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:

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) spike (S) variants govern transmissibility, responsiveness to vaccination, and disease severity. In a screen for new models of SARS-CoV-2 infection, we identify human H522 lung adenocarcinoma cells as naturally permissive to SARS-CoV-2 infection despite complete absence of angiotensin-converting enzyme 2 (ACE2) expression. Remarkably, H522 infection requires the E484D S variant; viruses expressing wild-type S are not infectious. Anti-S monoclonal antibodies differentially neutralize SARS-CoV-2 E484D S in H522 cells as compared to ACE2-expressing cells. Sera from vaccinated individuals block this alternative entry mechanism, whereas convalescent sera are less effective. Although the H522 receptor remains unknown, depletion of surface heparan sulfates block H522 infection. Temporally resolved transcriptomic and proteomic profiling reveal alterations in cell cycle and the antiviral host cell response, including MDA5-dependent activation of type I interferon signaling. These findings establish an alternative SARS-CoV-2 host cell receptor for the E484D SARS-CoV-2 variant, which may impact tropism of SARS-CoV-2 and consequently human disease pathogenesis.
["Mechanism", "Treatment"]