Prior to the emergence of antigenically distinct SARS-CoV-2 variants, reinfections were reported infrequently - presumably due to the generation of durable and protective immune responses . However, case reports also suggested that rare, repeated infections may occur as soon as 48 days following initial disease onset . The underlying immunologic deficiencies enabling SARS-CoV-2 reinfections are currently unknown . Here we describe a renal transplant recipient who developed recurrent, symptomatic SARS-CoV-2 infection - confirmed by whole virus genome sequencing - 7 months after primary infection . To elucidate the immunological mechanisms responsible for SARS-CoV-2 reinfection, we performed longitudinal profiling of cellular and humoral responses during both primary and recurrent SARS-CoV-2 infection . We found that the patient responded to the primary infection with transient, poor-quality adaptive immune responses . The patients immune system was further compromised by intervening treatment for acute rejection of the renal allograft prior to reinfection . Importantly, we also identified the development of neutralizing antibodies and the formation of humoral memory responses prior to SARS-CoV-2 reinfection . However, these neutralizing antibodies failed to confer protection against reinfection, suggesting that additional factors are required for efficient prevention of SARS-CoV-2 reinfection . Further, we found no evidence supporting viral evasion of primary adaptive immune responses, suggesting that susceptibility to reinfection may be determined by host factors rather than pathogen adaptation in this patient . In summary, our study suggests that a low neutralizing antibody presence alone is not sufficient to confer resistance against reinfection . Thus, patients with solid organ transplantation, or patients who are otherwise immunosuppressed, who recover from infection with SARS-CoV-2 may not develop sufficient protective immunity and are at risk of reinfection.