A patient with sickle cell disease develops sudden-onset severe anemia, reticulocytopenia, and absent erythroid precursors in the bone marrow during a febrile illness. Parvovirus B19 serology is positive. What is the pathophysiology of this aplastic crisis?

• A Parvovirus B19 infects mature red cells causing hemolysis via complement
• B Parvovirus B19 triggers autoimmune hemolysis via molecular mimicry with RBC antigens
• C Parvovirus B19 causes splenic sequestration of reticulocytes
• D Parvovirus B19 infects erythroid progenitors (BFU-E/CFU-E) via P antigen (globoside), halting erythropoiesis ✓

Explanation

Parvovirus B19 selectively infects erythroid progenitor cells (BFU-E and CFU-E) by binding to P antigen (globoside, CD36 complex) on their surface. This causes transient arrest of erythropoiesis (pure red cell aplasia) for 7–10 days. In normal individuals this is asymptomatic, but in sickle cell disease where RBC survival is markedly shortened, even brief interruption of erythropoiesis causes severe aplastic crisis with rapid hemoglobin drop and reticulocytopenia. The marrow shows absence or marked reduction of erythroid precursors with characteristic giant pronormoblasts.

Reference: Robbins & Cotran Pathologic Basis of Disease, 10th ed.

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