FOUR colony-stimulating factors influence the survival, proliferation, differentiation, and functional activation of myeloid hematopoietic cells: macrophage colony-stimulating factor (M-CSF), granulocyte colony-stimulating factor (G-CSF), granulocytemacrophage colony-stimulating factor (GM-CSF), and interleukin-3 (formerly known as multi-colony-stimulating factor).1 2 3 Various other cytokines and factors are also implicated in these processes, including interleukins 1, 5, 6, and 11 and the recently identified Steel factor (variously designated c-kit ligand, mast-cell growth factor, and stem-cell factor).4 , 5 Of these factors, only G-CSF and GM-CSF are commercially available for clinical use. G-CSF has been approved in the United States and major European countries for the reduction of infection after . . .

https://www.nejm.org/doi/pdf/10.1056/NEJM199207023270106?listPDF=true

Granulocyte Colony-Stimulating Factor and Granulocyte-Macrophage Colony-Stimulating Factor

Background Infection with human herpesvirus-6 (HHV-6) is nearly universal in infancy or early childhood. However, the course of this infection, its complications, and its potential for persistence or reactivation remain unclear. Methods We studied infants and children under the age of three years who presented to our emergency department with acute illnesses. Infants and young children without acute illness were studied as controls. HHV-6 infection was identified by blood-mononuclear-cell culture, serologic testing, and the polymerase chain reaction (PCR). Results No primary HHV-6 infection was found among 582 infants and young children with acute nonfebrile illnesses or among 352 controls without acute illness. Of 1653 infants and young children with acute febrile illnesses, 160 (9.7 percent) had primary HHV-6 infection, as documented by viremia and seroconversion. They ranged in age from 2 weeks to 25 months; 23 percent were under the age of 6 months. HHV-6 infections accounted for 20 percent of 365 vis...

https://www.nejm.org/doi/pdf/10.1056/NEJM199408183310703

Human Herpesvirus-6 Infection in Children -- A Prospective Study of Complications and Reactivation

Human herpesvirus 6 variant A (HHV-6A) and human herpesvirus 6 variant B (HHV-6B) are two closely related yet distinct viruses. These visuses belong to the Roseolovirus genus of the betaherpesvirus subfamily; they are most closely related to human herpesvirus 7 and then to human cytomegalovirus. Over 95% of people older than 2 years of age are seropositive for either or both HHV-6 variants, and current serologic methods are incapable of discriminating infection with one variant from infection with the other. HHV-6A has not been etiologically linked to any human disease, but such an association will probably be found soon. HHV-6B is the etiologic agent of the common childhood illness exanthem subitum (roseola infantum or sixth disease) and related febrile illnesses. These viruses are frequently active and associated with illness in immunocompromised patients and may play a role in the etiology of Hodgkin's disease and other malignancies. HHV-6 is a commensal inhabitant of brains; various neurologic manifestations, including convulsions and encephalitis, can occur during primary HHV-6 infection or in immunocompromised patients. HHV-6 and distribution in the central nervous system are altered in patients with multiple sclerosis; the significance of this is under investigation.

Human herpesvirus 6.

The authors present an account of haematopoietic growth factors which include the stem cell factor (SCF), factors stimulating granulocytomacrophage colonies (GM-CSF), granulocyte (G-CSF), monocytomacrophage (M-CSF) factors, erythropoietin (EPO) and also interleukin (IL) 1 to 11. Their main action is described as well as the site of action in haematopoiesis. In many of them participation in the pathogenesis of some diseases, incl. malignant ones, is anticipated. The preparation of growth factors in a recombinant-form and knowledge of their effect made it possible to use them in clinical practice. The authors mention possible indications, although in many their administration still has the character of clinical studies.

Hematopoietic growth factors. Biology and clinical applications

Greater than 80% of malaria-related mortality occurs in sub-Saharan Africa due to infections with Plasmodium falciparum. The majority of P. falciparum-related mortality occurs in immune-naive infants and young children, accounting for 18% of all deaths before five years of age. Clinical manifestations of severe falciparum malaria vary according to transmission intensity and typically present as one or more life-threatening complications, including: hyperparasitemia; hypoglycemia; cerebral malaria; severe malarial anemia (SMA); and respiratory distress. In holoendemic transmission areas, SMA is the primary clinical manifestation of severe childhood malaria, with cerebral malaria occurring only in rare cases. Mortality rates from SMA can exceed 30% in pediatric populations residing in holoendemic transmission areas. Since the vast majority of the morbidity and mortality occurs in immune-naive African children less than five years of age, with SMA as the primary manifestation of severe disease, this review will focus primarily on the innate immune mechanisms that govern malaria pathogenesis in this group of individuals. The pathophysiological processes that contribute to SMA involve direct and indirect destruction of parasitized and non-parasitized red blood cells (RBCs), inefficient and/or suppression of erythropoiesis, and dyserythropoiesis. While all of these causal etiologies may contribute to reduced hemoglobin (Hb) concentrations in malaria-infected individuals, data from our laboratory and others suggest that SMA in immune-naive children is characterized by a reduced erythropoietic response. One important cause of impaired erythroid responses in children with SMA is dysregulation in the innate immune response. Phagocytosis of malarial pigment hemozoin (Hz) by monocytes, macrophages, and neutrophils is a central factor for promoting dysregulation in innate inflammatory mediators. As such, the role of P. falciparum-derived Hz (PfHz) in mediating suppression of erythropoiesis through its ability to cause dysregulation in pro- and anti-inflammatory cytokines, growth factors, chemokines, and effector molecules is discussed in detail. An improved understanding of the etiological basis of suppression of erythropoietic responses in children with SMA may offer the much needed therapeutic alternatives for control of this global disease burden.

/pdf/severe-malarial-anemia-innate-immunity-and-pathogenesis-3ofmzvfyxe.pdf

Severe Malarial Anemia: Innate Immunity and Pathogenesis

Treatment of aplastic anemia in children with recombinant human granulocyte colony-stimulating factor.

The assay for detecting IgM neutralizing (NT) antibody activity to human herpesvirus-6 (HHV-6) was developed by using pretreatment of blood sample with staphylococcal protein A The activity was mostly present in IgM fractions of serum but not in IgA fractions separated by ultracentrifugation The assay was used for seroepidemiological studies for HHV-6 infection In primary HHV-6 infection, IgM NT antibodies appeared 5 to 7 days after onset of exanthem subitum, reached maximum titers at 2 to 3 weeks, and tended to decline to undetectable levels after 2 months In contrast, reactivation of HHV-6 observed in organ transplants showed somewhat greater degree of IgM NT antibody responses that persisted for 2 to 3 months and became undetectable 5 to 6 months after transplantation The level and persistence of NT antibody titers measured by the conventional method was generally greater than those of the IgM titers The prevalence of the IgM NT antibodies was examined in healthy individuals The antibody was first detected at 4 to 7 months of age (5%), reached maximum level at 8 to 11 months (40%), and was detectable by 4 to 6 years (17%) A few (4 to 5%) of adolescents and adults were positive for the antibody

IgM neutralizing antibody responses to human herpesvirus-6 in patients with exanthem subitum or organ transplantation.

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Treatment of aplastic anemia in children with recombinant human granulocyte colony-stimulating factor.

IgM neutralizing antibody responses to human herpesvirus-6 in patients with exanthem subitum or organ transplantation.