HIV-related Differences in Placental Immunology: Data From the PRACHITi Cohort in Pune, India

与 HIV 相关的胎盘免疫学差异:来自印度浦那 PRACHITi 队列的数据

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Background

Maternal HIV infection can affect placental immunology and expression of the neonatal crystallizable fragment receptor (FcRn), which allows transplacental antibody transfer. This study delineated differences in placental FcRn and T-cell expression by HIV status, with or without viral suppression.

Conclusions

Maternal HIV, even with viral suppression, is associated with lower placental FcRn expression and increased placental CD8+ T cells. These results suggest that dysregulation may not be completely reversed by antiretroviral therapy and could contribute to poorer infant outcomes, even in the absence of mother-to-child HIV transmission.

Methods

This observational cohort study in Pune, India, followed pregnant women with and without HIV through 1 year postpartum; 42 had placenta collected, stratified by HIV status. FcRn expression was analyzed by Western blot (normalized by GADPH) and compared using ImageJ. Placental CD4/CD8 abundance was assessed by immunofluorescent counting per high powered field.

Results

The median gestational age at delivery was 38.3 weeks (interquartile range [IQR] 37.5-39.1). Of 18 women living with HIV, all were on combined antiretroviral therapy with a median CD4 of 455 cells/mm3 (IQR 281-640) at entry and 429 cells/mm3 (IQR 317-686) at delivery. Ten had undetectable virus (≤40 copies/mL); of those with detectable virus, the median viral load was 151 copies/mL (IQR 118.15-539 334). Relative placental FcRn expression was lower in women living with HIV compared to without (median 0.54 vs 0.84, P = .01) and not associated with CD4 or viral load. Women with HIV had significantly higher abundance of placental CD8+ T cells, regardless of viral suppression, compared to women without. Conclusions: Maternal HIV, even with viral suppression, is associated with lower placental FcRn expression and increased placental CD8+ T cells. These results suggest that dysregulation may not be completely reversed by antiretroviral therapy and could contribute to poorer infant outcomes, even in the absence of mother-to-child HIV transmission.

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