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Removal of SARS-CoV-2 viral markers through a water reclamation facility.

ABSTRACT: There have been multiple reports of COVID-19 virus, SARS-CoV-2 RNA presence in influent wastewater of water reclamation facilities (WRFs) across the world. In this study, the removal of SARS-CoV-2 RNA was investigated in a WRF by collecting samples from various stages relayed to hydraulic retention time (HRT) and analyzed for viral RNA (N1 and N2) gene markers and wastewater characteristics. SARS-CoV-2 RNA was detected in 28 out of 28 influent wastewater and primary effluent samples. Secondary effluent showed 4 out of 9 positive samples, and all tertiary and final effluent samples were below the detection limit for the viral markers. The reduction was significant (p value < 0.005, one-way analysis of variance [ANOVA] test) in secondary treatment, ranging from 1.4 to 2.0 log₁₀ removal. Adjusted N1 viral marker had a positive correlation with total suspended solids, total Kjeldahl nitrogen, and ammonia concentrations (Spearman's ρ = 0.61, 0.67, and 0.53, respectively, p value < 0.05), while demonstrating a strongly negative correlation with HRT (Spearman's ρ = -0.58, p value < 0.01). PRACTITIONER POINTS: Viral RNA was present in all samples taken from influent and primary effluent of a WRF. SARS-CoV-2 gene marker was detected in secondary effluent in 4 out of 9 samples. Tertiary and final effluent samples tested nondetect for SARS-CoV-2 gene markers. Up to 0.5 and 2.0 log₁₀ virus removal values were achieved by primary and secondary treatment, respectively.

SUBMITTER: Gharoon N

PROVIDER: S-EPMC8661921 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:Severe viral infections, including SARS-COV-2, could trigger disruption of the balance between pro-oxidant and antioxidant mediators; the magnitude of which could reflect the severity of infection and lung injury. Using publicly available COVID-19 transcriptomic datasets, we conducted an in-silico analyses to evaluate the expression levels of 125 oxidative stress genes, including 37 pro-oxidant genes, 32 oxidative-responsive genes, and 56 antioxidant genes. Seven oxidative stress genes were found to be upregulated in whole blood and lung autopsies (MPO, S100A8, S100A9, SRXN1, GCLM, SESN2, and TXN); these genes were higher in severe versus non-severe COVID-19 leucocytes. Oxidative genes were upregulated in inflammatory cells comprising macrophages and CD8+ T cells isolated from bronchioalveolar fluid (BALF), and neutrophils isolated from peripheral blood. MPO, S100A8, and S100A9 were top most upregulated oxidative markers within COVID-19's lung autopsies, whole blood, leucocytes, BALF derived macrophages and circulating neutrophils. The calprotectin's, S100A8 and S100A9 were upregulated in SARS-COV-2 infected human lung epithelium. To validate our in-silico analysis, we conducted qRT-PCR to measure MPO and calprotectin's levels in blood and saliva samples. Relative to uninfected donor controls, MPO, S100A8 and S100A9 were significantly higher in blood and saliva of severe versus asymptomatic COVID-19 patients. Compared to other different viral respiratory infections, coronavirus infection showed a prominent upregulation in oxidative stress genes with MPO and calprotectin at the top of the list. In conclusion, SARS-COV-2 induce the expression of oxidative stress genes via both immune as well as lung structural cells. The observed correlation between oxidative stress genes dysregulation and COVID-19 disease severity deserve more attention. Mechanistical studies are required to confirm the correlation between oxidative stress gene dysregulation, COVID-19 severity, and the net oxidative stress balance.

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Removal of SARS-CoV-2 viral markers through a water reclamation facility.

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