High rates of congenital CMV infection in a highly CMV-endemic Ugandan population

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ID: 327337
2026
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Abstract
Abstract Background Globally, congenital CMV (cCMV) is one the most common infections during pregnancy, and can result in significant sequelae, including pregnancy loss, microcephaly, and sensorineural hearing loss (SNHL). Congenital transmission is influenced by maternal immunity, with higher risk of transmission in mothers previously naive to CMV infection. Despite this, a small body of evidence has demonstrated a high burden of congenital disease in populations with high rates of maternal preconception immunity to CMV. Here, we report on congenital CMV transmission rates and determinants in a highly CMV-endemic Ugandan population. Methods Clinical data and samples were collected from 1166 maternal-fetal dyads enrolled in a Ugandan malaria chemoprevention trial, including cord blood as well as longitudinal PBMC and serum from children through up to three years of life. Cord blood was screened by qPCR for CMV DNA and confirmed using digital droplet PCR. ELISA for CMV IgG was performed on pediatric samples at 56, 104, and 156 weeks to determine pediatric seroconversion. Results 39 of 1058 children screened were positive for congenital CMV (3.69%) (Figure 1). Placental malaria infection was significantly associated with congenital CMV (p=0.004); maternal HIV status was not significantly associated with congenital CMV transmission. In infants with cCMV, 13.2% had microcephaly <3%ile (n=5) and 21% of cCMV infants were born small for gestational age <3%ile (n=8); both were significantly associated with cCMV status (p=0.013, p=0.002, respectively). In children followed longitudinally from birth, 97.3% (248/255) acquired CMV IgG by three years of life. Conclusion Maternal preconception immunity to CMV has previously been associated with protection against congenital transmission. Despite this, we report here on a population with high rates of early life CMV acquisition and longstanding latent infection that nonetheless demonstrate both high rates of congenital CMV transmission and significant CMV-associated sequelae. While we have shown that co-infections influence this rate of transmission, these findings underscore the need to define why prior maternal CMV infection confers only partial protection against congenital CMV and to identify the immune pathways essential for preventing congenital transmission.
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Authors Amy KF Davis, Mary Prahl, Mikias Ilala, Justine Levan, Pam M Odorizzi, Mary Muhindo, Abel Kakuru, Moses R Kamya, Grant Dorsey, Margaret E. Feeney
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Journal journal of the pediatric infectious diseases society
Year 2026
DOI
10.1093/jpids/piag070/piag070.044
URL
https://academic.oup.com/jpids/article-pdf/15/Supplement_2/S19/70833271/piag070.044.pdf
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