SHILL ALERT! Cody Snodgres is REALLY Jerry Boswell of TX CCHR!

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Ultimate Theory - All The Pieces Put Together, Everything Explained - Virus Code Cracked - Sources Provided - TL;DR: T-cell infection silent first wave, infected macrophage delayed release time bomb, second wave antibody dependent enhancement more severe illness.
Grain of Salt
Here are some weird features of SARS-CoV-2, all of which make it quite different from other viruses:

Asymptomatic spread [link to www.discovermagazine.com (secure)]

High number of carriers who had no to mild symptoms [link to www.tellerreport.com (secure)]

Despite no massive immediate outbreak within the early weeks, evidence of very high R0 [link to wwwnc.cdc.gov (secure)]

Undulant symptoms, recurring sickness after "recovery" [link to www.usnews.com (secure)]

Leaps in severity, higher than expected death rate, higher number of sick young people than expected. [link to www.theguardian.com (secure)]

Low to no antibodies in recovered persons [link to www.scmp.com (secure)]

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Here's evidence about what SARS-CoV-2 can do:

Infects T-Cells (does not replicate in T-Cells, just enters them and kills them, killing the virus too) [link to www.nature.com (secure)]

Infects macrophages (no proof SARS-2 does this, but SARS could in vitro) [link to www.ncbi.nlm.nih.gov (secure)]

Macrophage infection feline coronaviruses cause granulomates (SARS-2 is basically a bat/animal virus, not a human coronavirus) [link to en.wikipedia.org (secure)]

Discussion of granulomatic disease: [link to en.wikipedia.org (secure)] [link to en.wikipedia.org (secure)] Basically, the innate immune system creates pockets meant to contain and dissolve pathogens, but some pathogens can survive this process and end up hiding in the pockets so the adaptive immune system won't end up developing antibodies because it can't "see" the disease.

Early evidence that SARS-2 might be causing Antibody Dependent Enhancement [link to www.nature.com (secure)]

Discussion of ADE in Dengue and in SARS vaccine development [link to en.wikipedia.org (secure)] With ADE (antibody dependent enhancement), a disease causes a mild first infection, and the body recovers, producing antibodies. Next time you get the disease, the adaptive immune system will identify it when antibodies bind to it, and will then hunt down and kill it off. When a close serotype of that disease, however, infects, the antibodies will bind to it, but instead of being killed, the disease will bind to immune cells for a "free ride" to spread more quickly through the body. This causes a far worse sickness. Dengue fever does this in vivo, but SARS vaccine research saw this effect in mice [link to journals.plos.org (secure)]

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Here's what I think SARS-2 does:

During the initial wave of infection, SARS-2 spreads insanely fast. You need up to 4 meters of distance to avoid airborne infection [link to www.japantimes.co.jp (secure)] . It lasts a long time on surfaces [link to www.webmd.com (secure)] . It's uniquely adapted to infect human cells easily [link to www.assaygenie.com (secure)] .

By attacking the T-cells which develop antibodies for SARS-2, the virus inhibits the immune response. This leads to no/mild symptoms in the infected, but these people are still very infected, and very infectious. At risk persons will get sick in these conditions. Most people will recover without even knowing they were sick. When the virus kills T-cells, it kills itself. Macrophages also are "eating" virions at this time as well. SARS-2 is usually defeated quite easily.

The adaptive immune system recovers, in some cases with little to no memory of SARS-2 infection. The innate immune system features macrophages which become infected. These "die" and become "granulomates" or little pockets where the virus is able to hide from the adaptive immune system.

This "hiding" cause a slow release of new virions over time as the granulomates break down and release the virions, the cause of undulant fevers and recurrant symptoms. Especially among patients whose adaptive immune system retains little to no memory of the virus, these fevers will feel like being mildly sick all over again.

When a new serotype (slightly mutated strain) of the virus is introduced things get worse - for example, the New York crisis is caused by the European strain introduced at the end of February [link to www.usatoday.com (secure)] , I'm assuming New York had a mostly unseen epidemic of the Wuhan strain from early January. The new serotype causes a cross infection with the ongoing release of the old serotype from the granulomates. This cross-infections activates ADE, which spreads both strains much more quickly and aggressively in the body. This is where the jump in serious cases occurs.

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