Transmission models for infectious diseases are typically formulated in terms of dynamics between individuals or groups with processes such as disease progression or recovery for each individual captured phenomenologically, without reference to underlying biological processes. Furthermore, the construction of these models is often monolithic: they do not allow one to readily modify the processes involved or include the new ones, or to combine models at different scales. We show how to construct a simple model of immune response to a respiratory virus and a model of transmission using an easily modifiable set of rules allowing further refining and merging the two models together. The immune response model reproduces the expected response curve of PCR testing for COVID-19 and implies a long-tailed distribution of infectiousness reflective of individual heterogeneity. This immune response model, when combined with a transmission model, reproduces the previously reported shift in the population distribution of viral loads along an epidemic trajectory. This article is part of the theme issue 'Technical challenges of modelling real-life epidemics and examples of overcoming these'.
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http://dx.doi.org/10.1098/rsta.2021.0307 | DOI Listing |
Sci Rep
December 2024
Interventional Oncology, Johnson & Johnson Enterprise Innovation, Inc, 10th Floor 255 Main St, 02142, Cambridge, Boston, MA, USA.
The introduction of anti-PD-1/PD-L1 therapies revolutionized treatment for advanced non-small cell lung cancer (NSCLC), yet response rates remain modest, underscoring the need for predictive biomarkers. While a T cell inflamed gene expression profile (GEP) has predicted anti-PD-1 response in various cancers, it failed in a large NSCLC cohort from the Stand Up To Cancer-Mark (SU2C-MARK) Foundation. Re-analysis revealed that while the T cell inflamed GEP alone was not predictive, its performance improved significantly when combined with gene signatures of myeloid cell markers.
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December 2024
IRCCS SYNLAB SDN, Naples, 80143, Italy.
LAG3 plays a regulatory role in immunity and emerged as an inhibitory immune checkpoint molecule comparable to PD-L1 and CTLA-4 and a potential target for enhancing anti-cancer immune responses. We generated 3D cancer cultures as a model to identify novel molecular biomarkers for the selection of patients suitable for α-LAG3 treatment and simultaneously the possibility to perform an early diagnosis due to its higher presence in breast cancer, also to achieve a theragnostic approach. Our data confirm the extreme dysregulation of LAG3 in breast cancer with significantly higher expression in tumor tissue specimens, compared to non-cancerous tissue controls.
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December 2024
State Key Laboratory for Diagnosis, Treatment of Infectious Diseases, National Clinical Research Center for Infectious Diseases, Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, The First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, 310003, China.
Influenza virus infections are a serious danger to people's health worldwide as they are responsible for seasonal flu outbreaks. There is an urgent need to improve the effectiveness and durability longevity of the immune response to influenza vaccines. We synthesized the CpG HP021 and examined the impact of it on the immune response to an influenza vaccine.
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December 2024
Key Laboratory of the Pest Monitoring and Safety Control of Crops and Forests of the Xinjiang Uygur Autonomous Region, College of Agronomy, Xinjiang Agricultural University, Urumqi, 830052, China.
Wheat stripe rust is a fungal disease caused by Puccinia striiformis f. sp. tritici.
View Article and Find Full Text PDFJ Neurovirol
December 2024
Department of Pharmacology and Physiology, Drexel University College of Medicine, Philadelphia, PA, 19102, USA.
Although antiretroviral therapy (ART) has dramatically improved the outlook of the HIV/AIDS pandemic, people living with HIV (PLWH) on suppressive therapy are still at higher risk for a range of comorbidities including cardiovascular disease (CVD) and HIV-associated neurocognitive disorders (HAND), among others. Chronic inflammation and immune activation are thought to be an underlying cause of these comorbidities. Many of the factors thought to drive chronic inflammation and immune activation in HIV overlap with factors known to induce trained immunity.
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