Maia Martcheva

Dr. Maia Martcheva

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Research Focus & Metrics

Academic Career Length

21Years (2006-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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25 April 2007 in Journal of The Royal Society Interface
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MMMaia Martcheva
Maia Martcheva
BBBenjamin Bolker
Benjamin Bolker
RHRobert D Holt
Robert D Holt
Host immune systems impose natural selection on pathogen populations, which respond by evolving different antigenic signatures. Like many evolutionary processes, pathogen evolution reflects an interaction between different levels of selection; pathogens can win in between-strain competition by taking over individual hosts (within-host level) or by infecting more hosts (population level). Vaccination, which intensifies and modifies selection by protecting hosts against one or more pathogen strains, can drive the emergence of new dominant pathogen strains—a phenomenon called vaccine-induced pathogen strain replacement . Here, we review reports of increased incidence of subdominant variants after vaccination campaigns and extend the current model for pathogen strain replacement, which assumes that pathogen strain replacement occurs only through the differential effectiveness of vaccines against different pathogen strains. Based on a recent theoretical study, we suggest a broader range of possible mechanisms, some of which allow pathogen strain replacement even when vaccines are perfect —that is, they protect all vaccinated individuals completely against all pathogen strains. We draw an analogy with ecological and evolutionary explanations for competitive dominance and coexistence that allow for tradeoffs between different competitive and life-history traits.

20 September 2016 in Bulletin of Mathematical Biology
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Journal Article
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NTNecibe Tuncer
Necibe Tuncer
HGHayriye Gulbudak
Hayriye Gulbudak
VCVincent L. Cannataro
Vincent L. Cannataro
MMMaia Martcheva
Maia Martcheva

1 May 2009 in Journal of Biological Dynamics
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Journal Article
Open access
MMMaia Martcheva
Maia Martcheva
In this paper we consider a non-autonomous multi-strain SIS epidemic model with periodic coefficients. Reproduction numbers and invasion reproduction numbers are derived which agree well with their counterparts usually derived from autonomous epidemic models. With conditions on these reproduction numbers typical results are obtained, such as the local and global stability of the disease-free equilibrium. Existence and uniqueness of a single-strain periodic solution is established. Based on conditions on the invasion reproduction numbers, local stability of the single-strain periodic solution is shown. In a two-strain version of the model, conditions for uniform strong persistence are derived, and coexistence of the two strains is established. Coexistence, however, does not occur if the transmission rates of the different strains are linearly dependent.

1 January 2019 in Journal of Biological Dynamics
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ASAmar Sha
Amar Sha
SSSudip Samanta
Sudip Samanta
MMMaia Martcheva
Maia Martcheva
JCJoydev Chattopadhyay
Joydev Chattopadhyay
This paper considers an eco-epidemiological model with disease in the prey population. The disease in the prey divides the total prey population into two subclasses, susceptible prey and infected prey. The model also incorporates fear of predator that reduces the growth rate of the prey population. Furthermore, fear of predator lowers the activity of the prey population, which reduces the disease transmission. The model is well-posed with bounded solutions. It has an extinction equilibrium, susceptible prey equilibrium, susceptible prey-predator equilibrium, and coexistence equilibria. Conditions for local stability of equilibria are established. The model exhibits fear- induced backward bifurcation and bistability. Extensive numerical simulations show the presence of oscillations and occurrence of chaos due to fear induced lower disease transmission in the prey population.

1 January 2010 in Mathematical Biosciences and Engineering
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Anuj MubayiAnuj Mubayi
Anuj Mubayi
CZChristopher Kribs Zaleta
Christopher Kribs Zaleta
MMMaia Martcheva
Maia Martcheva
CCCarlos Castillo-Chávez
Carlos Castillo-Chávez
A classical epidemiological framework is used to provide a preliminary cost analysis of the effects of quarantine and isolation on the dynamics of infectious diseases for which no treatment or immediate diagnosis tools are available. Within this framework we consider the cost incurred from the implementation of three types of dynamic control strategies. Taking the context of the 2003 SARS outbreak in Hong Kong as an example, we use a simple cost function to compare the total cost of each mixed (quarantine and isolation) control strategy from a public health resource allocation perspective. The goal is to extend existing epi-economics methodology by developing a theoretical framework of dynamic quarantine strategies aimed at emerging diseases, by drawing upon the large body of literature on the dynamics of infectious diseases. We find that the total cost decreases with increases in the quarantine rates past a critical value, regardless of the resource allocation strategy. In the case of a manageable outbreak resources must be used early to achieve the best results whereas in case of an unmanageable outbreak, a constant-effort strategy seems the best among our limited plausible sets.

1 January 2021 in Journal of Biological Dynamics
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Journal Article
Open access
MMMaia Martcheva
Maia Martcheva
NTNecibe Tuncer
Necibe Tuncer
Calistus NgonghalaCalistus Ngonghala
Calistus Ngonghala
We propose two models inspired by the COVID-19 pandemic: a coupled disease-human behaviour (or disease-game theoretic), and a coupled disease-human behaviour-economic model, both of which account for the impact of social-distancing on disease control and economic growth. The models exhibit rich dynamical behaviour including multistable equilibria, a backward bifurcation, and sustained bounded periodic oscillations. Analyses of the first model suggests that the disease can be eliminated if everybody practices full social-distancing, but the most likely outcome is some level of disease coupled with some level of social-distancing. The same outcome is observed with the second model when the economy is weaker than the social norms to follow health directives. However, if the economy is stronger, it can support some level of social-distancing that can lead to disease elimination.