# Adaptive Immunity and Persistent SARS-CoV-2 Replication

> **NIH NIH U01** · UNIVERSITY OF ALABAMA AT BIRMINGHAM · 2022 · $599,569

## Abstract

Project Summary/Abstract
The pandemic caused by the novel coronavirus, SARS-CoV-2 (SARS2) has so far infected greater than
3.5 million individuals and resulted in >138,000 deaths in the US. Although it has been suggested that
adaptive immunity plays an important role in improving clinical outcomes of patients infected with
SARS2, protective immune responses have not been specifically defined. Also, the variability in clinical
disease and outcome in patients with SARS2 infection has not been explained based on qualitative and
quantitative antiviral immune responses. Interestingly, a significant proportion of children with presumed
deficits in immune competence secondary to cancer chemotherapy and hematologic disorders have
been observed to shed virus from the upper respiratory tract for prolonged periods of time (>4 weeks),
even after complete resolution of clinical symptoms. This finding raises the possibility that specific
qualitative or quantitative deficits in adaptive immune responses in some individuals can result in
incomplete control of virus replication and prolonged virus shedding. Therefore, an understanding of the
immune responses that lead to control of virus shedding could help define correlates of protective
immunity and perhaps more importantly, determine the potential value of vaccines to limit spread of
SARS2 to unvaccinated populations. The major goal of our studies is to quantify adaptive immune
responses to SARS2 in a cohort of children with varying levels immune responsiveness and to relate
these responses to the control of virus shedding in the upper respiratory tract, thus allowing stratification
immune reactivity and control of virus replication. Defining relationships between variations in immune
competence and virus shedding could provide novel insight into the level and nature of adaptive
immunity, more specifically antiviral antibodies, that can restrict or eliminate viral shedding in SARS2
infected patients. Our studies will also identify SARS2 variants that arise during poorly controlled virus
replication in these patients as prolonged virus replication coupled with ineffective immunity offers an
ideal opportunity for the generation of viral variants. Analysis of these variants in terms of the quality and
quantity of SARS2 antibody responses will help elucidate the role of SARS2 sequence variation and
persistent virus replication as a mechanism for prolonged virus replication. Together, these studies will
test our hypothesis that variations in immune responsiveness contribute to prolonged viral replication
and shedding.

## Key facts

- **NIH application ID:** 10688349
- **Project number:** 4U01CA260462-02
- **Recipient organization:** UNIVERSITY OF ALABAMA AT BIRMINGHAM
- **Principal Investigator:** Suresh B Boppana
- **Activity code:** U01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2022
- **Award amount:** $599,569
- **Award type:** 4N
- **Project period:** 2020-09-22 → 2025-03-24

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10688349

## Citation

> US National Institutes of Health, RePORTER application 10688349, Adaptive Immunity and Persistent SARS-CoV-2 Replication (4U01CA260462-02). Retrieved via AI Analytics 2026-05-23 from https://api.ai-analytics.org/grant/nih/10688349. Licensed CC0.

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