Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), identified for the first time in Wuhan, China, causes coronavirus disease 2019 (COVID-19), which moved from epidemic status to becoming a pandemic. Since its discovery in December 2019, there have been countless cases of mortality and morbidity due to this virus. Several compounds such as chloroquine, hydroxychloroquine, lopinavir-ritonavir, and remdesivir have been tested as potential therapies; however, no effective treatment is currently recommended by regulatory agencies. Some studies on respiratory non-enveloped viruses such as adenoviruses and rhinovirus and some respiratory enveloped viruses including human respiratory syncytial viruses, influenza A, parainfluenza, SARS-CoV, and SARS-CoV-2 have shown the antiviral activity of cardiac glycosides, correlating their effect with Na+/K+-ATPase (NKA) modulation. Cardiac glycosides are secondary metabolites used to treat patients with cardiac insufficiency because they are the most potent inotropic agents. The effects of cardiac glycosides on NKA are dependent on cell type, exposure time, and drug concentration. They may also cause blockage of Na+ and K+ ionic transport or trigger signaling pathways. The antiviral activity of cardiac glycosides is related to cell signaling activation through NKA inhibition. Nuclear factor kappa B (NFκB) seems to be an essential transcription factor for SARS-CoV-2 infection. NFκB inhibition by cardiac glycosides interferes directly with SARS-CoV-2 yield and inflammatory cytokine production. Interestingly, the antiviral effect of cardiac glycosides is associated with tyrosine kinase (Src) activation, and NFκB appears to be regulated by Src. Src is one of the main signaling targets of the NKA α-subunit, modulating other signaling factors that may also impair viral infection. These data suggest that Src-NFκB signaling modulated by NKA plays a crucial role in the inhibition of SARS-CoV-2 infection. Herein, we discuss the antiviral effects of cardiac glycosides on different respiratory viruses, SARS-CoV-2 pathology, cell signaling pathways, and NKA as a possible molecular target for the treatment of COVID-19.

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The Mediterranean diet (MedDiet) consists of consumption of vegetables and healthy oils and have beneficial effects on metabolic and inflammatory diseases. Our goal here is to discuss the role of fatty acid content in MedDiet, mostly omega-3, omega-6, and omega-9 on malaria. Malaria affects millions of people around the globe. The parasite Plasmodium causes the disease. The metabolic and inflammatory alterations in the severe forms have damaging consequences to the host. The lipid content in the MedDiet holds anti-inflammatory and pro-resolutive features in the host and have detrimental effects on the Plasmodium. The lipids from the diet impact the balance of pro- and anti-inflammation, thus, lipids intake from the diet is critical to parasite elimination and host tissue damage caused by an immune response. Herein, we go into the cellular and molecular mechanisms and targets of the MedDiet fatty acids in the host and the parasite, reviewing potential benefits of the MedDiet, on inflammation, malaria infection progression, and clinical outcome.