Fig. 1
a | Infection with SARS-CoV-2 leads to activation of innate immunity and dendritic cells (DCs), which will drive the induction of virus-specific T cell and B cell responses. Little is currently known concerning the memory response to SARS-CoV-2, but this will be important for developing an effective vaccine. b | A predicted time-course of adaptive immunity to SARS-CoV-2. CTL, cytotoxic T lymphocyte; TFH, T follicular helper cell; TH, T helper cell; Treg, regulatory T cell.

Recent reports that antibodies to SARS-CoV-2 are not maintained in the serum following recovery from the virus have caused alarm. However, the absence of specific antibodies in the serum does not necessarily mean an absence of immune memory. University of Bergen researchers have just published a paper on Nature Reviews Immunology.

Immunity after infection with the coronaviruses may last from months to several years. Interestingly, cross-reactive immune responses to HCoVs may be boosted after severe infection; 12 of 20 patients infected with SARS-CoV had at least fourfold increases in IgG that cross-reacted with OC43 and/or 229E HCoVs.

It is still unclear how long immunity to SARS-CoV-2 lasts after recovery from infection. A recent report suggesting that antibodies to the virus may only be maintained for 2 months has caused speculation that ‘immunity’ to the virus may not be long lived.

Similarly, a rapid decline in antibodies was reported in mild cases, although with a half-life of approximately 21 days for IgG we would expect this decrease. It is important to remember that memory B cells and T cells may be maintained even if there are not measurable levels of serum antibodies. In this paper it’s outlined current understanding of B cell and T cell immunity to SARS-CoV-2 and potential immune correlates of protection that could inform vaccine efficacy studies 

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