The only known natural host cell of PB19 is the human erythroid progenitor cell. PB19 is a potent inhibitor of hematopoiesis. The cellular receptor for PB19 is globoside or P-antigen, which is found on erythrocyte progenitor cells, synovium, placental tissue, fetal myocardium, and endothelial cells. The B19-associated red blood cell aplasia is related to caspase-10–mediated apoptosis of erythrocyte precursors. Infection with PB19 is usually acquired through respiratory droplets, but the virus can also be transmitted by blood or blood products and vertically from mother to fetus. In children and adults, viremia develops 2 days after exposure and reaches its peak at ∼1 week. During the phase of viral replication and shedding, the patient is generally asymptomatic. When the typical rash (characterized by a “slapped cheek” appearance on the face and a “lace-like” erythematous rash on the trunk and extremities) or arthralgias develop, the patient is no longer infectious to others. Symptoms during pregnancy are nonspecific and include a flulike syndrome with a low-grade fever, sore throat, generalized malaise, and headache. Pregnant women rarely develop the characteristic “slapped cheek.” The fetus may become infected during the maternal viremic stage. Because of active erythropoiesis in the fetus with a shortened red-cell life span, marked fetal anemia, high-output cardiac failure, and fetal hydrops may develop. Myocarditis, and less often fetal hepatic infection, may contribute to fetal cardiac failure. Teratogenicity from PB19 has been described in case reports; also, one recent study found high prevalence of trisomy in pregnancy loss ascribable to PB19/erythrovirus infection. Despite that, PB19 is considered nonteratogenic based on large epidemiologic studies.