Presented at the 13th International Congress on Autoimmunity in Athens, Greece

Speaker: Laura Talamini

Key Takeaways:

  • COVID-19 was shown to induce the production of autoantibodies linked to spermatogenesis (a cell differentiation process that ensures the production of fertilizing sperm, which ultimately fuse with an egg to form a zygote)
  • Vaccination was not shown to induce autoantibodies linked to spermatogenesis
  • A cross-reactivity (the extent to which different antigens appear similar to the immune system) occurs against spermatogenesis-associated antigens in both males and females, highlighting the potential onset of new fertility disorders

Summary:

Talamini’s team focused on the reproductive system in their COVID-19-related research, due to its vulnerability to infections, the overexpression of ACE2 (entry receptor for SARS-CoV-2) in the testes and ovaries, and recent research demonstrating potential spermatogenesis impairment in COVID-19 patients (1) (2) (3) (4) (5) (6) (7) (8) (9) (10). Their objective was to assess the presence of immunoglobulin G (IgG) antibodies directed against spermatogenesis-related proteins in patients with acute and long COVID-19. This research has not yet been published.

When comparing the spike protein of SARS-CoV-2 and spermatogenesis-related proteins they observed shared long sequences (cross-reactivity) in four peptides and decided to focus on these peptides (peptides 1, 2, 3, and 4). They collected serum from COVID-19 patients in different countries as well as from normal healthy controls. The COVID-19 patient population was stratified into those with an acute COVID-19 infection and those with long COVID-19. Those with an acute COVID-19 infection showed elevated levels of antibodies against peptide 2 while those with long COVID showed elevated levels of antibodies against peptide 4. They also found that females with long COVID had more antibodies against peptide 2. They went on to compare their results with serum from those who had been vaccinated against COVID-19 and did not find the same elevated antibodies against peptides 2 and 4 in those individuals.

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