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The severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), known to cause the disease COVID-19, was declared a pandemic in early 2020. The objective of this review was to collate information regarding the potential of plants and natural products to inhibit coronavirus and targets associated with infection in humans and to highlight known drugs, which may have potential activity against SARS-CoV-2. Due to the similarity in the RNA genome, main proteases, and primary host receptor between SARS-CoV and SARS-CoV-2, a review was conducted on plants and secondary metabolites, which have shown activity against SARS-CoV. Numerous scientific reports on the potential of plants and secondary metabolites against SARS-CoV infection were found, providing important information on their possible activity against SARS-CoV-2. Based on current literature, 83 compounds have been identified with the potential to inhibit COVID-19. The most prominent selectivity was found for the alkaloid, lycorine, the lignan, savinin, and the abietane terpenoid, 8-beta-hydroxyabieta-9(11),13-dien-12-one with selectivity index values greater than 945, 667, and 510, respectively. Plants and their secondary metabolites, with activity against targets associated with the SARS-CoV infection, could provide valuable leads for the development into drugs for the novel SARS-CoV-2. The prospects of using computational methods to screen secondary metabolites against SARS-CoV targets are briefly discussed, and the drawbacks have been highlighted. Finally, we discuss plants traditionally used in Southern Africa for symptoms associated with respiratory viral infections and influenza, such as coughs, fever, and colds. However, only a few of these plants have been screened against SARS-CoV. Natural products hold a prominent role in discovering novel therapeutics to mitigate the current COVID-19 pandemic; however, further investigations regarding in vitro, in vivo, pre-clinical, and clinical phases are still required.

The purpose of this investigation was to try to understand the antibacterial mechanism of L-(-)-usnic acid isolated for the first time from fruticose lichen Usnea subfloridana using clinical isolates of methicillin-resistant Staphylococcus aureus (MRSA). The minimum inhibitory concentration (MIC) of L-(-)-usnic acid against the clinical isolates of MRSA and reference strain S. aureus MTCC-96 (SA-96) was in the range 25-50 μg/ml. Treatment of both reference and clinical strains (MRSA-ST 2071) with four-fold MIC concentrations (100-200 μg/ml) of L-(-)-usnic acid reduced the viability of cells without damaging the cell wall. However, the loss of 260 nm absorbing material and increase in propidium iodide uptake was observed in both of the strains. Similarly, a combined effect of L-(-)-usnic acid (25-50 μg/ml) and 7.5 % NaCl resulted in a reduced number of viable cells within 24 h in comparison to the control. These observations clearly indicate that L-(-)-usnic acid exerts its action by disruption of the bacterial membrane. Further, in vivo efficacy showed that L-(-)-usnic acid significantly (p < 0.001) lowered the microbial load of spleen at doses ranging from 1 to 5 mg/kg. Further, toxicity studies in infected mice at doses 20 times higher than the efficacious dose indicated L-(-)usnic acid to be safe. Paradoxically, L-(-)usnic acid exhibited changes in serum triglycerides, alkaline phosphatase (ALKP) and liver organ weight in the healthy mice administered with only 25 mg/kg body weight. The results obtained in this study showed that natural L-(-)-usnic acid exerts its antibacterial activity against MRSA by disruption of the cell membrane. Further, the natural L-(-)-usnic acid was found to be safe up to 100 mg/kg body weight, thereby, making it a probable candidate for treating S. aureus infections.

One-pot reactions of diorganotin oxides, R(2)SnO, with dimethyl sulfite under reflux conditions (125-127 degrees C) proceed via the Arbuzov rearrangement at the sulfur center, yielding the corresponding methoxydiorganotin methanesulfonates, R(2)Sn(OMe)OS(O)(2)Me [R = n-Pr (1), n-Bu (2), i-Bu (3), c-Hx (4)], as white, hygroscopic solids. These compounds react with beta-diketones [acetylacetone (Hacac), benzoylacetone (Hbzac), and dibenzoylmethane (Hbzbz)] to afford mixed-ligand organotin derivatives, R(2)Sn(X)OS(O)(2)Me [X = acac, R = n-Pr (5), n-Bu (6); X = bzac, R = n-Pr (7), n-Bu (8); X = bzbz, R = n-Pr (9), n-Bu (10), i-Bu (11)]. Selective hydrolysis of the Sn-OMe bond in 1-3 occurs, resulting in the isolation of (&mgr;-hydroxo)diorganotin methanesulfonates, R(2)Sn(OH)OS(O)(2)Me [R = n-Pr (12), n-Bu (13), i-Bu (14)]. All the compounds are characterized by elemental analyses and IR, multinuclear ((1)H, (13)C, and (119)Sn) NMR, and mass spectra. Unequivocal evidence of the presence of the methanesulfonate group is provided by the X-ray crystal structures of 6, 10, and 13. [For 6: trigonal space group R&thremacr; (No. 148), a = 28.664(1) Å, c = 13.056(1)Å, Z = 18. For 10: triclinic space group P&onemacr; (No. 2), a = 13.056(3) Å, b = 14.062(3) Å, c = 16.282(3) Å, Z = 4. For 13: triclinic space group P&onemacr; (No. 2), a = 9.089(2) Å, b = 12.040(2) Å, c =13.894(2) Å, Z = 2]. For 6 and 10, the solid-state structural analyses reveal dimeric structures with a bridging bidentate methanesulfonate group forming a centrosymmetric eight-membered ring. Compound 13 possesses a polymeric sheet structure with repeating 20-membered macrocycles (including two four-membered [Sn(OH)](2) rings) by virtue of the bridging bidentate methanesulfonate groups. A search for a possible pathway to give Arbuzov-rearranged products 1-4 leads us to speculate that there is an initial catalytic transformation of dimethyl sulfite to methyl methanesulfonate via intermediate compounds, Bu(2)Sn(OMe)(2) (A) and [Bu(2)SnOMe](2)O (B). A and B subsequently react with methyl methanesulfonate to give 1-4.

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