SARS-CoV-2 infection in alpha1-antitrypsin deficiency

Low Prevalence of Mild Alpha-1-Antitrypsin Deficiency in Hospitalized COVID-19-Patients

“…However, since there were so few patients with moderate-to-severe AATD, data were not considered robust enough for meaningful conclusions. 21 Finally, in our study, both patients with PI*MZ developed severe COVID-19 of whom one died. Yet, both patients had several other known risk factors for severe COVID-19 why this finding necessitates cautious interpretation.…”

“…Simultaneously, in patients with positive COVID-19-tests, “Death by COVID-19” was seen in 353 (0.083%) non-carriers and in 53 (0.088%) PI-gene mutation carriers (x 2 , p=0.69) in the UK Biobank study. 21 In addition, on the contrary to previous reports of a suggested association of moderate and severe AATD with severity of COVID-19, 4 the UK biobank study did neither identify moderate-to-severe AATD as a risk factor for SARS-CoV-2-positivity or “Death by COVID-19” when compared to non-carriers. However, since there were so few patients with moderate-to-severe AATD, data were not considered robust enough for meaningful conclusions.…”

“…While our study constitutes a small cohort of hospitalized COVID-19-patients, our findings are in line with recently published data from the United Kingdom (UK) Biobank, which showed 12,723 (3.0%) positive COVID-19 tests in 426,994 participants that were non-carriers of PI-gene mutations and 1670 (2.8%) positive COVID-19 tests in 60,509 participants that were carriers of any PI-gene mutation (MZ, MS, SZ, SS, ZZ). 21 …”

Correlation between α1-Antitrypsin Deficiency and SARS-CoV-2 Infection: Epidemiological Data and Pathogenetic Hypotheses

“…Unlike previous findings, Schneider and Strnad recently assessed the association between AATD and COVID-19 in the United Kingdom Biobank, a community-based cohort with >500,000 participants, and showed that the most common and mild AATD genotypes were not associated with increased SARS-CoV-2 infection rates or increased SARS-CoV-2 fatalities, whereas the number of severe AATD cases was too low to allow definitive conclusions to be drawn [ 32 ].…”

Advances in the development of therapeutic strategies against COVID-19 and perspectives in the drug design for emerging SARS-CoV-2 variants

“…Alpha-1 antitrypsin (α1AT) inhibits the protease activity of TMPRSS2 at physiological concentrations to restrain the entry and replication of SARS-CoV-2 in cell lines and primary cells [40] . A statistical study based on 500,000 people shows that mild α1-Antitrypsin deficiency (AATD) genotypes were not associated with increased SARS-CoV-2 infection rates or fatalities [41] . For the lack of α1AT makes it easier to activate TMPRSS2, severe AATD patients may be susceptible to SARS-CoV-2 [42] , [43] .…”