A COVID-19 Patient with Repeatedly Undetectable SARS-CoV-2 Antibodies

Goetz, Lianna; Yang, Jianbo; Greene, Wallace; Zhu, Yusheng

doi:10.1093/jalm/jfaa137

Cited by 11 publications

(13 citation statements)

References 7 publications

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“…The current knowledge about COVID-19 in cases with underlying immunodeficiency is scarce [18][19][20][21][22][23][24]. Comparing to previous data reported mainly primary antibody deficient and male patients with COVID-19 infection (Table S4), we did not observe the dominancy of infected patients in this PID category despite their high frequency among the national registry with no deceased patient.…”

Section: Discussioncontrasting

confidence: 85%

Impact of SARS-CoV-2 Pandemic on Patients with Primary Immunodeficiency

et al. 2020

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Although it is estimated that COVID-19 life-threatening conditions may be diagnosed in less than 1:1000 infected individuals below the age of 50, but the real impact of this pandemic on pediatric patients with different types of primary immunodeficiency (PID) is not elucidated. The current prospective study on a national registry of PID patients showed that with only 1.23 folds higher incidence of infections, these patients present a 10-folds higher mortality rate compared to population mainly in patients with combined immunodeficiency and immune dysregulation. Therefore, further management modalities against COVID-19 should be considered to improve the survival rate in these two PID entities using hematopoietic stem cell transplantation and immunomodulatory agents.

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Section: Discussioncontrasting

confidence: 85%

Impact of SARS-CoV-2 Pandemic on Patients with Primary Immunodeficiency

et al. 2020

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“…Conformational change of spike protein to postfusion form may cause failure to form neutralizing antibodies in many individuals against natural infections as well as in response to vaccines. Whereas, any such report from the running trials of COVID‐19 vaccines are still not known, failure to form neutralizing antibodies (directed to spike proteins) against natural SARS‐CoV‐2 infection in some patients has been occasionally reported 33–35 …”

Section: Sars‐cov‐2‐specific Virulence Factorsmentioning

confidence: 99%

SARS‐CoV‐2‐specific virulence factors in COVID‐19

Kumar

Prasoon

Kumari

et al. 2020

Journal of Medical Virology

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The paucity of knowledge about severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2)‐specific virulence factors has greatly hampered the therapeutic management of patients with coronavirus disease 2019 (COVID‐19). Recently, a cluster of studies appeared, which presented empirical evidence for SARS‐CoV‐2‐specific virulence factors that can explain key elements of COVID‐19 pathology. These studies unravel multiple structural and nonstructural specifics of SARS‐CoV‐2, such as a unique FURIN cleavage site, papain‐like protease (SCoV2‐PLpro), ORF3b and nonstructural proteins, and dynamic conformational changes in the structure of spike protein during host cell fusion, which give it an edge in infectivity and virulence over previous coronaviruses causing pandemics. Investigators provided robust evidence that SARS‐CoV‐2‐specific virulence factors may have an impact on viral infectivity and transmissibility and disease severity as well as the development of immunity against the infection, including response to the vaccines. In this article, we are presenting a summarized account of the newly reported studies.

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“…Some patients with very little Ab response still can effectively clear COVID‐19 (Goetz, Yang, Greene, & Zhu, 2020),…”

Section: Covid‐19 Convalescent Plasma Contains Important Exosomes Likmentioning

confidence: 99%

“…These differences between results of the current huge FDA Mayo clinic study and prior experiences, suggest that something is very different in this case of use of convalescent plasma in very ill COVID‐19 patients. The result could have to do with the particularly meager role of Ab and associated other dysfunctional aspects of the particular immune response in COVID‐19 patients (Frey et al., 2008; Goetz et al., 2020; Hassanpour et al., 2020; Kaneko et al., 2020; Kreer et al., 2020; Lucas et al., 2020; Okoye et al., 2014; Quinti et al., 2020; Robbiani et al., 2020; Rosendahl Huber et al., 2014; Seow et al., 2020; Soresina et al., 2020; Thornton & Harel, 2020; Yoshikawa et al., 2019), or perhaps negative acting exosomes in the convalescent plasma.…”

Section: Covid‐19 Convalescent Plasma Contains Important Exosomes Likmentioning

confidence: 99%

“…At the moment, it is not clear that convalescent plasma works at all in COVID‐19 despite the mistaken FDA blessing as an approved emergency therapy that has resulted in huge recruiting programs throughout the country for a therapy that likely will have little effect. There is sufficient alternate evidence, like recovery of patients with little or no antibodies (Goetz et al., 2020; Seow et al., 2020; Soresina et al., 2020; Thornton & Harel, 2020), to postulate that the antibodies actually have little effect and that immune resistance is principally due to T cell mechanisms not represented by the exosomes that may still be in a pro‐illness mode. This would account for the observations that COVID‐19 convalescent plasma has weak beneficial effects compared to what was expected.…”

Section: Conclusion Per Convalescent Plasmamentioning

confidence: 99%

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COVID‐19 therapy with mesenchymal stromal cells (MSC) and convalescent plasma must consider exosome involvement: Do the exosomes in convalescent plasma antagonize the weak immune antibodies?

Askenase

2020

J of Extracellular Vesicle

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Exosome extracellular vesicles as biologic therapy for COVID‐19 are discussed for two areas. The first involves the growing use of mesenchymal stromal cells (MSCs) for the profound clinical cytokine storm and severe pneumonia in COVID‐19 patients. Instead, it is recommended to treat alternatively with their MSC‐released exosomes. This is because many reports in the literature and our data have shown that the release of exosomes from the in vivo administered MSC is actually responsible for their beneficial effects. Further, the exosomes are superior, simpler and clinically more convenient compared to their parental MSC. Additionally, in the context of COVID‐19, the known tendency of MSC to intravascularly aggregate causing lung dysfunction might synergize with the pneumonia aspects, and the tendency of MSC peripheral vascular micro aggregates might synergize with the vascular clots of the COVID‐19 disease process, causing significant central or peripheral vascular insufficiency. The second exosome therapeutic area for severe COVID‐19 involves use of convalescent plasma for its content of acquired immune antibodies that must consider the role in this therapy of contained nearly trillions of exosomes. Many of these derive from activated immune modulating cells and likely can function to transfer miRNAs that acting epigenetically to also influence the convalescent plasma recipient response to the virus. There is sufficient evidence, like recovery of patients with antibody deficiencies, to postulate that the antibodies actually have little effect and that immune resistance is principally due to T cell mechanisms. Further, COVID‐19 convalescent plasma has remarkably weak beneficial effects if compared to what was expected from many prior studies. This may be due to the dysfunctional immune response to the infection and resulting weak Ab that may be impaired further by antagonistic exosomes in the convalescent plasma. At the least, pre selection of plasma for the best antibodies and relevant exosomes would produce the most optimum therapy for very severely affected COVID‐19 patients.

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A COVID-19 Patient with Repeatedly Undetectable SARS-CoV-2 Antibodies

Cited by 11 publications

References 7 publications

Impact of SARS-CoV-2 Pandemic on Patients with Primary Immunodeficiency

Impact of SARS-CoV-2 Pandemic on Patients with Primary Immunodeficiency

SARS‐CoV‐2‐specific virulence factors in COVID‐19

COVID‐19 therapy with mesenchymal stromal cells (MSC) and convalescent plasma must consider exosome involvement: Do the exosomes in convalescent plasma antagonize the weak immune antibodies?

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