TWiV 736: Rhapsody in T with Alessandro Sette

March 28, 2021

Alessandro Sette joins TWiV to discuss the role of T cells in COVID-19, the finding that amino acid changes in SARS-CoV-2 variants of concern have a negligible impact on T cell reactivity in convalescent patients and vaccinees, and whether a next generation vaccine should include more viral proteins than spike.

Hosts: Vincent Racaniello, Alan Dove, Rich Condit, and Kathy Spindler

Guest: Alessandro Sette

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Intro music is by Ronald Jenkees

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4 comments on “TWiV 736: Rhapsody in T with Alessandro Sette

  1. Jung Choi Mar 28, 2021

    HIV also has a much higher mutation rate than SARS-CoV2, further facilitating its ability to evolve resistance to individual hosts.

  2. Aspirating before intramuscular injection used to be standard practice in vaccination. At some point in time it was concluded that it really didn’t have any merit because there are no large vessels in the usual sites (deltoid in adults and older kids, vastus lateralis in infants).

  3. Chris Mar 29, 2021

    Bravo, Bravo, Alessandro! Excellent, clear explanation of T-cell roles in fighting infection.

  4. Janet Mar 30, 2021

    I loved this episode! Cheerful Dante 🙂 or as Camus said “one must imagine Sisyphus happy’.
    There is hope for us humans given all of you’s cheerful persistance, indefatigable curiosity and sheer blo0dy-mindedness 🙂
    Questions (hopefully not too daft!): how do T cell and B cell responses interact especially with regards to memory of infection? Does a memory T cell implicate (sometimes;always;ever;never?) a corresponding memory B cell response. if so, what would be the mechanism, cytokines?
    Is there a triaging energy-wise- T cell response less costly if effective, antibodies only if infection lasts (how long?) or damages (How much/where?)
    Do self-reactive T cells and self-reactive B cells get eliminated in similar ways and would this also process have any way of feeding back/ interacting?
    Additionally, could a T cell epitope recognised in Sars CoV 2 or vaccine ‘call up’ a related pre-existing but previously not pathological auto-antibody response? vis ‘Antinuclear Autoantibodies in Health: Autoimmunity Is Not a Synonym of Autoimmune Disease’, Pashnina et al.
    In agammglobulinemia- does this point to antibodies being a double-edged sword in SARS CoV 2 infection and does this indicate that people under immuno-suppresant therapy may not always suffer severe Covid19? The long duration of infection in one case that was studied for variant emergence apart- I think that was a cancer patient rather than auto-immune though. Is anyone aware of studies along this line?
    I am still intrigued by the difference in experience of the pandemic wrt to ethnicity as it plays out in migrated populations. Is this just age demographics at play or is there something else going on, maybe along the lines of increased prevalence of autoimmune pathology and e.g schizophrenia (hypothesised by some to be-at least partly- of immune etiology) found in this population as immigrant vs in originating locations. Could there be immune dysregulation in absence of host-adaption-related early-life pathogen exposures? (e.g survival of ‘Immune amnesia’ following measles infection as a goldilocks threshold for local immune fitness).