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T-cell recognition is a mych more important thing; works for at least 17 years with the close relative: SARS-COV-1. That bodes well for SARS-COV-2 as well, look at Sweden (and New York).

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That depends on whether CD4/CD8+ dysregulation continues long after infection ceases and if there is a recovery if new CD8+ T cells have antigen recognition. If the imbalance continues or if there isn't antigen recognition in CD8+ T cells it is more likely to result in an over-reactive immune response. CD4 T cells call up cytokines, CD8+ T cells kill the virus. Lacking virus kill off things go out of control.

Which may be the cause in several cases of second infections that are worse then the initial infection. Elevated CD4 cells may also be the initiating factor for longhaulers.