Government Scientists: COVID-19 Rebound Not Caused by Impaired Immune Response

Colorized scanning electron micrograph of a cell infected with the Omicron strain of SARS-CoV-2 virus particles (purple), isolated from a patient sample. Credit: NIAID

Detailed analysis of eight patients published.

Findings from a small study of eight patients suggest that ongoing COVID-19 study at the NIH Clinical Center in Bethesda, Maryland, and other local hospitals. As part of the study, participants provided blood and other samples as well as access to their COVID-19 medical records.Six participants (three men and three women with a median age of 42 years) who took Paxlovid within four days of initial symptom onset and then experienced recurrent symptoms were included in the study to evaluate COVID-19 rebound. Two participants (a 54-year-old man and a 35-year-old woman) experienced recurrent symptoms and did not take Paxlovid. Finally, a control group included six people who had COVID-19 but did not experience symptom rebound. All participants were previously vaccinated and boosted against COVID-19, and none developed severe disease requiring hospitalization during acute infection or rebound. Investigators collected data on each participant’s clinical course and performed laboratory tests on blood and nasal swab samples.Researchers found no evidence of genetic mutations that would indicate participants who experienced COVID-19 rebound were infected with a strain of SARS-CoV-2 that was resistant to Paxlovid. Additionally, they found no evidence of delayed development of antibodies in participants experiencing rebound after taking Paxlovid. In fact, investigators detected robust SARS-CoV-2 T-cell responses in rebound patients. Overall, the level of T-cell responses was greater in rebound patients than in patients with early acute COVID-19 who did not experience rebound. Infectious SARS-CoV-2 was detected by viral culture in one out of eight rebound participants.According to the authors, the findings indicate that rebound symptoms could be partially driven by the robust cellular immune response to residual viral DOI: 10.1093/cid/ciac663Irini Sereti, M.D., chief of the HIV Pathogenesis Section in the Laboratory of Immunoregulation, part of NIAID’s Division of Intramural Research, is available for comment.