ABSTRACT
-This study aims to determine spectrum of bacterial infection in patients with severe acute respiratory syndrome coronavirus-2 infection at the time of hospital admission and identify changes in hematological biomarkers of COVID19 severity. A retrospective study was conducted in blood cultures from patients suspected to have sepsis were included in the study. Patients were grouped based on SARS-CoV-2 RT-PCR result as positive, negative, or not tested. For the purposes of classifying blood cultures by SARS-CoV-2 RT-PCR status, hematological parameters were analyzed. Out off 825 blood sample, 466 samples was positive for blood culture identified by conventional and Automatic blood culture system - Vitek 2. Among these 466 patients, 211(45.2%) were positive for SARS-CoV2 virus and 255 (54.7%) were negative for SARS-CoV2 virus by RT-PCR. Regarding CRP Total number of CRP positive samples was 654, CRP negative samples was 84 and CRP was not done for 87samples. The total number of IL6 positive samples was 83 and IL6 negative samples were not evaluated for 125 patients. The concern of Bacterial sepsis in COVID-19 patients due to the above organisms based on our study over the period of one year. Consequently, it is important to pay attention to bacterial co-infections in critical patients diagnosed for COVID-19. Copyright © Global Science Publications.
ABSTRACT
Enveloped viruses utilize the host cell secretory pathway to synthesize viral glycoproteins and direct them to sites of assembly. Using an image-based screen, we identified two thiopurines, 6-thioguanine (6-TG) and 6-thioguanosine (6-TGo), that selectively disrupted the processing and accumulation of influenza A virus glycoproteins hemagglutinin (HA) and neuraminidase (NA). Selective disruption of IAV glycoprotein processing and accumulation by 6-TG and 6-TGo correlated with unfolded protein response (UPR) activation. 6-TG and 6-TGo also inhibited replication of the human coronavirus OC43 (HCoV-OC43), which correlated with UPR/ISR activation and diminished accumulation of ORF1ab and nucleocapsid (N) mRNAs, which suggests broader disruption of coronavirus gene expression in ER-derived cytoplasmic compartments. The chemically similar thiopurine 6-mercaptopurine (6-MP) had little effect on the UPR and did not affect IAV or HCoV-OC43 replication. Consistent with reports on other CoV Spike (S) proteins, ectopic expression of SARS-CoV-2 S protein caused UPR activation. 6-TG inhibited accumulation of full length S0 or furin-cleaved S2 fusion proteins, but spared the S1 ectodomain. DBeQ, which inhibits the p97 AAA-ATPase required for retrotranslocation of ubiquitinated misfolded proteins during ER-associated degradation (ERAD) restored accumulation of S0 and S2 proteins in the presence of 6-TG, suggesting that 6-TG induced UPR accelerates ERAD-mediated turnover of membrane-anchored S0 and S2 glycoproteins. Taken together, these data indicate that 6-TG and 6-TGo are effective host-targeted antivirals that trigger the UPR and disrupt accumulation of viral glycoproteins. Importantly, our data demonstrate for the first time the efficacy of these thiopurines in limiting IAV and HCoV-OC43 replication in cell culture models.