Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) remains an ongoing therapeutic challenge among patients with antibody deficiencies, herein referred to as immunocompromised patients [1, 2]. Among immunocompromised patients, the ability to generate endogenous antibodies against SARS-CoV-2 in response to either natural infection or vaccination is frequently absent or attenuated compared with healthy individuals [1–3]. This impaired immunogenicity among immunocompromised patients is associated with increased vulnerability to SARS-CoV-2 infection, poor clinical outcomes, and, in some patients, persistent or smoldering SARS-CoV-2 infections that last for months or even years [4–6]. In patients with smoldering SARS-CoV-2 infection, acute respiratory distress syndrome (ARDS) pathophysiology is usually not seen. This is because the immunocompromised state also limits the patient’s ability to generate the systemic inflammatory response that is central to ARDS. Patients with smoldering SARS-CoV-2 infections also demonstrate prolonged viral shedding, including novel variants that evolve in the immunocompromised host [7]. In this context, evolution of new viral variants in immunocompromised patients that are resistant to various therapies could theoretically put the general population at risk for a new wave of infection [8–10].
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Senefeld et al. (2023) studied this question.
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