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Severe COVID-19 virus reactivation following treatment for B cell acute lymphoblastic leukemia

TLDR
This case illustrates the risks of treating recently recovered COVID-19 patients with immunosuppressive therapy, particularly lymphocyte- and antibody-depleting therapy, and raises new questions about the potential of SARS-CoV-2 reactivation.
Abstract
SARS-CoV-2 has infected millions of people worldwide, but little is known at this time about second infections or reactivation. Here, we report a case of a 55-year-old female undergoing treatment for CD20+ B cell acute lymphoblastic leukemia who experienced a viral reactivation after receiving rituximab, cytarabine, and dasatinib. She was initially hospitalized with COVID-19 in April and developed a high antibody titer with two negative nasal polymerase chain reaction (PCR) swabs for SARS-CoV-2 on discharge. After recovery, she resumed treatment in June for her leukemia, which included rituximab, cytarabine, and dasatinib. She promptly lost her COVID-19 antibodies, and her nasal PCR turned positive in June. She developed a severe COVID-19 pneumonia with lymphopenia, high inflammatory markers, and characteristic bilateral ground-glass opacities on chest CT, requiring high-flow nasal cannula and transfer to the intensive care unit. She received steroids, anticoagulation, and convalescent plasma, and within 48 h she was off oxygen. She was discharged home in stable condition several days later. Given the short time frame from leukemia treatment to PCR positivity and the low case rate in mid-June in New York City, reinfection appears to have been unlikely and SARS-CoV-2 reactivation is a possible explanation. This case illustrates the risks of treating recently recovered COVID-19 patients with immunosuppressive therapy, particularly lymphocyte- and antibody-depleting therapy, and raises new questions about the potential of SARS-CoV-2 reactivation.

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Long COVID or Post-acute Sequelae of COVID-19 (PASC): An Overview of Biological Factors That May Contribute to Persistent Symptoms

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COVID-19 and autoimmune diseases.

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Mechanisms underlying low-clinical responses to PD-1/PD-L1 blocking antibodies in immunotherapy of cancer: a key role of exosomal PD-L1.

TL;DR: In this article, the role of exosomal PDL-1 in the therapeutic resistance to anti-PD-1/PD-L1 treatment was reviewed. But, despite impressive treatment outcomes, some patients show poor response to PD-1 and PD-L 1 blockade.
References
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Journal ArticleDOI

SARS-CoV-2-specific T cell immunity in cases of COVID-19 and SARS, and uninfected controls.

TL;DR: Infection with betacoronaviruses induces multi-specific and long-lasting T cell immunity against the structural N protein, and SARS-CoV-2-reactive T cells were found in individuals who had recovered from SARS or COVID-19 and in unexposed donors, although with different patterns of immunoreactivity.
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Lymphopenia in severe coronavirus disease-2019 (COVID-19): Systematic review and meta-analysis

TL;DR: A systematic review and meta-analysis showed that lymphopenia on admission was associated with poor outcome in patients with COVID-19 and the association between lymphocyte count and composite poor outcome was affected by age.
Journal ArticleDOI

False negative of RT-PCR and prolonged nucleic acid conversion in COVID-19: Rather than recurrence.

TL;DR: It is found that 15 (21.4%) patients experienced a “turn positive” of nucleic acid detection by RT‐PCR test for SARS‐CoV‐2 after two consecutive negative results, which may be related to the false negative of RT‐ PCR test and prolongeducleic acid conversion.
Journal ArticleDOI

Clinical characteristics of severe acute respiratory syndrome coronavirus 2 reactivation.

TL;DR: Findings from this small group of cases suggested that there was currently evidence for reactivation of SARS-CoV-2 and there might be no specific clinical characteristics to distinguish them.
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