Table 1.

Microbes triggering bone marrow (BM) failure.

Microbe	Effects on hematopoiesis	Mechanism(s)	Target cells	Reference
Virus
Parvovirus B19	Various cytopenias	Apoptosis of target cells	Erythroid progenitor	(43, 47–50)
	Anemia	Excessive inflammatory signals IL1-β, IL6, tumor necrosis factor-α, and interferon (IFN)-γ
	Pure red cells aplasia
	Aplastic anemia (AA)
	Thrombocytopenic Purpura
Epstein–Barr virus	Thrombocytopenia	Excessive inflammatory signals: TNF-α and IFN-γ	HPSC	(54–58)
	AA	HPSC inhibition by virus-specific T-cells	T-cells
	Pure red cells aplasia
Dengue virus	Leukopenia	Apoptosis of progenitor cells	Hematopoietic stem progenitor cells, megakaryocyte progenitor	(62–65, 69, 70)
	Thrombocytopenia	Excessive inflammatory signal: multiple cytokines
	Severe AA
HAAA	AA	Excessive inflammatory signals	Indirectly HPSC?	(74–76)
		T-cell activation
		Multiple cytokines
Cytomegalovirus	AA	Stromal function failure	Mesenchymal stem cells	(77, 78)
	Anemia
Human herpes virus-6	Anemia	Apoptosis of target cells?	Granulocyte macrophage	(79, 80)
	Pancytopenia		Megakaryocyte progenitors
HIV	Anemia	Excessive growth of bacterial	HPSC	(36, 40)
		Sustained activation of pathogen recognition receptors (PRRs), TLRs by LPS or other pathogen-associated molecular patterns (PAMPs)
Bacteria
Anaplasma phagocytophilum	Pancytopenia	Excessive inflammatory signals	Circulating granulocyte	(85–88)
		Myelosuppressive cytokines
Ehrlichia chaffeensis	Pancytopenia		Granulocyte	(89, 90)
	Anemia
	Thrombocytopenia
Tuberculosis	Pancytopenia	Granuloma infiltration in BM	BM niche	(91–93)
		Maturation arrest?
		Hypersplenism?	HPSC?
		Histiocytic hyperplasia?
Dysbiosis	Anemia?	Persistent release of PAMPs?	HPSC?	(11, 34, 36, 38, 40)
	AA?	Sustained stimulation of HPSCs via PRRs?