There is no definitive data on whether those with PI are more likely to get COVID-19 than others. However, there have been studies looking at PI and the course of COVID-19, including severe COVID-19, MIS-C/MIS-A, and long COVID.
Importantly, age, regardless of any other factor, is the single greatest risk factor for developing severe COVID-19. An analysis of adults hospitalized in 2020 that adjusted for chronic conditions found that:
PIs that disrupt the type I interferon response like TLR7 deficiency or autoimmune polyendocrinopathy syndrome type 1 (APS-1, also known as autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy or APECED) place individuals at very high risk for developing severe COVID-19. The interferon response is critical for controlling the virus early on and, without it, the virus spreads rapidly in the body.
The data for most other types of PI are less definitive. However, a large CDC study looking at healthcare records found that adults with PI and COVID-19 who went to the emergency room were hospitalized, were admitted to the ICU, were put on ventilators, and died at higher rates than those without PI. The increased risk ranged from 1.4 (ventilation or death) to 2.4 (hospitalization) times higher than those without PI.
In addition to PI, certain medical conditions, including some that tend to co-occur with or result from PI (bolded below), make it more likely that someone will develop severe COVID-19.
Medical treatments and behaviors can also be risk factors for severe COVID-19, including:
Risk factors are cumulative, which means that the risk of developing severe COVID-19 increases for every additional risk factor a person has. For example, a person who is 18 years old with an antibody deficiency (one risk factor) is less likely to become severely ill with COVID-19 than someone who is 65 years old with an antibody deficiency and bronchiectasis (three risk factors).
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