Correct Answer: A. Parvovirus B-19
Parvovirus B-19 (erythrovirus) is the classic viral cause of transient aplastic anemia, particularly in children and immunocompromised patients. The virus has a tropism for erythroid progenitor cells (BFU-E and CFU-E) in the bone marrow, causing direct cytolytic infection and temporary cessation of red cell production. This results in a reticulocytopenic anemia lasting 7–10 days in immunocompetent individuals, though it may persist longer in immunocompromised hosts. The hallmark is a "giant pronormoblast" — a large, immature erythroid precursor with viral inclusions visible on bone marrow examination. In healthy children, this transient aplasia is often clinically silent because normal RBC lifespan (~120 days) masks the brief production halt. However, in patients with underlying hemolytic anemias (sickle cell, hereditary spherocytosis, G6PD deficiency), parvovirus B-19 causes aplastic crisis — acute severe anemia with reticulocytopenia, fever, and joint pain (arthralgia/arthritis). The diagnosis is confirmed by IgM serology or PCR. Management is supportive; transfusion is reserved for symptomatic anemia. This is a self-limited condition in immunocompetent hosts, distinguishing it from other viral causes of bone marrow suppression.
Why the other options are wrong
B. Polio — Poliovirus causes acute flaccid paralysis via motor neuron destruction, not bone marrow suppression. While polio can cause systemic illness, it does not target erythroid progenitors or cause aplastic anemia. This is a distractor that tests knowledge of polio's true pathophysiology. C. HIV — HIV causes chronic, progressive bone marrow suppression (pancytopenia) through direct infection of CD4+ T cells and macrophages, leading to persistent anemia, thrombocytopenia, and leukopenia — not transient aplasia. HIV-related anemia develops over months to years, not acutely. The question specifies 'transient,' which excludes HIV. D. HHV-8 — HHV-8 (Human Herpesvirus 8) is the causative agent of Kaposi sarcoma and is associated with lymphoproliferative disorders in immunocompromised patients, not aplastic anemia. It does not target erythroid progenitors. This is a distractor testing knowledge of HHV-8's true oncogenic role.
High-Yield Facts
- Parvovirus B-19 causes transient aplastic anemia by direct cytolytic infection of erythroid progenitor cells (BFU-E, CFU-E) in the bone marrow.
- Aplastic crisis occurs in patients with underlying hemolytic anemias (sickle cell, hereditary spherocytosis); presents with acute severe anemia, reticulocytopenia, fever, and arthralgia.
- Giant pronormoblasts (large immature RBC precursors with viral inclusions) are pathognomonic on bone marrow examination in parvovirus B-19 infection.
- IgM serology or PCR confirms parvovirus B-19 diagnosis; reticulocytopenia distinguishes it from other causes of anemia.
- Self-limited in immunocompetent hosts (7–10 days); may persist weeks to months in immunocompromised patients (HIV, transplant recipients).
- Fifth disease (erythema infectiosum) is the classic childhood presentation; adults present with polyarthropathy (wrists, knees, ankles).
Mnemonics
PARVOVIRUS B-19 TARGETS Parvo → Progenitors (erythroid) → Production halt → Pancytopenia (transient). Remember: Parvo = Progenitor killer. APLASTIC CRISIS TRIGGERS (in hemolytic anemias) PARVOVIRUS = Parvovirus B-19 is THE viral cause. Sickle cell patients recognize sudden severe anemia + reticulocytopenia + fever as aplastic crisis until proven otherwise.
NBE Trap
NBE pairs parvovirus B-19 with "transient" to lure students who confuse it with HIV or other chronic viral causes of bone marrow suppression. The key discriminator is the self-limited 7–10 day duration in immunocompetent hosts, not chronic progressive anemia.
Clinical Pearl
In Indian pediatric practice, parvovirus B-19 is often missed in children with sickle cell disease (common in tribal and Dravidian populations) presenting with acute severe anemia and reticulocytopenia — the aplastic crisis is life-threatening and requires urgent transfusion. A simple reticulocyte count (low, not high) is the bedside clue that differentiates this from hemolytic crisis.
_Reference: Robbins Ch. 13 (Hematopoietic and Lymphoid Systems); Harrison Ch. 211 (Viral Infections); OP Ghai Ch. 10 (Pediatric Hematology)_