This is a really great summary and reference document, thanks for writing this! I have two comments:
1. There is a difference between detectable levels of RNA/DNA/Antigen and an active, transmissible infection. While most of the time this is not important when thinking about a global surveillance system, it is good to keep in mind especially in PoP testing.
Edit: You address my point 1 in your Part 2
2. You write:
However, while we can use animal surveillance systems to regularly monitor animals’ health and collect samples, we lack the capability of characterizing the pathogens effectively so as to predict their virulence and transmissibility to humans. This is a serious problem as it is infeasible to analyze and monitor every single pathogen strain found in animals. Microbiologists are working on this problem, but until then, zoonotic surveillance may not be suitable as an early-warning system
Kevin Esvelt has convincingly argued that we should not do this, because this would publish what and where viruses or pathogens are that could cause a pandemic to bad actors. It seems related to your point on “Potential for Dual-Use by Bad Actors”. While the technology itself may not be used by bad actors, the information gathered would immediately be an information hazard which could be used by bad actors.
Again, thanks a lot for this overview of the topic!
The infectious period and the symptomatic period, and how they interact, is generally more important than how long a pathogen can lay “dormant”. However, HIV is an example of when a case can be infectious even during the dormant period- that is very concerning, it’s like asymptomatic transmission for COVID-19 but on a much larger scale. People are certainly concerned about a pathogen that has an infectious period that starts before the symptomatic period- it’s even bolded on the slidedeck from the presentation you linked to:
“I have bolded this because in multiple modeling studies, and in experience...if a disease is contagious during the incubation period, when you’re not sick, then it’s very, very hard to control”.
There will certainly be some patients who die in the next few decades from some damage the SARS-CoV-2 infection did to an organ system or from immune system dysregulation from a SARS-CoV-2 infection. Novel pathogens that infect large swathes of the population often have longer term effects. Following the 1889 “Russian flu” pandemic there was even a noticeable increase in suicides among flu victims (https://macsphere.mcmaster.ca/handle/11375/14366; it was likely not a flu but in fact a novel coronavirus!). However, the magnitude is nowhere near the level needed to bring SARS-CoV-2 into GCBR status. While it is true that people can die of measles, EBV, or herpes after recovering from an acute infection, this is by no means likely. HIV is the outlier here, but it has meaningful differences from SARS-CoV-2: it has a much, much higher mutation rate, it uses reverse transcriptase to integrate its genome into the host cell’s genome, and it preferentially attacks immune cells (measles also attacks the immune system in a different way, by attacking memory cells). So yes, in my opinion, we are out of the woods with COVID-19 with regards to GCBRs.
The main countermeasure to pathogens that take a while to cause symptoms is good epidemiologic surveillance systems. This “starts the clock” faster on countermeasures. Ideally, you would want a pathogen agnostic system, like what is being worked on at the Nucleic Acid Observatory. There’s a game called Plague Inc that models this one aspect well- the sooner humanity realizes something is spreading, the sooner they slow the spread and create cures.