Immune Responses to SARS-CoV-2 in Solid Organ Transplant Recipients.

Purpose of Review: Coronavirus disease 2019 (COVID-19) is caused by a complex interplay between severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) dynamics and host immune responses. Hosts with altered immunity, including solid organ transplant recipients, may be at increased risk of complications and death due to COVID-19. A synthesis of the available data on immune responses to SARS-CoV-2 infection is needed to inform therapeutic and preventative strategies in this special population.
Recent Findings: Few studies have directly compared immune responses to SARS-CoV-2 between transplant recipients and the general population. Like non-transplant patients, transplant recipients mount an exuberant inflammatory response following initial SARS-CoV2 infection, with IL-6 levels correlating with disease severity in some, but not all studies. Transplant recipients display anti-SARS-CoV-2 antibodies and activated B cells in a time frame and magnitude similar to non-transplant patients-limited data suggest these antibodies can be detected within 15 days of symptom onset and may be durable for several months. CD4 + and CD8 + T lymphopenia, a hallmark of COVID-19, is more profound in transplant recipients, but SARS-CoV-2-reactive T cells can be detected among patients with both mild and severe disease.
Summary: The limited available data indicate that immune responses to SARS-CoV-2 are similar between transplant recipients and the general population, but no studies have been sufficiently comprehensive to understand nuances between organ types or level of immunosuppression to meaningfully inform individualized therapeutic decisions. The ongoing pandemic provides an opportunity to generate higher-quality data to support rational treatment and vaccination strategies in this population.
Competing Interests: Conflict of InterestDr. Phadke was supported in part by Imagine, Innovate, and Impact (I3) Funds from the Emory University School of Medicine and through the Georgia CTSA NIH award (UL1-TR002378). Dr. Scanlon was supported by the NIH R38 Stimulating Access to Research in Residency (StARR) grant through the NIH/NIAID (5R38AI140299-02). Dr. Jordan reports receiving grants and non-financial support from CSL Behring during the preparation of this manuscript, and grants and personal fees from CSL Behring, Hansa Biopharma, Regeneron, and Amplyx outside the submitted work. Dr. Jordan has patents for the use of IL-6 inhibitors for desensitization and treatment of antibody-mediated rejection in transplant recipients, the use of clazakizumab to desensitize and improve renal transplantation in HLA-sensitized patients and to treat chronic antibody-mediated rejection of organ transplants, and the use of calcineurin inhibitor–free CTLA4-Ig with anti-IL-6/IL-6R for long-term immunosuppression in solid organ transplant recipients, all licensed to CSL Behring. All are outside the submitted work. Dr. Rouphael was supported by the Immunophenotyping Assessment in a COVID-19 Cohort (IMPACC) grant through the NIH/DAIT (5U19AI090023).
(© The Author(s), under exclusive licence to Springer Nature Switzerland AG part of Springer Nature 2021.)