The following is a summary of “Nasopharyngeal angiotensin converting enzyme 2 (ACE2) expression as a risk-factor for SARS-CoV-2 transmission in concurrent hospital associated outbreaks,” published in the February 2024 issue of Infectious Disease by Nikiforuk et al.
Researchers started a retrospective study to investigate if nasopharyngeal levels of angiotensin converting enzyme two (ACE2) in patients were linked to further transmission during hospital SARS-CoV-2 outbreaks in British Columbia, Canada.
They merged epidemiological case data with public health lab records and viral lineage calls (from whole genome sequencing) to reconstruct concurrent outbreaks through infection tracing network analysis. ACE2 and RNA viral load were measured with PCR. The transmission network identified secondary cases. Using Poisson and Negative Binomial regression models, bivariate and multivariable analyses estimated the ACE2 transcription’s association with the number of secondary SARS-CoV-2 cases.
The results showed 76 potential transmission events among 103 infection-tracing transmission network cases. Bivariate comparisons indicated no difference in ACE2 transcription between patients and healthcare workers (P=0.86). High ACE2 transcription was found in 98.6% of transmission events where the primary or secondary case had above-average ACE2. Multivariable analysis revealed a difference in the association between ACE2 transcription (log2 fold-change) and the number of secondary transmission events between patients and healthcare workers. In healthcare workers, Negative Binomial regression estimated that a one-unit change in ACE2 transcription decreased the number of secondary cases (β = -0.132, 95% CI: -0.255 to -0.0181) adjusting for RNA viral load. In patients, a one-unit change in ACE2 transcription increased the number of secondary cases (β = 0.187, 95% CI: 0.0101 to 0.370), adjusting for RNA viral load. Sensitivity analysis showed no ACE2 relationship in healthcare workers but confirmed a positive association in patients.
Investigators concluded that hospitalized patients with higher ACE2 levels may spread COVID-19 more easily, but further research is needed.
Source: bmcinfectdis.biomedcentral.com/articles/10.1186/s12879-024-09067-9