Main characteristics of a COVID Superspreader

Would you prefer to know if you were one?

Superspreaders are unable to control viral replication in the nasal passage and sinuses, therefore have higher viral loads for longer periods of time. Instead of infecting just 3 people they may infect up to 20!

A superspreader will tend to have asymptomatic infection and sometimes only test themselves after someone in close contact tests positive.

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The basic characteristics of this superspreader group are likely to be -

• Aged 35 to 45 years

• Female more likely than male

• Not usually obese

• Non-smokers

• *High probability of food sensitivities - Gluten, dairy, nuts (this is based on my own anecdotal observations, not the paper below).

Von Stemann, Jakob Hjorth, et al. "Prevalence and correlation of cytokine-specific autoantibodies with epidemiological factors and C-reactive protein in 8,972 healthy individuals: results from the Danish Blood Donor Study." PloS one 12.6 (2017): e0179981.

Additional characteristics of Superspreaders

Prior recurrent Upper Respiratory Tract Infections (URTI’s) - Some individuals have a history of frequent colds, sometimes multiple episodes in a year. The natural immune system tends to have protection for about 18 months to 2 years, before the next viral infection. Recurrent infection can point to interferon autoantibodies, which block the immune alarm when having an active viral infection.

Multiple COVID-19 infections - These individuals may have previously recurrent URTI’s and also get Covid on multiple occasions. This still points to interferon blocking through autoantibodies.

Vaccination Status - Covid vaccines have focused the immune system on using spike protein as the primary target. This means that even minor changes to the viral spike protein may evade mucosal immunity. Additionally, injectable vaccines are poor stimulators for mucosal IgA antibodies with higher risk of infection.

Haller-Kikkatalo, Kadri, et al. "Demographic associations for autoantibodies in disease-free individuals of a European population." Scientific Reports 7.1 (2017): 44846.

Abers, Michael S., et al. "Neutralizing type‐I interferon autoantibodies are associated with delayed viral clearance and intensive care unit admission in patients with COVID‐19." Immunology and cell biology 99.9 (2021): 917-921.

This interesting thought pattern came out of a recent post regarding the higher risk of severe COVID-19 in persons with interferon autoantibodies. My research suggests that this immune dysfunction was present prior to the COVID-19 infection.

Why is it important?

Interferon is the first signal to warn the body that virus is present and occurs in the upper airway. With interferon autoantibodies, it is likely that the signal will be delayed and allow the virus to get into the lungs undetected. This is the predisposition for severe disease when combined with elevated serum ACE-2.

COVID-19: The truth about super-spreaders