You are presented with a paragraph from a COVID-19 literature. Classify the topics of this piece of text by choosing from the following categories:

- Epidemic Forecasting: The content relates to predictions about the spread of COVID-19.
- Treatment: The paragraph discusses therapeutic methods or medication for COVID-19.
- Prevention: The content covers measures to prevent the spread of COVID-19.
- Mechanism: The paragraph explains the biological mechanisms of the virus.
- Case Report: The content is a report of a COVID-19 case.
- Transmission: The paragraph discusses how COVID-19 is transmitted.
- Diagnosis: The content is about diagnosing COVID-19 in individuals.

Your classification should be provided as an element within a JSON array. The array should be formatted with topics enclosed in double quotes and separated by commas, following the JSON format, for example: ["Topic1", "Topic2", ...]. Include all applicable topics within the array. Your output should be a valid JSON array, and no additional text should be included in your response.

Article:

Early and persistent activation of complement is considered to play a key role in the pathogenesis of COVID-19. Complement activation products orchestrate a proinflammatory environment that might be critical for the induction and maintenance of a severe inflammatory response to SARS-CoV-2 by recruiting cells of the cellular immune system to the sites of infection and shifting their state of activation towards an inflammatory phenotype. It precedes pathophysiological milestone events like the cytokine storm, progressive endothelial injury triggering microangiopathy, and further complement activation, and causes an acute respiratory distress syndrome (ARDS). To date, the application of antiviral drugs and corticosteroids have shown efficacy in the early stages of SARS-CoV-2 infection, but failed to ameliorate disease severity in patients who progressed to severe COVID-19 pathology. This report demonstrates that lectin pathway (LP) recognition molecules of the complement system, such as MBL, FCN-2 and CL-11, bind to SARS-CoV-2 S- and N-proteins, with subsequent activation of LP-mediated C3b and C4b deposition. In addition, our results confirm and underline that the N-protein of SARS-CoV-2 binds directly to the LP- effector enzyme MASP-2 and activates complement. Inhibition of the LP using an inhibitory monoclonal antibody against MASP-2 effectively blocks LP-mediated complement activation. FACS analyses using transfected HEK-293 cells expressing SARS-CoV-2 S protein confirm a robust LP-dependent C3b deposition on the cell surface which is inhibited by the MASP-2 inhibitory antibody. In light of our present results, and the encouraging performance of our clinical candidate MASP-2 inhibitor Narsoplimab in recently published clinical trials, we suggest that the targeting of MASP-2 provides an unsurpassed window of therapeutic efficacy for the treatment of severe COVID-19.
["Mechanism", "Treatment"]