Impairment of the immunological and neurological synapses by respiratory viruses. Implications for vaccine design.

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Respiratory viruses are a leading cause of bronchiolitis and pneumonia worldwide, due an inefficient viral immunity even after disease resolution. These viruses can cause severe symptoms both in the respiratory and nervous systems, such as bronchiolitis and encephalopathy, respectively. We have observed that some respiratory viruses prevent the proper function of immune cells, such as T cells and dendritic cells, by impairing the immunological synapse assembly between these cells. Inhibition of the immunological synapse could work as a major virulence factor by impairing host immunity and enhancing susceptibility to reinfection. Further, respiratory viruses can cause a learning impairment due to inflammation at the central nervous system. Due to alterations on the blood brain barrier after infection, elements of the immune system enter the CNS impairing the normal function of neurons and astrocytes in the host. Based on these data, we have generated novel vaccine approaches to strengthen the immunological synapse leading to protective immunity against these respiratory pathogens and preventing CNS damage. These findings have permitted us to design a vaccine for SARS-CoV-2, which is currently in preclinical evaluation.

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Webinar: Tracking SARS-CoV-2 in Ghana

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This seminar will discuss the analysis of 2 sets of SARS-CoV-2 sequences which include imported and circulating viruses at the inception of Ghana’s outbreak, and circulating viruses 2-3 months after Ghana’s first reported cases. They will present on the adaptations on the ARCTIC protocols they carried out in sequencing batch, discuss the benefits inured by the ARCTIC V3 primers and relative ease of sequencing on the MiSeq and Nanopore platforms. They will also analyse the Ghanaian viruses, describe their evolution relative to other SARS-CoV-2 outbreaks and the observed transmission patterns in Southern Ghana.

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COVID-19 in immunodeficient patients

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Kathleen Sullivan will share her insights on:

  • Immune compromise and the risk for severe COVID-19
  • Primary immune deficiencies and COVID-19, what we know and what we don’t know
  • Vaccine options for people living with primary immunodeficiencies

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The impacts of psychological stress on virus-associated immune responses: unignorable challenges in the COVID-19 pandemic immunity

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The pandemic outbreak of the highly contagious coronavirus (COVID-19) has become a major threat to our physical health. Simultaneously, the rapid spread of COVID-19 and the resulting countermeasures (particularly lockdowns) are negatively affecting our mental well-being, due to disease progression-induced fear and fatigue, social distancing and isolation, family conflicts during quarantine, supply shortages, unemployment, and mounting financial burdens. Accumulating evidence suggests that stress is associated with an increased susceptibility to, and severity of, viral infection, which can be at least partially explained by systemic changes in anti-viral innate and adaptive immunity, as well as dysregulated inflammatory and autoimmune responses. Furthermore, pandemic-related psychological stress may influence the efficacy of viral vaccines. Thus, deciphering the underlying molecular links between psychological stress and viral infection-associated immune-inflammatory alternations will provide novel insights into the development of optimal therapeutic interventions and prophylactic vaccines.

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Longitudinal immune profiling reveals distinct features of COVID-19 pathogenesis

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Elizabeth Mann and Madhvi Menon will discuss findings from their recent longitudinal immune profiling study with admitted COVID-19 patients across four hospitals in Manchester at the height of the pandemic in the UK. They find key immune signatures that track with disease severity and can potentially be used to identify patients upon admission that are destined for intensive care. They also determine how immune responses change throughout the disease course and how this differs in patients with milder disease that recover compared with patients who go on to become severe/critical.

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Webinar: Ramos B cell engineering for the evaluation of the humoral anti-SARS-CoV-2 immunity

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Michael Reth and his team are studying how the B cell antigen receptor (BCR) and the B cell surface is organized in resting and activated B cells for the sensing of foreign antigens. They learned that the BCR and many B cell surface markers are highly organized at nanoscale distances. In their studies they are using the CRISPR/Cas9 method to rapidly generate loss- or gain-of-function mutants of the Burkitt lymphoma cell line Ramos as specific cell line. They thus have generated Ramos B cells which are lacking all four components of the BCR and replaced the antigen receptor by the spike protein of SARS-CoV-2. This allows them to test for SARS-COV-2 spike specific antibody responses and monoclonal antibodies by flow cytometry. The first results of their assays will be discussed in the presentation. The webinar will be moderated by Rita Carsetti.

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Webinar: Prevention and Therapy of COVID-19 with Monoclonal Antibodies

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Hans-Martin Jäck summarizes the COVID-19 pandemic and CoV-2-host cell interactions. He introduces the concept of passive immunisation and active vaccination to prevent and protect from COVID-19, and he provides an overview of the current clinical serum and vaccine trials, finishing the webinar with a review on the production of human CoV-2 neutralising antibodies in transgenic mice with an entirely human antibody repertoire. 

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Webinar: Seeking correlates of protection and correlates of pathology in COVID-19 patients

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In this webinar, Professor Adrian Hayday will share with us, an overview of a completed deep immunophenotyping of 100 patients and controls, with approximately 200,000 data points.
Professor Adrian Hayday began studying immunology in 1982 at MIT, where he and his colleagues first described the wholly unanticipated T-cell receptor gamma chain genes. Establishing that γδ T-cells are distinct from conventional T-cells, Professor Hayday and his colleagues demonstrated that γδ T-cells generate rapid responses to tissue dysregulation to monitor tissue integrity, rather than showing highly specific responses to pathogens, as is the case for conventional T and B cells.

Over the course of his career, Professor Hayday has authored over 200 papers, the majority of which are original research contributions. He has received many awards, including the William Clyde deVane Medal, Yale College’s highest honour for scholarship and teaching, an honorary fellowship from King’s College London, and the King’s College Business Award. He was elected to lead the British Society of Immunology (2005-09), and is an elected fellow of the Academy of Medical Sciences and of the Royal Society.He is currently a Professor of Immunobiology at King’s College London, a Clinical Academic Group leader at King’s Health Partners, and Group Leader at the Francis Crick Institute where he is an Assistant Research Director. 

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