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Modelling Covid-19 Dynamics With Periodic Contact Rates, Waning Vaccine Immunity and Temporary Cross Immunity

This paper presents a novel delay differential equation model incorporating periodic contact rates, waning vaccine immunity, and temporary cross-immunity to analyze the transmission dynamics of COVID-19, demonstrating that disease eradication is achievable when the basic reproduction number falls below unity under specific parameter regimes.

Original authors: FAROUK SAAD, Shehu Maitama, Mubarak Zurmi, Ali Althobaiti, Chanakarn Kiataramkul, Usman Salihu, Musa Danyaro, Idris Ahmed

Published 2026-09-29
📖 5 min read🧠 Deep dive

Original authors: FAROUK SAAD, Shehu Maitama, Mubarak Zurmi, Ali Althobaiti, Chanakarn Kiataramkul, Usman Salihu, Musa Danyaro, Idris Ahmed

Original paper licensed under CC BY 4.0 (https://creativecommons.org/licenses/by/4.0/). ✨ This is an AI-generated explanation of the paper below. It is not written or endorsed by the authors. For technical accuracy, refer to the original paper. Read full disclaimer

In the study of how diseases move through populations, scientists often look for the hidden rhythms that drive an outbreak. Just as the seasons change the way people interact, the spread of an infectious virus is rarely a straight line; it pulses and shifts with time. A critical factor in this dance is the concept of immunity. When a person recovers from an illness or receives a vaccine, their body builds a shield against future infection. However, this shield is not always permanent. Over time, the protection can fade, a process known as waning immunity, leaving individuals vulnerable once again. Furthermore, vaccines are rarely perfect; they may prevent severe sickness but still allow the virus to pass through, and the virus itself can change, creating new strains that might bypass existing defenses. Understanding how these factors—changing contact patterns, fading protection, and imperfect vaccines—interact is essential for predicting whether a disease will vanish or continue to circulate.

A team of researchers has built a new mathematical model to explore these exact dynamics in the context of the coronavirus pandemic. Rather than assuming that people's behavior and their immunity remain constant, the team created a system that accounts for the fact that contact rates between people fluctuate over time, much like the changing seasons. They also incorporated the reality that vaccine protection does not last forever and that immunity gained from a previous infection might only be temporary. By weaving these elements together, the researchers aimed to see how a disease behaves when it faces a population that is partially vaccinated, partially immune, and constantly changing its exposure to the virus.

The researchers constructed a detailed simulation that divides the population into groups: those who are susceptible, those who are vaccinated, those infected with the first strain of the virus, those infected with a second strain, and those who have recovered. A key feature of their work is the inclusion of a time delay, which represents the period of temporary cross-immunity. This is the window of time after recovering from one strain during which a person is protected from catching a different strain, before that protection eventually wears off. The model also tracks how the rate at which people meet each other changes periodically, reflecting real-world patterns where social interaction rises and falls.

Through their analysis, the team discovered a specific condition under which the disease can be completely wiped out. They found that if the basic reproduction number—a measure of how many new infections one sick person causes on average—stays below a critical threshold, the disease will eventually die away. This threshold depends heavily on how effective the vaccine is, how quickly immunity fades, and how often people come into contact with one another. The study shows that even an imperfect vaccine can be powerful enough to stop an outbreak, but only if the coverage is high enough and the protection lasts long enough. If the immunity fades too quickly, or if the contact rates spike too high, the disease can find a way to persist, leading to recurring waves of infection.

The researchers ran computer simulations to test these ideas, adjusting the speed at which immunity wanes and the rate at which people get vaccinated. In scenarios where the vaccination rate was high and immunity faded slowly, the number of infected people dropped steadily over time. However, when the protection from the vaccine or previous infection faded rapidly, the system became unstable. The simulations showed that rapid waning could lead to sustained oscillations, where the number of cases rises and falls in a predictable but dangerous pattern, preventing the disease from ever fully disappearing. The inclusion of the time delay for cross-immunity added another layer of complexity, causing peaks in infection to arrive later than they would in a simpler model, which suggests that the timing of outbreaks can be harder to predict when temporary immunity is involved.

A sensitivity analysis performed by the authors revealed which factors matter most. The results indicated that the baseline rate at which people contact one another is the most influential factor in driving the spread of the virus. While the effectiveness of the vaccine and the speed of immunity loss are also critical, the frequency of human interaction plays the dominant role. This implies that public health strategies must focus not only on vaccination but also on managing how people interact, especially during periods when the virus is likely to spread more easily. The study suggests that relying solely on vaccination without addressing contact rates may not be enough to control the disease if the protection provided by the vaccine is not strong or long-lasting.

The researchers acknowledge that their model is a simplification of a complex reality. It assumes that new people enter the population at a constant rate and does not account for differences in age or location, which can significantly affect how a disease spreads. Additionally, the model focuses on vaccination for the first strain and does not fully explore the dynamics of booster shots or the competition between multiple evolving strains. Despite these limitations, the work provides a clear framework for understanding how periodic changes in behavior and the temporary nature of immunity can shape the long-term future of an epidemic. The findings suggest that to keep a disease at bay, societies must maintain high vaccination coverage and be prepared to adjust their social behaviors as the seasons change, recognizing that the shield of immunity is not a permanent wall but a barrier that requires constant reinforcement.

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