Luuydin ja koronavirus

(1)  Sarsin osalta  mainittu reaktiivinen hemofagosytoosi.

Bone Marrow  (Luuydin)  ja   koronavirukset fokuksessa.

https://ajp.amjpathol.org/article/S0002-9440(10)61329-6/fulltext#cesec80

In some cases, evidence of reactive hemophagocytosis or bone marrow hypoplasia was present.^{13, 25, 38} In other cases, however, active bone marrow without reactive hemophagocytosis has been demonstrated.¹¹ In situ hybridization and IHC have detected neither viral genomic sequences nor antigens.^{30, 31} Both viral isolation and RT-PCR performed on bone marrow were negative.^{11, 25, 31}

 2)  Voisiko  SARS2 infektiossa kehittyöä jollekulle hemofagosytoottinen oireyhtymä luuytimeen?
Tästä näkyy muutama maininta netissä   " Harvemmin esiintyy reaktiivista hemofagosytoosia" LÄHDE:
 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1829448/

3)  Mitä tarkoittaa HEMOFAGOSYTOOSI? 

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4062561/

Hemophagocytosis is the engulfment of hematopoietic cells by activated macrophages acting outside of usual immune system regulations. Hemophagocytic lymphohistiocytosis (HLH) covers a wide array of related diseases including HLH, autosomal recessive familial HLH (FHL), familial erythrophagocytic lymphohistiocytosis, viral-associated hemophagocytic syndrome, and autoimmune-associated macrophage activation syndrome (MAS). These disorders feature severe cytopenias due to this uncontrolled hemophagocytosis. Other laboratory signs and clinical symptoms result from disordered immune regulation and cytokine storm. The term primary HLH refers to an underlying genetic abnormality causing the disorder, whereas secondary HLH indicates that the disorder is secondary to underlying conditions such as infection, autoimmune/rheumatologic, malignant, or metabolic conditions. For the purposes of this review, FHL will indicate cases with a primary genetic cause, secondary HLH will refer to cases secondary to infection, malignancy, or metabolic disorders, and MAS will refer to cases associated with autoimmune diseases.

Much has been learned about HLH in the 75 years since it was first discovered. One of the earliest descriptions of the disease was in 1939 when Scott and Robb-Smith1 described a disorder featuring erythrophagocytosis by proliferating histiocytes in the lymphoreticular system and called it “histiocytic medullary reticulosis” or HMR. It was later classified among malignant histiocytosis. Later in 1952, the familial form of HLH, FHL, was more fully described by Farquhar and Claireaux2 with the cases of two siblings who succumbed to HLH, and later in 1958, another sibling from this same family presented in the same manner.3 Risdall was among the first to describe a viral association with HLH and proposed that the condition be called virus-associated HLH, distinct from malignant histiocytosis.4 In the years since, researchers have recognized the wide scope of this disease and the fact that infection often triggers both primary and secondary HLH. Regardless of cause, physiologically, HLH is characterized by defective cytotoxic cell function coupled with unbridled macrophage activity, leading to excessive cytokine production, subsequent immune dysregulation, and tissue damage. Left untreated, the dysregulated inflammatory response causes severe neutropenia, and patients often die from bacterial or fungal infections. The condition carries high morbidity and mortality.5 Long-term survival in 1983 was estimated to be as low as 4%.6 The median survival without treatment is estimated at <2 a="" aria-expanded="false" aria-haspopup="true" class=" bibr popnode tag_hotlink tag_tooltip" href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4062561/#b6-jbm-5-069" id="__tag_383968853" months.="" role="button">6