There is an imperative need to determine the durability of adaptive immunity to SARS-CoV-2. We enumerated SARS-CoV-2-reactive CD4+ and CD8+ 28 T 29 cells targeting S1 and M proteins and measured RBD-specific serum IgG over a period 30 of 2-6 months after symptoms onset in a cohort of subjects who had recovered from 31 severe clinical forms of COVID-19

Experimental evidence supports a major role of neutralizing antibodies (NtAb) and 54 skewed Th1 functional immune responses in preventing and controlling SARS-CoV-2 55 infection [1-4]. Epitopes eliciting NtAb have been mapped within all SARS-CoV-2 56 structural proteins; among these, NtAbs targeting the receptor binding domain (RBD) of 57 the viral spike protein (S) appear to display maximum specificity and potency [5-7]. 58 Broad specificity to structural and non-structural proteins has been reported across SARS-CoV-2-reactive CD4+ and CD8+ 59 T cells, of which S, membrane (M) and 60 nucleocapsid (N) proteins are immunodominant in most individuals [8-18]. Both SARS61 CoV-2-specific NtAb and T cells are readily detectable in a large proportion of acute or 62 short-term convalescent COVID-19 patients [8-18], although the strength of adaptive 63 immune responses may be modulated by the severity of the disease [1-4]. Data on 64 SARS-CoV infection suggest that memory B and T cells have a potential for long65 lasting persistence (over years) [19,20], yet the durability of SARS-CoV-2 adaptive 66 immunity remains to be established. Determining whether SARS-CoV-2 B- and T-cell 67 responses persist over time following natural infection or after vaccination seems of 68 paramount relevance in designing effective public health policies to prevent virus 69 transmission and spread. In the current study we enumerated SARS-CoV-2-reactive CD4+ and CD8+ 70 T cells targeting S and M proteins, and measured IgG antibodies 71 binding to RBD of S protein, along a timeframe of up to 6 months after symptoms onset 72 in a cohort of recovered COVID-19 patients who had been hospitalized due to severe 73 clinical forms of the disease.

Thanks and Regards,

Alpine

Associate Editor

Journal of Clinical Trials

clinicaltrials@eclinicalsci.com