:mrow>
                  <mml:mtext>d</mml:mtext>
                  <mml:mi>t</mml:mi>
                </mml:mrow>
              </mml:mfrac>
              <mml:mo>=</mml:mo>
              <mml:mo>−</mml:mo>
              <mml:mfrac>
                <mml:mrow>
                  <mml:mtext>d</mml:mtext>
                  <mml:mi>V</mml:mi>
                </mml:mrow>
                <mml:mrow>
                  <mml:mtext>d</mml:mtext>
                  <mml:mi>I</mml:mi>
                </mml:mrow>
              </mml:mfrac>
              <mml:mo>=</mml:mo>
              <mml:mo>−</mml:mo>
              <mml:mrow>
                <mml:mo>(</mml:mo>
                <mml:mrow>
                  <mml:msup>
                    <mml:mi>I</mml:mi>
                    <mml:mn>3</mml:mn>
                  </mml:msup>
                  <mml:mo>+</mml:mo>
                  <mml:mi>a</mml:mi>
                  <mml:mi>I</mml:mi>
                  <mml:mo>+</mml:mo>
                  <mml:mi>b</mml:mi>
                </mml:mrow>
                <mml:mo>)</mml:mo>
              </mml:mrow>
            </mml:mrow>
          </mml:math>
        </disp-formula>
        <p>So equilibrium points satisfy:</p>
        <disp-formula id="FD8">
          <mml:math>
            <mml:mrow>
              <mml:msup>
                <mml:mi>I</mml:mi>
                <mml:mn>3</mml:mn>
              </mml:msup>
              <mml:mo>+</mml:mo>
              <mml:mi>a</mml:mi>
              <mml:mi>I</mml:mi>
              <mml:mo>+</mml:mo>
              <mml:mi>b</mml:mi>
              <mml:mo>=</mml:mo>
              <mml:mn>0</mml:mn>
            </mml:mrow>
          </mml:math>
        </disp-formula>
        <p>This cubic equation is the core of cusp bifurcation behavior.</p>
      </sec>
      <sec id="sec7dot3">
        <title>7.3. Interpretation in SEIRV Epidemic Modeling</title>
        <p>In an SEIRV reduction:</p>
        <p>State variable</p>
        <p><inline-formula><mml:math><mml:mi> I </mml:mi></mml:math></inline-formula><bold>: infected class (dominant slow variable)</bold></p>
        <p>Control parameters (typical mapping)</p>
        <p>Define:</p>
        <p><inline-formula><mml:math><mml:mi> a </mml:mi></mml:math></inline-formula><bold>: effective linear epidemic pressure:</bold><inline-formula><mml:math><mml:mrow><mml:mi> a </mml:mi><mml:mo> ~ </mml:mo><mml:mrow><mml:mo> ( </mml:mo><mml:mrow><mml:msub><mml:mi> ℛ </mml:mi><mml:mn> 0 </mml:mn></mml:msub><mml:mo> − </mml:mo><mml:mn> 1 </mml:mn></mml:mrow><mml:mo> ) </mml:mo></mml:mrow><mml:mo> − </mml:mo><mml:msub><mml:mi> c </mml:mi><mml:mn> 1 </mml:mn></mml:msub><mml:mi> ν </mml:mi><mml:mo> + </mml:mo><mml:msub><mml:mi> c </mml:mi><mml:mn> 2 </mml:mn></mml:msub><mml:mi> ω </mml:mi></mml:mrow></mml:math></inline-formula><inline-formula><mml:math><mml:mi> b </mml:mi></mml:math></inline-formula><bold>: external or asymmetry forcing:</bold><inline-formula><mml:math display="inline"><mml:mi> b </mml:mi></mml:math></inline-formula> ~importation rate, behavioral shifts, seasonal forcing</p>
      </sec>
      <sec id="sec7dot4">
        <title>7.4. Epidemic Meaning of Cusp Geometry</title>
        <p>The cusp catastrophe explains:</p>
        <p><bold>1) Bistability</bold></p>
        <p>Two possible stable epidemic states:</p>
        <p><inline-formula><mml:math><mml:mrow><mml:mi> I </mml:mi><mml:mo> = </mml:mo><mml:mn> 0 </mml:mn></mml:mrow></mml:math></inline-formula> disease-free<inline-formula><mml:math><mml:mrow><mml:mi> I </mml:mi><mml:mo> = </mml:mo><mml:msup><mml:mi> I </mml:mi><mml:mo> * </mml:mo></mml:msup><mml:mo> &gt; </mml:mo><mml:mn> 0 </mml:mn></mml:mrow></mml:math></inline-formula> endemic</p>
        <p><bold>2) Sudden outbreak jump</bold></p>
        <p>A small parameter change in <inline-formula><mml:math><mml:mi> a </mml:mi></mml:math></inline-formula> or <inline-formula><mml:math><mml:mi> b </mml:mi></mml:math></inline-formula> causes:</p>
        <p>smooth variation → then abrupt jump in infection level</p>
        <p><bold>3) Hysteresis</bold></p>
        <p>If parameters are reversed:</p>
        <p>system does NOT return along the same pathepidemic persists even after <inline-formula><mml:math><mml:mrow><mml:msub><mml:mi> ℛ </mml:mi><mml:mn> 0 </mml:mn></mml:msub><mml:mo> &lt; </mml:mo><mml:mn> 1 </mml:mn></mml:mrow></mml:math></inline-formula></p>
      </sec>
      <sec id="sec7dot5">
        <title>7.5. Cusp Set (Bifurcation Surface)</title>
        <p>The cusp bifurcation occurs when equilibria merge:</p>
        <disp-formula id="FD9">
          <mml:math>
            <mml:mrow>
              <mml:mn>4</mml:mn>
              <mml:msup>
                <mml:mi>a</mml:mi>
                <mml:mn>3</mml:mn>
              </mml:msup>
              <mml:mo>+</mml:mo>
              <mml:mn>27</mml:mn>
              <mml:msup>
                <mml:mi>b</mml:mi>
                <mml:mn>2</mml:mn>
              </mml:msup>
              <mml:mo>=</mml:mo>
              <mml:mn>0</mml:mn>
            </mml:mrow>
          </mml:math>
        </disp-formula>
        <p>Meaning:</p>
        <p>inside this curve → 3 equilibria (bistability)outside → 1 equilibrium (monostable)</p>
      </sec>
      <sec id="sec7dot6">
        <title>7.6. Numerical SEIRV Example (Illustrative)</title>
        <p>Let: <inline-formula><mml:math><mml:mrow><mml:mi> a </mml:mi><mml:mo> = </mml:mo><mml:mo> − </mml:mo><mml:mn> 0.2 </mml:mn></mml:mrow></mml:math></inline-formula> and <inline-formula><mml:math><mml:mrow><mml:mi> b </mml:mi><mml:mo> = </mml:mo><mml:mn> 0.05 </mml:mn></mml:mrow></mml:math></inline-formula></p>
        <p>Then:</p>
        <disp-formula id="FD10">
          <mml:math>
            <mml:mrow>
              <mml:mi>V</mml:mi>
              <mml:mrow>
                <mml:mo>(</mml:mo>
                <mml:mi>I</mml:mi>
                <mml:mo>)</mml:mo>
              </mml:mrow>
              <mml:mo>=</mml:mo>
              <mml:mfrac>
                <mml:mn>1</mml:mn>
                <mml:mn>4</mml:mn>
              </mml:mfrac>
              <mml:msup>
                <mml:mi>I</mml:mi>
                <mml:mn>4</mml:mn>
              </mml:msup>
              <mml:mo>−</mml:mo>
              <mml:mn>0.1</mml:mn>
              <mml:msup>
                <mml:mi>I</mml:mi>
                <mml:mn>2</mml:mn>
              </mml:msup>
              <mml:mo>+</mml:mo>
              <mml:mn>0.05</mml:mn>
              <mml:mi>I</mml:mi>
            </mml:mrow>
          </mml:math>
        </disp-formula>
        <p><bold>Interpretation:</bold></p>
        <p>bistable regime (near cusp region)system may switch between: disease-free state, endemic outbreak state</p>
      </sec>
      <sec id="sec7dot7">
        <title>7.7. Epidemic Interpretation Summary</title>
        <p>A cusp catastrophe in SEIRV means:</p>
        <p>gradual changes in vaccination or transmissionproduce abrupt epidemic transitionssystem exhibits: bistability, hysteresis loops, tipping points</p>
      </sec>
      <sec id="sec7dot8">
        <title>7.8. Key Takeaway</title>
        <p>The cusp potential provides a geometric explanation for sudden epidemic outbreaks in SEIRV models, in which infection dynamics are governed by a quartic landscape with two control parameters, thereby capturing bistability and hysteresis [<xref ref-type="bibr" rid="B13">13</xref>]-[<xref ref-type="bibr" rid="B15">15</xref>].</p>
      </sec>
    </sec>
    <sec id="sec8">
      <title>8. Bifurcation and Sudden Transition Behavior</title>
      <p>The SEIRV model exhibits rich bifurcation structures depending on vaccination and transmission intensity. In particular:</p>
      <p>Increasing <inline-formula><mml:math><mml:mi> ν </mml:mi></mml:math></inline-formula> (vaccination rate) shifts the system toward the disease-free regime.Increasing <inline-formula><mml:math><mml:mi> β </mml:mi></mml:math></inline-formula> leads to forward bifurcation and possible endemic persistence.When nonlinear feedback (e.g., immunity waning <inline-formula><mml:math><mml:mi> ω </mml:mi></mml:math></inline-formula> ) is strong, the system may exhibit backward bifurcation, where <inline-formula><mml:math><mml:mrow><mml:msub><mml:mi> ℛ </mml:mi><mml:mn> 0 </mml:mn></mml:msub><mml:mo> &lt; </mml:mo><mml:mn> 1 </mml:mn></mml:mrow></mml:math></inline-formula> still allows endemic equilibria.</p>
      <p>Catastrophe theory explains such behavior as the crossing of a fold surface in parameter space, where equilibria disappear or suddenly emerge.</p>
    </sec>
    <sec id="sec9">
      <title>9. Interpretation of Catastrophic Transitions</title>
      <p>In epidemiological terms, catastrophe corresponds to abrupt transitions such as:</p>
      <p>Sudden outbreak emergence after a gradual increase in contact rateRapid collapse of infection due to vaccination threshold crossingCoexistence of multiple stable states (endemic and disease-free)</p>
      <p>These transitions are not smooth and cannot be fully captured by classical linear stability theory alone.</p>
    </sec>
    <sec id="sec10">
      <title>10. Dynamical Structure</title>
      <p>The SEIRV catastrophe model reveals that:</p>
      <p>Epidemic systems are inherently nonlinear and multi-stableControl parameters can trigger discontinuous transitionsVaccination and immunity loss critically shape the geometry of equilibrium surfacesCatastrophe theory provides a unified explanation for sudden epidemic shifts</p>
    </sec>
    <sec id="sec11">
      <title>11. Conclusions</title>
      <p>This study demonstrated that SEIRV epidemic dynamics can be effectively reinterpreted through the framework of catastrophe theory, particularly the cusp catastrophe model. By reducing the high-dimensional SEIRV system to a lower-dimensional infection subsystem, the evolution of the infected class was shown to be representable in gradient form using a potential function with quartic structure and two control parameters.</p>
      <p>The resulting potential landscape provides a geometric interpretation of epidemic behavior, where equilibrium states correspond to critical points of the potential. In this context, the disease-free and endemic equilibria emerge as stable minima, while unstable states act as transition barriers between them. The analysis highlights that small continuous variations in epidemiological parameters—such as transmission rate, vaccination rate, and immunity waning—can lead to abrupt qualitative changes in system behavior.</p>
      <p>In particular, the cusp catastrophe formulation explains key nonlinear phenomena observed in epidemic systems, including bistability, hysteresis, and sudden outbreak transitions. These features cannot be fully captured by classical threshold-based approaches such as basic reproduction number analysis alone. Instead, the cusp structure reveals the existence of multiple coexisting equilibria and critical tipping surfaces that govern regime shifts between disease-free and endemic states.</p>
      <p>Overall, the integration of SEIRV modeling with catastrophe theory provides a powerful theoretical framework for understanding nonlinear epidemic transitions. It enhances the interpretability of complex disease dynamics and offers deeper insight into how control strategies such as vaccination and behavioral interventions can prevent catastrophic outbreaks. This approach opens new directions for further analytical and computational studies in nonlinear epidemiology, particularly in the study of multistability and critical transitions in infectious disease systems.</p>
    </sec>
  </body>
  <back>
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