Parvovirus is a known culprit of transient red cell aplasia (TRCA) in children with sickle cell disease (SCD). Few reports have previously described the association between the virus and acute splenic sequestration crisis (ASSC) in the same patient. Here, we are shedding light on such a potentially serious combination by reporting two cases of siblings with SCD complicated with concurrent ASSC and TRCA and presenting a review of the relevant literature.

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We present a mortality case showcasing t(9;11)-positive acute myeloid leukemia/juvenile myelomonocytic leukemia (AML/JMML) overlap to shed light on this lethal molecular subtype of AML. In this case, the flawed assumption that JMML was to blame impeded the prompt undertaking of appropriate treatment for AML in our 14-month-old patient. This article aims to scrutinize the catastrophic sequel of such an overlap in leukemia and refutes the contemporary diagnostic methods.

Juvenile myelomonocytic leukemia (JMML) is the most confusing mimicker of KMT2A-rearranged acute myeloid leukemia (AML). Clinical presentation, age of susceptibility (infancy or early childhood) and abnormal monocytosis are common clinical features. To complicate matters, JMML morphologically resemble acute myelomonocytic leukemia (AML M4) and distinction must be made based on accurate blast and promonocyte counts. As treatment significantly varies, AML/JMML overlap can lead to catastrophic consequences that can be avoided by timely management. Therefore, meticulous knowledge of JMML is essential to treat patients with hematologic malignancies. The pathognomic feature of JMML is increased infiltration of the peripheral blood, bone marrow, and viscera by abnormal myelomonocytic cells. Molecular diagnostics has generated substantial dividends in dissecting the genetic basis of JMML. We can now molecularly confirm the diagnosis of JMML in approximately over 90% of patients who harbor driver mutations in KRAS, NRAS, PTPN11, NF1, or CBL genes. The presence of monosomy 7 is a classic feature of JMML that can support the diagnosis in many cases. On the other hand, cytogenetics and Fluorescence in situ hybridization analysis (FISH) are indispensable to differentiate KMT2A-rearranged AML from JMML. In particular, AML with t(9;11) is associated with monocytic features that can be easily mistaken for JMML.

The primary target for vaccine design and anti-viral therapeutics for the deadly severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causing coronavirus disease 2019 (COVID-19) is the coronavirus surface spike (S) glycoprotein. Like other enveloped viruses, S glycoproteins are masked by a dense sugar “coat” of host-derived glycans that mediate immune evasion by molecular mimicry through shielding the immunogenic surface proteins from host immune responses. Paradoxically, this same protective glycan shield can make these sugar-coated viruses vulnerable to immune attack by soluble lectins of the innate immune system that are still able to recognise these glycans as pathogen-associated molecular patterns (PAMPs) leading to complement activation. In reality, recombinant lectins that target virus-associated glycans have the potential to be used as anti-viral agents; and therefore, binding of recombinant lectins to viruses could represent a paradigm shift for viral infection therapy. Likewise, SARS-CoV-2- associated glycans can offer novel targets for recombinant lectins as innovative anti-SARSCoV-2 agents. Unfortunately, pharmacological hurdles currently constrain the entry of recombinant lectins into clinical trials but more vigorous research into potentially useful modifications of these agents can truly develop a new landscape of anti-viral lectin-based therapeutics.