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gandhi, s., klein, j., robertson, a., pena-hernandez, m. a.,
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lin, m. j., roychoudhury, p., lu, p., fournier, j., ferguson, d., mohamed bakhash, s. a., muenker, m. c., srivathsan, a., wunder, e. a., kerantzas, n., wang, w., pyle, a., wilen, c. b., ogbuagu, o., greninger ,
sars-cov-2 remdesivir resistance mutations have been generated in vitro but have not been reported in patients receiving treatment with the antiviral agent. we present a case of an immunocompromised patient with acquired b-cell deficiency who developed an indolent, protracted course of sars-cov-2 infection. remdesivir therapy alleviated symptoms and produced a transient virologic response, but her course was complicated by recrudescence of high-grade viral shedding. whole genome sequencing identified a mutation, e802d, in the nsp12 rna-dependent rna polymerase which was not present in pre-treatment specimens. in vitro experiments demonstrated that the mutation conferred a ~6-fold increase in remdesivir ic50 but resulted in a fitness cost in the absence of remdesivir. sustained clinical and virologic response was achieved after treatment with casirivimab-imdevimab. although the fitness cost observed in vitro may limit the risk posed by e802d,
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, this case illustrates the importance of monitoring for remdesivir resistance and the potential benefit of combinatorial therapies in immunocompromised patients with sars-cov-2 infection.
