SARS-CoV-2 Vaccination and Clinical Presentation of COVID-19 in Patients Hospitalized during the Delta- and Omicron-Predominant Periods

Evidence suggests that monovalent vaccine formulations are less effective against the Omicron SARS-CoV-2 than against previous variants. In this retrospective cohort study of hospitalized adults with PCR-confirmed COVID-19 during the Delta (October–November 2021) and Omicron (January–April 2022) variant predominant periods in Slovenia, we assessed the association between primary vaccination against SARS-CoV-2 and progression to critically severe disease (mechanical ventilation or death). Compared with the 529 patients hospitalized for acute COVID-19 during the Delta period (median age 65 years; 58.4% men), the 407 patients hospitalized during the Omicron period (median age 75 years; 50.6% men) were older, more often resided in long-term care facilities, and had higher Charlson comorbidity index scores. After adjusting for age, sex, the Charlson comorbidity index, the presence of immunocompromising conditions, and vaccination status, the patients admitted during the Omicron period had comparable odds of progressing to critically severe disease to those admitted during the Delta period. The 334/936 (35.7%) patients completing at least primary vaccination had lower odds of progression to critically severe disease and shorter hospital stay than unvaccinated patients; however, the protective effect of vaccination was less pronounced during the Omicron than during the Delta period. Although the Omicron variant appeared to better evade immunity induced by monovalent vaccines than the Delta variant, vaccination against SARS-CoV-2 remained an effective intervention to decrease morbidity and mortality in COVID-19 patients infected with the Omicron variant

Sporadic hepatitis A virus PCR false-positive results observed during reflex testing of serum samples previously tested for Anti-HAV antibodies and caused by contamination with HAV RNA present in the reagents of the commercial Anti-HAV immunoassay

Hepatitis A diagnosis relies on serology and occasionally on hepatitis A virus (HAV) RNA detection. For timely diagnosis and the avoidance of drawing additional blood, molecular testing is often performed as reflex testing by using blood specimens that were initially sent for anti-HAV serology. Reflex molecular testing is preferably performed from different sample aliquots, but, for limited sample quantities, it uses samples that have been preprocessed in an immunoassay analyzer. In 2012, we first observed sporadic HAV RNA-positive cases that were inconsistent with patients’ serological profiles and/ or medical histories, suggesting that occasional laboratory contamination was causing false-positive PCR results. Multiple external quality assurance (EQA) and laboratory surface contamination checks were performed, questionable specimens were tested with various HAV RNA tests, and follow-up serum/stool samples were collected. All contamination-check samples and samples from healthy individuals tested HAV RNA-negative, and the laboratory successfully passed all EQAs. The HAV RNA-positive results were reproducible with various HAV RNA assays. No patients seroconverted, and their follow-up samples were consistently HAV RNA-negative. Finally, a detailed review of testing protocols revealed a correlation between HAV RNA false positivity and preceding anti-HAV testing with the Cobas-e411 automated immunoassay analyzer. HAV RNA was detected in the Cobas-e411 anti-HAV reagents, with the HAV sequences matching those from the false-positive samples. Preceding anti-HAV testing using two other immunoassay analyzers did not result in subsequent HAV RNA false positivity during reflex testing. The Cobas-e411 pipetting procedure with a single pipette tip collecting samples and anti-HAV reagents contaminated the original sample with the HAV RNA that was present in the immunoassay’s reagents, thereby resulting in HAV RNA false positivity during the reflex testing