OBJECTIVE: The objectives of this paper are to gain a better understanding of the key presenting symptoms of COVID-19 in HCWs in a district specialist hospital, to establish the proportion of symptomatic COVID-19 cases among HCWs and its severity and to determine the time taken from onset of symptoms or perceived exposure to diagnostic testing.
METHODOLOGY: This is a retrospective descriptive analysis of clinical characteristics of subjects infected with COVID-19 among HCW in HTI. Their demography and clinical characteristics were recorded.
RESULTS: There were 47 HCW in HTI who tested positive for COVID-19. The mean age of the patients was 37.5 years old. 7 patients (15.2%) had at least more than one comorbidity. Average duration of time from perceived close contact to onset of symptom was 4.5 days, while the mean duration of time from symptoms to first positive RT-PCR result was 3.4 days. Six patients (13.0%) were asymptomatic throughout, whereas 40 (87.0%) had at least one symptom prior to hospitalization. The most commonly reported symptoms were fever (65.2%), sore throat (39.1%) and cough (37.0%). In terms of severity of symptoms, the majority of patients experienced mild symptoms (Group 2, 52.2%). Two patients (4.3%) with multiple comorbidities had severe disease requiring ICU admission and mechanical ventilation. There were no mortalities, and the longest staying patient was hospitalized for 18 days. The high rates of infectivity among HCW in HTI can be attributed to working in close proximity while in the asymptomatic incubation phase, while no HCW directly involved in the care of COVID-19 positive patients were tested positive.
CONCLUSION: We report that HCW share similar clinical characteristics of COVID-19 infection as those of non HCW patients in earlier studies. The infection can spread rapidly within healthcare settings via close contacts among infected HCWs. As such, we advocate distancing when working and usage of personal protective equipment when treating patients with respiratory illness to reduce transmission of COVID-19.
METHODS: Here we describe the clinical course of 10 consecutive TBE patients with outcome assessment at discharge and after 12 month using a modified Rankin Scale. Patients underwent cerebral MRI after confirmation of diagnosis and before discharge. (18)F-FDG PET/CT scans were performed within day 5 to day 14 after TBE diagnosis. Extended analysis of coagulation parameters by thrombelastometry (ROTEM® InTEM, ExTEM, FibTEM) was performed every other day after confirmation of TBE diagnosis up to day 10 after hospital admission or discharge.
RESULTS: All patients presented with a meningoencephalitic course of disease. Cerebral MRI scans showed unspecific findings at predilection areas in 3 patients. (18)F-FDG PET/CT showed increased glucose utilization in one patient and decreased (18)F-FDG uptake in seven patients. Changes in coagulation measured by standard parameters and thrombelastometry were not found in any of the patients.
DISCUSSION: Glucose hypometabolism was present in 7 out of 10 TBE patients reflecting neuronal dysfunction in predilection areas of TBE virus infiltration responsible for development of clinical signs and symptoms.
RESULTS: ARG2 promotes tumorigenesis by increasing cellular proliferation, migration, invasion and vasculogenic mimicry in GBM cells, at least in part due to overexpression of MMP2/9. The nor-NOHA significantly reduced migration and tube formation of ARG2-overexpressing cells. HCMV immediate-early proteins (IE1/2) or its downstream pathways upregulated the expression of ARG2 in U-251 MG cells. Immunostaining of GBM tissue sections confirmed the overexpression of ARG2, consistent with data from subsets of Gene Expression Omnibus. Moreover, higher levels of ARG2 expression tended to be associated with poorer survival in GBM patient by analyzing data from TCGA.
METHODS: The role of ARG2 in tumorigenesis was examined by proliferation-, migration-, invasion-, wound healing- and tube formation assays using an ARG2-overexpressing cell line and ARG inhibitor, N (omega)-hydroxy-nor-L-arginine (nor-NOHA) and siRNA against ARG2 coupled with functional assays measuring MMP2/9 activity, VEGF levels and nitric oxide synthase activity. Association between HCMV and ARG2 were examined in vitro with 3 different GBM cell lines, and ex vivo with immunostaining on GBM tissue sections. The viral mechanism mediating ARG2 induction was examined by siRNA approach. Correlation between ARG2 expression and patient survival was extrapolated from bioinformatics analysis on data from The Cancer Genome Atlas (TCGA).
CONCLUSIONS: ARG2 promotes tumorigenesis, and HCMV may contribute to GBM pathogenesis by upregulating ARG2.