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Infectious Disease Talks

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Talks related to infectious diseases
URL: http://talks.cam.ac.uk/show/index/29729
Updated: 3 min 39 sec ago

Fri 16 Feb 15:00: Title to be confirmed

Fri, 26/01/2024 - 12:00
Title to be confirmed

Abstract not available

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Fri 02 Feb 15:00: Disorder at different length scales from a chromatin perspective

Fri, 26/01/2024 - 11:59
Disorder at different length scales from a chromatin perspective

Abstract not available

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Tue 06 Feb 12:00: Airway Biology at the Nanoscale

Tue, 23/01/2024 - 15:41
Airway Biology at the Nanoscale

A significant frontier in Spatial Biology is the construction of an integrated view of tissue function within its native environment at the cellular and molecular levels. In this seminar, we will explore how the combination of nanometre-scale imaging modalities, AI segmentation algorithms, and protein-protein interaction mapping in human tissue models is providing a novel perspective on airway biology and creating opportunities for translational medicine research. The primary focus will be on the respiratory epithelium, a critical tissue that safeguards our lungs by serving as the first line of defence against bacteria, viruses, and particulate matter. We will provide examples illustrating how this multimodal spatial biology approach is revealing the molecular mechanisms underlying airway protection from pathogens.

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Fri 19 Jan 13:00: ILC2 regulation of tissue-localised immunity... and beyond

Fri, 19/01/2024 - 00:34
ILC2 regulation of tissue-localised immunity... and beyond

Andrew McKenzie FRS F MedSci is a molecular biologist and group leader in the Medical Research Council (MRC) Laboratory of Molecular Biology (LMB).

The next Cambridge Immunology and Medicine Seminar will take place on Friday 19th January 2024, starting at 1:00 pm, in the Ground Floor Lecture Theatre, Jeffrey Cheah Biomedical Centre (JCBC)

Host: Professor Menna Clatworthy, Professor of Translational Immunology, University of Cambridge.

For anyone who can’t attend in person, please join the Cambridge Immunology and Medicine Seminar on Zoom:

Please note the Zoom link has changed from previous communications.

Join Zoom Meeting: https://cam-ac-uk.zoom.us/j/89741634903?pwd=dzcxbU45NjAwQXo1dmlNMjR3V0lUUT09

Meeting ID: 897 4163 4903 Passcode: 539740

Refreshments will be available following the Seminar.

If you have a question about this talk, please contact Ruth Paton.

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Wed 31 Jan 16:00: Reassessing red blood cell invasion in malaria parasites Please note 16:00 start time for this seminar

Thu, 18/01/2024 - 17:01
Reassessing red blood cell invasion in malaria parasites

Malaria parasites rely on cycles of cellular invasion and intracellular growth to proliferate within the blood stream, a process which underpins symptoms of the disease. The cycles of cellular invasion and intracellular growthThe adaptation of P. knowlesi (Pk) to culture in human erythrocytes presents exciting opportunities to study erythrocyte invasion biology. Two major protein families have been studied extensively in P. falciparum (Pf): the erythrocyte binding-like proteins (EBPs/EBAs) and the reticulocyte binding-like proteins (RBLs/RHs). These proteins are hypothesized to have overlapping but critical roles during the invasion process. The zoonotic malaria parasite P. knowlesi, has a smaller repertoire of these proteins, and much larger and polarised invasive stages known as merozoites.

Employing a conditional knockout approach, we’ve demonstrated distinct roles for the two families at different invasion stages, including a specific role for RBL proteins in the initial identification and deformation of target host erythrocytes. Furthermore, we’ve unearthed new features that prompt a significant reassessment of invasion. Notably, we’ve discovered that Pk merozoites can engage in productive gliding motility prior to invasion, and we’ve corrected a longstanding assumption in merozoite topology – the merozoite apex is actually located in the wider end of the cell, contrary to prior beliefs. These findings unveil new aspects of this complex process and introduce fresh tools and techniques to deepen our understanding of invasion across all malaria parasite species. Finally, we will demonstrate how the new genetic tools emerging from studies in basic biology of malaria parasite can be readily adapted to facilitate vaccine, drug and diagnostics targeting a broader range of malaria parasite species.

Please note 16:00 start time for this seminar

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Tue 05 Mar 12:00: Endocrine signaling and physiological constraint drive a reproduction-immunity tradeoff in Drosophila

Thu, 18/01/2024 - 15:54
Endocrine signaling and physiological constraint drive a reproduction-immunity tradeoff in Drosophila

Life history tradeoffs between reproductive output and immune performance are commonly observed throughout the animal kingdom but are rarely understood mechanistically. In the insect Drosophila melanogaster, reproductive investment reduces resistance to bacterial infection. We have found that the reduction in immunity can be traced to the cost of producing eggs, and that mating-induced changes in hormone balance regulate the differential investment in fecundity versus immunity. However, rather than arising through an adaptive shift in allocation of energetic resources from one process to the other, the tradeoff seems to originate in physiological constraints and overburdening of the fat body tissue. We observe natural genetic polymorphism for the magnitude of post-mating immune suppression but it is largely uncorrelated with reproductive output, potentially limiting the opportunity for evolutionary optimization. Thus, while reproduction and immune performance are observed to trade off in D. melanogaster as would be expected under classical life history theory, the mechanism and evolutionary potential may not conform to classical expectations.

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Wed 21 Feb 12:00: Title to be confirmed

Thu, 18/01/2024 - 15:52
Title to be confirmed

Abstract not available

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Tue 13 Feb 12:00: Title to be confirmed

Thu, 18/01/2024 - 15:50
Title to be confirmed

Abstract not available

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Wed 31 Jan 16:00: TBC Please note 16:00 start time for this seminar

Thu, 18/01/2024 - 11:47
TBC

Abstract not available

Please note 16:00 start time for this seminar

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Wed 24 Jan 14:00: Short term forecasting of Acute Respiratory Infections and their impact on NHS hospital pressures for situational awareness over Winter.

Thu, 18/01/2024 - 09:45
Short term forecasting of Acute Respiratory Infections and their impact on NHS hospital pressures for situational awareness over Winter.

Mitigations put in place during the SARS -Cov-2 pandemic supressed the transmission of seasonal respiratory viruses. There was an anticipated resurgence of non-COVID-19 seasonal respiratory diseases in Winter 2022-23 which were much harder to predict following extremely low pandemic baselines. These diseases caused an additive burden on healthcare systems, in the context of ongoing COVID -19 waves. We developed modelling methods to short term forecast a range of acute respiratory infections (COVID-19, Influenza, RSV ) at a range of geographies and metrics meaningful to healthcare managers. These forecasts used a range of Generalised Additive Models, time series techniques, leading indicators, and ensemble methods to improve assessments of trends.

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Fri 09 Feb 15:00: Therapeutic manipulations of phosphatases and kinases controlling protein quality control systems: From the bench, to the clinic and back

Thu, 18/01/2024 - 08:58
Therapeutic manipulations of phosphatases and kinases controlling protein quality control systems: From the bench, to the clinic and back

The deposition of misfolded proteins is a defining feature of many age-dependent human diseases, including the increasingly prevalent neurodegenerative diseases. Why aggregation-prone proteins accumulate in aged cells remains largely unclear. Cells normally strive to ensure that proteins get correctly folded and have powerful and sophisticated mechanisms to maintain protein homeostasis (proteostasis) under adverse conditions. However, with age and in diseases, the cellular defence systems against misfolded proteins are overwhelmed, leading to the accumulation of misfolded proteins with devastating consequences for cells and organism. In principle, improving the cells’ ability to deal with misfolded proteins could represent a generic approach to reduce the pathology in diverse protein misfolding diseases. My lab has identified powerful small drug-like molecules that safely boost a natural defence system against misfolded. These small molecules inhibit serine/threonine phosphatases controlling the termination of a proteostatic pathway, an interesting finding because phosphatases were previously thought to be undruggable. The inhibitors have demonstrated therapeutic effects in various models of neurodegenerative diseases. This work demonstrates that generic approaches aimed at helping cells to survive protein quality control failures can be useful to prevent protein misfolding diseases, including the devastating neurodegenerative diseases. One of these inhibitors, Sephin1, has passed through favourable Phase 1 clinical trials in 2019 and is being now developed for Charcot-Marie-Tooth disease and amyotrophic lateral sclerosis. In 2011, Guanabenz was found beneficial in a phase 2 clinical trial in ALS , 10 years after we reported its proteostasis-boosting activity.

The work on these inhibitors has perked our interest in serine/threonine phosphatases, a class of very important yet poorly characterized enzymes. In a recent tour de force, we have deployed a combination of approaches to elucidate the mechanism by which an eIF2 phosphatase recruits its large substrate.

Expanding our toolbox, we recently made the unexpected discovery that broadly used ATP -competitive inhibitors of eIF2 kinases can paradoxically increase eIF2 phosphorylation by directly binding to and activating a sister kinase resulting in functional activation of the pathway rather than the intended inhibition. These findings have broad relevance to kinases.

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Tue 06 Feb 12:00: Airway Biology at the Nanoscale

Mon, 15/01/2024 - 12:55
Airway Biology at the Nanoscale

A significant frontier in Spatial Biology is the construction of an integrated view of tissue function within its native environment at the cellular and molecular levels. In this seminar, we will explore how the combination of nanometre-scale imaging modalities, AI segmentation algorithms, and protein-protein interaction mapping in human tissue models is providing a novel perspective on airway biology and creating opportunities for translational medicine research. The primary focus will be on the respiratory epithelium, a critical tissue that safeguards our lungs by serving as the first line of defence against bacteria, viruses, and particulate matter. We will provide examples illustrating how this multimodal spatial biology approach is revealing the molecular mechanisms underlying airway protection from pathogens.

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Tue 30 Jan 12:00: Reciprocal gut/body interactions in health and disease

Mon, 15/01/2024 - 12:51
Reciprocal gut/body interactions in health and disease

The adult intestine is a major barrier epithelium and coordinator of multi-organ functions. Stem cells constantly repair the intestinal epithelium by adjusting their proliferation and differentiation to tissue intrinsic as well as micro- and macro-environmental signals. How these signals integrate to control intestinal and whole-body homeostasis is largely unknown. Addressing this gap in knowledge is central to an improved understanding of intestinal pathophysiology and its systemic consequences. Combining Drosophila and mammalian model systems my laboratory studies fundamental mechanisms driving intestinal regeneration and tumourigenesis including complex inter-organ signaling, which I will discuss during my seminar including: 1- Interactions between the intestine and its microenvironment influencing intestinal regeneration and tumourigenesis. 2- Impact of changes in intestinal homeostasis to whole-body physiology.

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Tue 23 Jan 12:00: Adaptation of the cytoskeleton for pathogenicity in the malaria parasite

Mon, 15/01/2024 - 12:45
Adaptation of the cytoskeleton for pathogenicity in the malaria parasite

To ensure disease transmission, the malaria parasite undergoes multiple rounds of metamorphosis, as it entirely alters its cell morphology to promote uptake and establishment in the mosquito vector and human host. Two cytoskeletal components play essential roles in this process: microtubules and actin.

Within each new ecological niche, microtubules drive the single-celled parasite’s successive cellular transformations. Microtubules have been studied extensively and their architecture and composition are established to be highly conserved. Using focussed ion beam milling and electron cryo tomography, we recently studied distinct stages in the Plasmodium falciparum life cycle. This revealed that the parasite has microtubules which are evolved to undertake specific roles in each life cycle stage with structures that are strikingly different from the well-studied canonical microtubules in vertebrates.

While unique microtubules drive cellular transformations, filamentous actin ensures several parasite stages can migrate between different niches. These stages utilise a unique form of motility, termed gliding motility, which relies on a specialised actomyosin motor system. Our recent work on actively gliding parasites sheds light on this process and highlights novel roles of parasite actin in other cellular locations. Together, this work provides unanticipated insights into adaptations of the parasite’s cytoskeleton, highlighting areas of novelty where the parasite has diverged from the biology of the host.

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Fri 19 Jan 12:00: Modelling optimal intervention strategies for animal diseases in data poor settings This talk will be streamed and will be accessible remotely once it has started, with raven login here: https://cambridgelectures.cloud.panopto.eu...

Mon, 15/01/2024 - 09:21
Modelling optimal intervention strategies for animal diseases in data poor settings

Abstract: Emerging diseases of livestock can devastate the agricultural industry and have a severe impact upon livestock exports. It is therefore vital to provide tools to assess the risk associated with infectious diseases and establish surveillance and intervention protocols that will reduce the cost of such outbreaks in the future. In this presentation, I will discuss the role of infectious disease models in supporting contingency planning for livestock disease outbreaks. These models typically require data on locations, sizes and species compositions of farms, as well as detailed information on any animals that are infected with the disease. However, in many settings such data are not available. I will therefore demonstrate how models can support infectious disease control in settings where such detailed data are not accessible and how surveillance resources should be targeted to reduce model uncertainty and provide accurate predictions regarding the future spread of disease.

Bio: Prof. Mike Tildesley is a Professor of Infectious Disease Modelling at the University of Warwick. He has an interest in the predictive power of models in the early stages of emerging disease outbreaks and in communicating modelling results to policy advisors. He has extensive experience of modelling livestock disease systems, including Foot-and-Mouth Disease (FMD) and Highly Pathogenic Avian Influenza (HPAI). Prof. Tildesley has advised the UK Government’s Department for the Environment, Food and Rural Affairs, the US Department of Agriculture and the Food and Agriculture Organisation of the United Nations about strategies for control of livestock diseases including FMD and HPAI . From March 2020 to March 2022, He was a member of the Scientific Pandemic Influenza Modelling Operational group (SPI-M-O), and worked extensively on COVID -19, providing policy advice to the UK government.

This talk will be streamed and will be accessible remotely once it has started, with raven login here: https://cambridgelectures.cloud.panopto.eu/Panopto/Pages/Sessions/List.aspx#folderID=%220c72d750-7bc0-4938-88f2-ae7c00b8c25d%22

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