Congenital Rubella Syndrome with Rubella Virus‐associated Generalized Brownish Macules, Indurated Erythemas, Papules, and Pigmentation

Senô, Akemi; Tada, Jôji; Matsuura, Hironori; Arata, Jirô; Isomura, Hiroki; Kitamura, Tatsuya; Oda, Megumi; Katow, Shigetaka

doi:10.1111/j.1346-8138.1994.tb01747.x

Cited by 8 publications

(1 citation statement)

References 7 publications

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“…Virus egress was equally efficient from A549 (Figure 1B), another human cell culture tested here. Moreover, attempts to identify intracellular virus in tissues of CRS fetuses were mostly unsuccessful indicating efficient RV secretion from cells in vivo [48,49]. Taken together these observations suggest that the wtRV egress mechanism is fine-tuned to human cells or possibly to particular human cell types.…”

Section: Discussionmentioning

confidence: 99%

Persistent Infection of Human Fetal Endothelial Cells with Rubella Virus

et al. 2013

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Cardiovascular abnormalities are the leading cause of neonatal death among patients with congenital rubella syndrome (CRS). Although persistence of rubella virus (RV) in fetal endothelium has been repeatedly suggested as a possible cause of cardiovascular birth defects, evidence of the permissiveness of fetal endothelial cells to RV is lacking. In this study we evaluated the ability of RV to infect and persist in primary fetal endothelial cells derived from human umbilical vein (HUVEC). We found that wild type (wt) low passage clinical RV productively infected HUVEC cultures without producing cytopathology or ultrastructural changes. RV did not inhibit host cell protein synthesis, cell proliferation, or interfere with the cell cycle. Persistently infected cultures were easily established at low and high multiplicities of infection (MOI) with both laboratory and wt clinical RV strains. However, synchronous infections of entire HUVEC monolayers were only observed with clinical RV strains. The release of infectious virions into media remained at consistently high levels for several subcultures of infected HUVEC. The results indicate that macrovascular fetal endothelial cells are highly permissive to RV and allow slow persistent RV replication. The findings provide more evidence for the suggestion that vascular pathologies in CRS are triggered by persistent rubella virus infection of the endothelium.

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Section: Discussionmentioning

confidence: 99%