Severe acute respiratory syndrome coronavirus (SARS-CoV)-2 is the agent responsible for the coronavirus disease 2019 (COVID-19) global pandemic. SARS-CoV-2 is closely related to SARS-CoV, which caused the 2003 SARS outbreak. Although numerous reagents were developed to study SARS-CoV infections, few have been applicable to evaluating SARS-CoV-2 infection and immunity. Current limitations in studying SARS-CoV-2 include few validated assays with fully replication-competent wild-type virus. We have developed protocols to propagate, quantify, and work with infectious SARS-CoV-2. Here, we describe: (1) virus stock generation, (2) RT-qPCR quantification of SARS-CoV-2 RNA; (3) detection of SARS-CoV-2 antigen by flow cytometry, (4) quantification of infectious SARS-CoV-2 by focus-forming and plaque assays; and (5) validated protocols for virus inactivation. Collectively, these methods can be adapted to a variety of experimental designs, which should accelerate our understanding of SARS-CoV-2 biology and the development of effective countermeasures against COVID-19.

Plasmodium parasite entrance and exit: Sweats and fever are the hallmarks of malaria. Red blood cells are the replication factories for malaria parasites. Fever occurs when the parasites' merozoite stages burst en masse from red blood cells into the circulation. Nasamu et al. and Pino et al. discovered that two parasite proteases, plasmepsin IX and X, are essential for mass cell exit (see the Perspective by Boddey). Plasmepsin X is also used by the merozoites to enter a fresh red blood cell to continue the replicative cycle. These two plasmepsins act by regulating the maturation of enzymes required to disrupt host cell membranes. Because these functions are essential for the parasite, the authors used protease inhibitors to show that plasmepsins provide potential drug targets. Science , this issue p. 518 , p. 522 ; see also p. 445