You just need to have general information about how acquired immunity works. But since you're being a credentials Nazi, I teach the immune system as either part of a college biology or human anatomy and physiology class. I have a BS and MS in biology, and have 30 hours of genetics courses at the PhD level from the early 2000's. I've done both PCR and rtPCR, so I know how to interpret the text from your excerpt.
Your "know more than anyone else on the planet" bullshit is not helpful in the least. And let me return some of your nitpicking - it's "rigid", not "ridgid." See how that kind of thing feels? If you want to have a conversation, have a civilized one. Don't go all deplorable and attack someone simply because they disagree with what you want to believe.
It's very well-established scientific fact that exposure to a disease very consistently results in antibodies against that disease (as long as someone survives the initial illness), and at least partial immunity to a second illness. The idea that COVID-19 is somehow different from every other disease that has been characterized is an extraordinary claim. Extraordinary claims require extraordinary evidence, and you don't provide anything.
I have a few things to say about the excerpt you've posted.
First, if you're going to post an excerpt from a specific paper, please provide the link that that paper and not to a review article that neither contains the information you excerpted nor contains a link to the information you excerpted. It's just common courtesy, and you should respect the authors, as well as us, enough to do so.
Second, the excerpt does not mention immunity. It says that new viral particles were found after discharge. The excerpt does not make clear whether the antiviral regimen was continued at home. Oseltamivir (which is otherwise known as Tamiflu) is a neuraminidase inhibitor, which acts to prevent viral release from previously infected cells. It does not prevent new infection of cells. Ceasing treatment could very well result in previously infected cells releasing new viral particles. Not having access to the actual paper, I can't tell exactly what was involved in the post-release quarantine. What I see suggests that Tamiflu may be a palliative that could lessen the severity of the disease if administered in early stages. However, the methodology that I can see does not constitute a valid study for establishing that.
Third, rtPCR is extremely sensitive and can result in a positive test from a very low viral load. From what I could see, there was no way to ascertain whether that viral load in those postrecovery patients could result in resumption of symptoms or being contagious.
Fourth, and most importantly, there is no mention of immune response. There is no mention of antibody titer. This means that the excerpt you provided does absolutely nothing to buttress your apparent position that COVID-19 does not provoke antibody production or immunity. The excerpt only states that new viral particles were found by rtPCR a few days later. The fact that you were apparently unaware that this excerpt does not support your position suggests that you have quite a lot to learn about how immunity works, and that you would be well-served to do more listening and less bomb-tossing.
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