Multiorgan tropism of SARS-CoV-2 lineage B.1.1.7

Due to the development of novel functionalities, distinct SARS-CoV-2 variants such as B.1.1.7 fuel the current pandemic. B.1.1.7 is not only more transmissible, but may also cause an increased mortality compared to previous SARS-CoV-2 variants. Human tissue analysis of the SARS-CoV-2 lineage B.1.1.7 is urgently needed, and we here present autopsy data from 7 consecutive SARS-CoV-2 B.1.1.7 cases. The initial RT-qPCR analyses from nasopharyngeal swabs taken post mortem included typing assays for B.1.1.7. We quantitated SARS-CoV-2 B.1.1.7 viral load in autopsy tissue of multiple organs. Highest levels of SARS-CoV-2 B.1.1.7 copies normalized to ß-globin were detected in the respiratory system (lung and pharynx), followed by the liver and heart. Importantly, SARS-CoV-2 lineage B.1.1.7 was found in 100% of cases in the lungs and in 85.7% in pharynx tissue. Detection also in the kidney and brain highlighting a pronounced organ tropism. Comparison of the given results to a former cohort of SARS-CoV-2 deaths during the first wave in spring 2020 showed resembling organ tropism. Our results indicate that also SARS-CoV-2 B.1.1.7 has a relevant organ tropism beyond the respiratory tract. We speculate that B.1.1.7 spike protein’s affinity to human ACE2 facilitates transmission, organ tropism, and ultimately morbidity and mortality. Further studies and larger cohorts are obligatory to proof this link.

WED 141 Pathological correlates of age at death in multiple sclerosis

IntroductionFew studies have investigated which pathological features, including systemic vascular disease (VD), associate with younger age at death in multiple sclerosis (MS) and this constitutes the aim of the present study.MethodsA post mortem MS brain autopsy tissue was studied for 1)systemic VD scores 2)% brain plaque area and activity from a)frontal plus occipital white matter(WM), b)pons, and c)basal ganglia(BG), 3)frontal plus occipital cortex. These pathology measures, sex, disease duration (DD), and cause of death, were fitted into a regression model to explain age at death.Results34 MS cases (mean age 61.6±13.05 years, 58.8% females, DD 20.2±13.45 years) were included. Age at death decreased with increasing WM+pons+ BG (r=−0.382, r=0.02) and cortical (r=−0.299, p=0.03) demyelination, and WM+pons+ BG active plaques (r=−0.326, p=0.011) but increased with DD(r=0.298, p=0.016) and VD(r=0.329, p<0.0001). In the regression model only cortical demyelination (b=−0.39, p=0.014), DD (b=0.36, p=0.009) and VD (b=0.64, p=0.001) persisted.ConclusionHigher cortical demyelination associated with younger age at death. Systemic VD did not associate with younger age at death in this MS cohort.