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1.
J Environ Sci Health A Tox Hazard Subst Environ Eng ; 58(7): 694-705, 2023.
Article in English | MEDLINE | ID: covidwho-2317443

ABSTRACT

The mismanagement of consumer-discarded plastic waste (CDPW) has raised global environmental concerns about climate change. The COVID-19 outbreak has generated ∼1.6 million tons of plastic waste per day in the form of personal protective equipment (masks, gloves, face shields, and sanitizer bottles). These plastic wastes are either combustible or openly dumped in aquatic and terrestrial environments. Open dumping upsurges emerging contaminants like micro-nano plastics (MNPs) that directly enter the ecosystem and cause severe impacts on flora and fauna. Therefore, it has become an utmost priority to determine sustainable technologies that can degrade or treat MNPs from the environment. The present review assesses the sources and impacts of MNPs, various challenges, and issues associated with their remediation techniques. Accordingly, a novel sustainable circular model is recommended to increase the degradation efficiency of MNPs using biochemical and biological methods. It is also concluded that the proposed model does not only overcome environmental issues but also provides a sustainable secondary resource to meet the sustainable development goals (SDGs).


Subject(s)
COVID-19 , Plastics , Humans , Microplastics , Ecosystem , COVID-19/epidemiology , COVID-19/prevention & control
2.
Front Immunol ; 12: 660632, 2021.
Article in English | MEDLINE | ID: covidwho-1325522

ABSTRACT

The novel SARS-CoV-2virus that caused the disease COVID-19 is currently a pandemic worldwide. The virus requires an alveolar type-2 pneumocyte in the host to initiate its life cycle. The viral S1 spike protein helps in the attachment of the virus on toACE-2 receptors present on type-2 pneumocytes, and the S2 spike protein helps in the fusion of the viral membrane with the host membrane. Fusion of the SARS-CoV-2virus and host membrane is followed by entry of viral RNA into the host cells which is directly translated into the replicase-transcriptase complex (RTC) following viral RNA and structural protein syntheses. As the virus replicates within type-2 pneumocytes, the host immune system is activated and alveolar macrophages start secreting cytokines and chemokines, acting as an inflammatory mediator, and chemotactic neutrophils, monocytes, natural NK cells, and CD8+ T cells initiate the local phagocytosis of infected cells. It is not the virus that kills COVID-19 patients; instead, the aberrant host immune response kills them. Modifying the response from the host immune system could reduce the high mortality due to SARS-CoV-2 infection. The present study examines the viral life cycle intype-2 pneumocytes and resultant host immune response along with possible therapeutic targets.


Subject(s)
COVID-19/immunology , COVID-19/therapy , Immunomodulation , SARS-CoV-2/pathogenicity , Alveolar Epithelial Cells/metabolism , Alveolar Epithelial Cells/pathology , Alveolar Epithelial Cells/virology , Angiotensin-Converting Enzyme 2/metabolism , COVID-19/pathology , COVID-19/virology , Cytokines/immunology , Cytokines/metabolism , Host-Pathogen Interactions/immunology , Humans , Immunity , Macrophages, Alveolar/immunology , Macrophages, Alveolar/metabolism , SARS-CoV-2/physiology
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