Adaptive immune determinants of viral clearance and protection in mouse models of SARS-CoV-2
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Abstract
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has caused more than 160 million infections and more than 3 million deaths worldwide. Although effective vaccines are currently being deployed, the adaptive immune determinants that promote viral clearance and confer protection remain poorly defined. Using mouse models of SARS-CoV-2, we demonstrate that both humoral and cellular adaptive immunity contribute to viral clearance in the setting of primary infection. Furthermore, we find that either convalescent mice or mice that receive mRNA vaccination are protected from both homologous infection and infection with a variant of concern, B.1.351. In addition, we find that this protection is largely mediated by antibody response and not cellular immunity. These results highlight the in vivo protective capacity of antibodies generated to both vaccine and natural infection.
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Quantification of TRM cells has yielded variable results using different modified mRNA vaccine constructs in a mouse model, ranging from detection in the lungs to absence in the same tissue despite using much higher doses of 2-5 μg.
“Quantification of TRM cells has yielded variable results, as reported by others, using different modified mRNA vaccine constructs in a mouse model, ranging from their detection in the lungs14 to absence in the same tissue15 despite using it at much higher doses of 2–5 µg.”
From Efficacy of an unmodified bivalent mRNA vaccine against SARS-CoV-2 variants in female small animal models (2023) · cites this paper as [14]
The Main Text reports that vaccinated mice did not develop high levels of lung-resident memory T cells, supporting the absence attributed to this source. But it specifies a 1 µg Pfizer-BioNTech mRNA vaccine dose, not the claimed 2–5 µg; the separate citation for detection in lungs is outside this verdict. (LLM, conf=0.90)
Experimental — accuracy not yet measuredDepletion of CD8+ T cells following immunization with mRNA vaccine, prior to SARS-CoV-2 challenge, led to different outcomes in a transgenic mouse model, possibly due to the vaccine dose used and variability in nAb concentrations.
“Depletion of CD8+ T cells following immunization with mRNA vaccine, prior to SARS-CoV-2 challenge, led to different outcomes in a transgenic mouse model, possibly due to the vaccine dose used and variability in nAb concentrations14,35.”
From Efficacy of an unmodified bivalent mRNA vaccine against SARS-CoV-2 variants in female small animal models (2023) · cites this paper as [14]
The Main Text (Fig. 4 discussion; page unavailable) describes CD8+ T-cell depletion before SARS-CoV-2 challenge in mRNA-vaccinated K18-hACE2 transgenic mice. It reports similar disease protection and viral RNA levels in depleted and control mice, not a different outcome caused by depletion. The paper specifies a 1 µg vaccine dose but does not attribute differing outcomes to dose or variability in neutralizing-antibody concentrations. (LLM, conf=0.86)
Experimental — accuracy not yet measuredLowering the CV2CoV dose to 0.1 μg mRNA reduced levels of neutralizing antibodies and protected only 50% of challenged mice.
“Lowering the CV2CoV dose to 0.1 µg mRNA reduced levels of neutralizing antibodies and protected only 50% of challenged mice (Fig. S1a, c), which is in line with previous studies using modified mRNA for immunization14.”
From Efficacy of an unmodified bivalent mRNA vaccine against SARS-CoV-2 variants in female small animal models (2023) · cites this paper as [14]
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- Authors
- Israelow, B., Mao, T., Klein, J., Song, E., Menasche, B., Omer, S. B., & Iwasaki, A.
- Affiliations
- Yale University (US)
- Department of Immunobiology, Yale University School of Medicine, New Haven, CT, USA.
- Department of Laboratory Medicine, Yale University School of Medicine, New Haven, CT, USA.
- Howard Hughes Medical Institute (US)
- Corresponding author
- Iwasaki, Akiko
- ORCID
- Venue
- Science Immunology
- Published
- 2021-10-29
- Volume
- 6
- Issue
- 64
- Pages
- eabl4509-eabl4509
- ISSN
- 2470-9468 (ISSN-L)
- PMC
- PMC8142653
- OpenAlex
- W3197127917
- Cited by
- 189
- References
- 52
- Citations by year
- 2026: 9 · 2025: 23 · 2024: 26 · 2023: 43 · 2022: 67 · 2021: 21
- FWCI
- 13.05
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Science Immunology (publishedVersion)
- bioRxiv (Cold Spring Harbor Laboratory) (acceptedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (submittedVersion)
- Funders
- Howard Hughes Medical Institute
- Yale University
- National Institutes of Health (UL1TR001863)
- National Cancer Institute (F30CA239444)
- National Institute of General Medical Sciences (T32GM007205)
- National Institute of Allergy and Infectious Diseases (R01AI157488, K08AI163493, T32AI007019, T32AI007517)
- Topics
- Health Sciences › Medicine › Infectious Diseases › SARS-CoV-2 and COVID-19 Research
- Life Sciences › Immunology and Microbiology › Immunology › Immune responses and vaccinations
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › vaccines and immunoinformatics approaches
- Keywords
- SARS-CoV-2, adaptive immunity, viral clearance, humoral immunity, cell-mediated immunity, antibody response, mRNA vaccination, B.1.351 variant, Omicron variant, COVID-19 protection, mouse model
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