Abstract
An understanding of protective immunity to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is critical for vaccine and public health strategies aimed at ending the global coronavirus disease 2019 (COVID-19) pandemic. A key unanswered question is whether infection with SARS-CoV-2 results in protective immunity against reexposure. We developed a rhesus macaque model of SARS-CoV-2 infection and observed that macaques had high viral loads in the upper and lower respiratory tract, humoral and cellular immune responses, and pathologic evidence of viral pneumonia. After the initial viral clearance, animals were rechallenged with SARS-CoV-2 and showed 5 log10 reductions in median viral loads in bronchoalveolar lavage and nasal mucosa compared with after the primary infection. Anamnestic immune responses after rechallenge suggested that protection was mediated by immunologic control. These data show that SARS-CoV-2 infection induced protective immunity against reexposure in nonhuman primates.
Highlights
An understanding of protective immunity to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is critical for vaccine and public health strategies aimed at ending the global coronavirus disease 2019 (COVID-19) pandemic
Individuals who recover from certain viral infections typically develop virus-specific antibody responses that provide robust protective immunity against reexposure, but some viruses, such as HIV-1 [17], do not generate protective natural immunity
We have demonstrated that SARS-CoV-2 infection in rhesus macaques provides protective efficacy against SARS-CoV-2 rechallenge
Summary
Dovirus neutralization assay [10] (Fig. 2B) and a live virus neutralization assay [11, 12] (Fig. 2C). Low but detectable levels of sgmRNA were still observed in four of nine animals in NS on day 1 after rechallenge, but sgmRNA levels declined quickly (Fig. 5E) and median peak sgmRNA levels in NS were >4.8 log lower after rechallenge compared with after the primary challenge (P = 0.0003, two-sided Mann-Whitney test; Fig. 5F). Consistent with these data, plaque assays in BAL and NS samples after rechallenge showed no recoverable virus and plaque levels were lower than those after the primary infection All animals developed anamnestic antibody responses after rechallenge regardless of the presence or absence of residual viral RNA or sgmRNA in BAL or NS, so we speculate that the protective efficacy against rechallenge was mediated by rapid immunologic control
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