Evidence of robust memory T‐cell responses in patients with chronic myeloproliferative neoplasms following infection with severe acute respiratory syndrome coronavirus‐2 (SARS‐CoV‐2)

• Published in: British Journal of Haematology 2021-05, Vol.193 (4), p.692-696
• Main Authors: Harrington, Patrick, Harrison, Claire N., Dillon, Richard, Radia, Deepti H., Rezvani, Katayoun, Raj, Kavita, Woodley, Claire, Curto‐Garcia, Natalia, O’Sullivan, Jennifer, Saunders, Jamie, Kordasti, Shahram, Ali, Sahra, Lavallade, Hugues, McLornan, Donal P.
• Format: Article
• Language: English
• Subjects: Chronic infection; CML; Coronaviruses; Correspondence; COVID‐19; Hematology; immunity; myeloproliferative neoplasm; Severe acute respiratory syndrome coronavirus 2; T cell
• ISSN: 0007-1048; 1365-2141
• DOI: 10.1111/bjh.17402

Collaborative cohort analyses reporting clinical sequelae following SARS‐CoV‐2 infection in patients with either a classical ‘Philadelphia Chromosome’ negative myeloproliferative neoplasm (MPN) or chronic myeloid leukaemia (CML) have recently been published.2, 3 Outcomes were varied but, to date, older patients, those with myelofibrosis (MF) and those who had sudden discontinuation of the Janus kinase (JAK) inhibitor (JAKi) ruxolitinib had worse outcomes. Chronic MPN, in particular MF, are associated with a pro‐inflammatory state and inherent dysregulation of pivotal natural killer (NK) cell, regulatory T‐cell and effector T‐cell function.4 These heterogeneous defects are likely modified by patient age, disease subtype and stage. [...]complex adaptive immune responses to significant viral challenges may potentially be attenuated by tyrosine kinase inhibitors (TKI), JAKi and other cytoreductive therapies. Given the immunomodulatory effects of JAKi such as ruxolitinib on B‐cell, T‐cell, NK‐cell and dendritic‐cell function, delineation of immune responsiveness in SARS‐CoV‐2 infected patients with MPN on such agents is required.4, 7, 8 T‐cell ‘fate’ following SARS‐CoV‐2 exposure appears dynamic, dependent on both host characteristics and indeed the severity of infection.9-11 As suggested by Altmann et al.,12 responses to SARS‐CoV‐2 can in fact become ‘uncoupled’ with discordant B‐ and T‐cell priming and memory. [...]the importance of a memory T‐cell response is intimated by evidence from the SARS‐CoV‐1 infection, whereby patients demonstrated relatively transient antibody responses with longer lasting T‐cell immunity.13 Further understanding of such is paramount for correct timing of immunosuppressive drugs in the disease course, optimisation of assays to assess surrogate correlates of longer‐term ‘protection’ and underpinning of future vaccination strategies.