A 61-year-old man was referred to the haematology department with progressive lymphadenopathy and weight loss. He was receiving haemodialysis for end-stage renal failure secondary to IgA nephropathy. He had been off immunosuppressive therapy for three years after a failed renal transplant. Needle-core biopsy of a supraclavicular node demonstrated Epstein–Barr virus (EBV)-positive classical Hodgkin lymphoma [EBV viral polymerase chain reaction (PCR) 4800 copies/ml; log10 3·68]. Fluorodeoxyglucose-positron emission tomography/computed tomography (FDG-PET/CT) revealed avid stage IIIs disease (left image, PET scan, and supplementary image PET/CT). Shortly after diagnosis he was admitted with breathlessness and wheeze and was diagnosed with PCR-positive SARS-CoV-2 pneumonia. After 11 days of best supportive ward-based care he was discharged to convalesce at home. No corticosteroid or immunochemotherapy was administered.

Four months later, palpable lymphadenopathy had reduced and an interim PET/CT scan revealed widespread resolution of the lymphadenopathy and reduced metabolic uptake throughout (right image and supplementary image). The EBV viral PCR had also fallen to 413 copies/ml (log10 2·62).

We hypothesise that the SARS-CoV-2 infection triggered an anti-tumour immune response, as has been described with other infections in the context of high-grade non-Hodgkin lymphoma.1 The putative mechanisms of action include cross-reactivity of pathogen-specific T cells with tumour antigens and natural killer cell activation by inflammatory cytokines produced in response to infection.