bioRxiv : the preprint server for biology · 2026
Post-infection immune response in adults with COVID-19 with and without nirmatrelvir-ritonavir treatment and virologic rebound.
СтатьяПрепринтНазвание и аннотация: Перевод в очереди
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Ghimire Dibya, Hasund Chloe M, Colangeli John Bianchi, Liew May Y, Abar Emory, Barry Mamadou, Alexandrescu Andrew, Kotzen Benjamin L, Reynolds Zahra, Passell Eliza, Mandell Chase, Smith-Sparks Zoie, Su Karry, Boucau Julie, Glover Owen T, Leeman Brooke, Edelstein Gregory E, Choudhary Manish C, Li Yijia, Patel Naomi, Sparks Jeffrey A, Barczak Amy K, Li Jonathan Z, Siedner Mark J, Lemieux Jacob E
Аннотация
BACKGROUND: Nirmatrelvir-ritonavir (N-R) reduces morbidity and mortality from COVID-19 in high-risk individuals; however, N-R use has been associated with risk of SARS-CoV-2 virologic rebound. The mechanisms contributing to virologic rebound after N-R treatment are currently unknown. One plausible mechanism is that antiviral treatment may alter the development of immune responses to SARS-CoV-2 infection, thereby contributing to rebound after cessation of therapy.
METHODS: We profiled immune responses in a case-ascertained, longitudinal, prospective cohort of ambulatory individuals with COVID-19. Participants were grouped according to whether virological rebound occurred and whether they had received N-R treatment. We assessed antibody, T-cell, and innate responses.
RESULTS: We observed no differences in the binding or neutralizing antibody, T-cell, and innate immune responses between participants with virologic rebound compared to participants without virologic rebound. N-R use was associated with slightly weaker antibody responses overall, even after adjustment for immunosuppression.
CONCLUSION: Virologic rebound after N-R treatment is likely driven by non-immune mechanisms.
FUNDING: The project was supported by the National Institutes of Health (R01 AI 138801) and the Massachusetts Consortium on Pathogen Readiness. Its contents are solely the responsibility of the authors and do not necessarily represent the official views of the NIH.
METHODS: We profiled immune responses in a case-ascertained, longitudinal, prospective cohort of ambulatory individuals with COVID-19. Participants were grouped according to whether virological rebound occurred and whether they had received N-R treatment. We assessed antibody, T-cell, and innate responses.
RESULTS: We observed no differences in the binding or neutralizing antibody, T-cell, and innate immune responses between participants with virologic rebound compared to participants without virologic rebound. N-R use was associated with slightly weaker antibody responses overall, even after adjustment for immunosuppression.
CONCLUSION: Virologic rebound after N-R treatment is likely driven by non-immune mechanisms.
FUNDING: The project was supported by the National Institutes of Health (R01 AI 138801) and the Massachusetts Consortium on Pathogen Readiness. Its contents are solely the responsibility of the authors and do not necessarily represent the official views of the NIH.