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Piklu Mallick

Publications and source records attributed to Piklu Mallick.

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Mechanics of Pandemics

COVID-19 and previous pandemics have shown how diseases can disrupt, threaten, and transform daily life. Since pathogens and societies are continuously evolving, every pandemic is different. However, certain fundamental principles of disease transmission appear to hold true across different outbreaks. These ``mechanisms'' are grounded in natural laws or the very structure of our biology and societies. This paper compiles ten fundamental mechanisms, curated by a multidisciplinary team with backgrounds spanning public health, medicine, epidemiology, political science, mathematics, physics, and psychology. These mechanisms, although perhaps underappreciated, substantially shape how pandemics unfold and are controlled. The better we succeed in understanding these mechanisms and establishing this knowledge in our societies, the better we will be able to prepare for future pandemics and respond appropriately when they occur.

q-bio.PE

Stability and bifurcations of a minimal model for the effect of PrEP-related risk compensation in epidemics of sexually transmitted infections

HIV pre-exposure prophylaxis (PrEP) drastically reduces the risk of HIV infection if taken as prescribed, providing almost perfect protection even during unprotected sexual intercourse. Although this has been transformative in reducing new HIV infections among high-risk populations, it has also been linked to an increase in risk practices -- a phenomenon known as risk compensation -- thereby favoring the spread of other sexually transmitted infections (STIs) deemed less severe. In this paper, we study a minimal compartmental model describing the effect of risk awareness and risk compensation due to PrEP on the spread of other STIs among a high-infection-risk group of men who have sex with men (MSM). The model integrates three key elements of risk-mediated behavior and PrEP programs: (i) HIV risk awareness drives self-protective behaviors (such as condom use and voluntary STI screening); (ii) individuals on PrEP are subject to risk compensation, but (iii) are required to screen for asymptomatic STIs frequently. We derived the basic reproduction number of the system, $R_0$, and found a transcritical bifurcation at $R_0=1$, where the disease-free equilibrium becomes unstable and an endemic equilibrium emerges. This endemic equilibrium is asymptotically stable wherever it exists. We identified critical thresholds in behavioral and policy parameters that separate these regimes and analyzed typical values for plausible parameter choices. Beyond the specific epidemiological context, the model serves as a general framework for studying nonlinear interactions between behavioral adaptation, preventive interventions, and disease dynamics, providing insights into how feedback mechanisms can lead to non-trivial responses in epidemic systems. Finally, our model can be easily extended to study the effect of interventions and risk compensation in other STIs.

q-bio.PE

Testing Paradox May Explain Increased Observed Prevalence of Bacterial STIs among MSM on HIV PrEP: A Modeling Study

HIV pre-exposure Prophylaxis (PrEP) has become essential for global HIV control, but its implementation coincides with rising bacterial STI rates among men who have sex with men (MSM). While risk-compensation behavioral changes like reduced condom use are frequently reported, we examine whether intensified asymptomatic screening in PrEP programs creates surveillance artifacts that could be misinterpreted. We developed a compartmental model to represent the simultaneous spread of HIV and chlamydia (as an example of a curable STI), integrating three mechanisms: 1) risk-mediated self-protective behavior, 2) condom use reduction post-PrEP initiation, and 3) PrEP-related asymptomatic STI screening. Increasing PrEP uptake may help to reduce chlamydia prevalence, only if the PrEP-related screening is frequent enough. Otherwise, the effect of PrEP can be disadvantageous, as the drop in self-protective actions caused by larger PrEP uptake cannot be compensated for. Additionally, the change in testing behavior may lead to situations where the trend in the number of positive tests is not a reliable sign of the actual dynamics. We found a plausible mechanism to reconcile conflicting observational evidence on the effect of PrEP on STI rates, showing that simultaneous changes in testing and spreading rates may generate conflicting signals, i.e., that observed trends increase while true prevalence decreases. Asymptomatic screening, together with personalized infection treatment to minimize putative pressure to generate antibiotic resistance, is one of the key determinants of the positive side effects of PrEP in reducing STI incidence.

q-bio.PE