This is a particularly important metric for any testing program, because it gives a sense of whether enough testing is being done to accurately capture the true positive rate. For instance, the WHO recommends that to ensure adequate testing, the % positive rate should be at or below 5% for at least 14 consecutive days: https://coronavirus.jhu.edu/testing/testing-positivity

Take away: Waning antibodies don’t necessarily mean that immunity will also decrease, because other components of the immune system retain “memory” for an infection and can combat invaders even after antibody counts have gone down.

The claim: “If you were infected with the novel coronavirus, a new study suggests that your immunity to the virus could decline within months.”

The evidence: This study [1], along with others [2], does indeed show evidence for declining neutralizing antibodies within a few months after infection; however, antibody counts alone are not enough to predict whether a patient will have durable immunity to a virus. Neutralizing antibodies are generated by B cells, a type of immune cell that patrols the body looking for their molecular targets. Some B cells carry “memory,” a quality that allows them to respond quickly when they see a virus or pathogen that they have encountered before, which allows them to pump out large quantities of antibody rapidly to fight the infection [3]. It’s actually normal in many viral infections for antibody levels within the blood to wane over time; the real concern is whether there are enough memory B cells to generate new antibodies at a moment’s notice.

In addition to B cells, a second type of immune cell known as a “T cell” is critical for predicting durable immunity. Like B cells, some T cells carry “memory” and can patrol the body for years looking for their targets. Some T cells play a role in helping B cells produce antibodies quickly, and other T cells can actually target the infection directly [4]. Studies have now shown that T cell responses can persist after SARS-CoV-2 infection, and some patients even have T cells that can react to SARS-CoV-2 due to “cross-reactivity,” likely from preexisting immunity from common cold viruses that share some characteristics of SARS-CoV-2. While this cross-reactivity does not guarantee immunity, the presence of robust B and T cell responses is important, and could be more predictive than presence of antibodies alone.

This article, written by a two well-known immunologists and COVID-19 experts at Yale University, provides a nice summary of the data that puts these claims in context [6].

This explanation is garbled and misstated. Genetic material is stored in DNA in the nucleus of the cell. Messenger RNA (mRNA) molecules carry the information stored within the DNA to the rest of the cell. Both DNA and RNA are a type of molecule called a "nucleic acid." Once outside the nucleus, the information in the messenger RNA can then be read, or "translated," to create proteins, such as the spike protein used by SARS-CoV-2. These proteins in turn carry out a wide variety of tasks that allow cells to function. This process is known as the "Central Dogma of Molecular Biology".

This is an oversimplification that dismisses research findings on particularly vulnerable activities. For instance, superspreading events have been linked to certain activities, as detailed here. For instance, a study of 110 case-patients from 11 clusters in Japan, linked all clusters to closed environments, including fitness centers, shared eating environments, and hospitals. The authors found an 18.7x risk of transmission in closed environments than open environments. Therefore, it is inaccurate to say "there are no activities that we can point to as extremely vulnerable."