Background: Preterm birth (PTB) rates are high in human immunodeficiency virus (HIV)-infected populations, even when on treatment. Still, only a subset of all births in HIV-infected pregnant women result in PTB, suggesting that risk factors other than HIV infection itself are also important. Inflammation is a known risk factor in uninfected populations, but its role in HIV-infected population have not been studied; in addition, the immune pathways involved are not clear and noninvasive immune markers with predictive value are lacking. Our objective was to determine the association of select markers of inflammation with PTB in HIV-1-infected pregnant women. Methods: Within a randomized trial of pregnant women receivingnevirapine (Six-Week Extended-Dose Nevirapine [SWEN] trial), we nested a case-control study (n = 107; 26 cases, 81 controls) to determine the association of maternal inflammation with PTB. Cases were defined as PTB (<37 weeks' gestational age). We assessed inflammation by measuring plasma levels of markers of general inflammation (C-reactive protein [CRP]), intestinal barrier dysfunction (intestinal fatty acid binding protein [I-FABP]), and microbial translocation/monocyte activation (soluble CD14 [sCD14] and CD163 [sCD163]). Multivariable logistic regression was used to determine the odds of PTB per log2 increase of each marker. Results: In multivariable models, there was increased odds of PTB per unit increase of log2 sCD14 (adjusted odds ratio [aOR], 2.45; 95% confidence interval [CI], 1.24-4.86), log2 sCD163 (aOR, 3.87; 95% CI, 1.43-10.49), and log2 I-FABP (aOR, 2.28; 95% CI, 1.18-4.41) but not log2 CRP (aOR, 0.72; 95% CI, .48-1.09). Conclusions: Our results show that select immune markers can identify women at higher risk for PTB in HIV-1-infected populations and suggest that modulating gut barrier integrity and microbial translocation may affect PTB. Clinical Trials Registration: NCT00061321.
RCT Entities:
Background: Preterm birth (PTB) rates are high in human immunodeficiency virus (HIV)-infected populations, even when on treatment. Still, only a subset of all births in HIV-infected pregnant women result in PTB, suggesting that risk factors other than HIV infection itself are also important. Inflammation is a known risk factor in uninfected populations, but its role in HIV-infected population have not been studied; in addition, the immune pathways involved are not clear and noninvasive immune markers with predictive value are lacking. Our objective was to determine the association of select markers of inflammation with PTB in HIV-1-infected pregnant women. Methods: Within a randomized trial of pregnant women receiving nevirapine (Six-Week Extended-Dose Nevirapine [SWEN] trial), we nested a case-control study (n = 107; 26 cases, 81 controls) to determine the association of maternal inflammation with PTB. Cases were defined as PTB (<37 weeks' gestational age). We assessed inflammation by measuring plasma levels of markers of general inflammation (C-reactive protein [CRP]), intestinal barrier dysfunction (intestinal fatty acid binding protein [I-FABP]), and microbial translocation/monocyte activation (soluble CD14 [sCD14] and CD163 [sCD163]). Multivariable logistic regression was used to determine the odds of PTB per log2 increase of each marker. Results: In multivariable models, there was increased odds of PTB per unit increase of log2 sCD14 (adjusted odds ratio [aOR], 2.45; 95% confidence interval [CI], 1.24-4.86), log2 sCD163 (aOR, 3.87; 95% CI, 1.43-10.49), and log2 I-FABP (aOR, 2.28; 95% CI, 1.18-4.41) but not log2 CRP (aOR, 0.72; 95% CI, .48-1.09). Conclusions: Our results show that select immune markers can identify women at higher risk for PTB in HIV-1-infected populations and suggest that modulating gut barrier integrity and microbial translocation may affect PTB. Clinical Trials Registration: NCT00061321.
Authors: Mary G Fowler; Min Qin; Susan A Fiscus; Judith S Currier; Patricia M Flynn; Tsungai Chipato; James McIntyre; Devasena Gnanashanmugam; George K Siberry; Anne S Coletti; Taha E Taha; Karin L Klingman; Francis E Martinson; Maxensia Owor; Avy Violari; Dhayendre Moodley; Gerhard B Theron; Ramesh Bhosale; Raziya Bobat; Benjamin H Chi; Renate Strehlau; Pendo Mlay; Amy J Loftis; Renee Browning; Terence Fenton; Lynette Purdue; Michael Basar; David E Shapiro; Lynne M Mofenson Journal: N Engl J Med Date: 2016-11-03 Impact factor: 91.245
Authors: Jennifer Y Chen; Heather J Ribaudo; Sajini Souda; Natasha Parekh; Anthony Ogwu; Shahin Lockman; Kathleen Powis; Scott Dryden-Peterson; Tracy Creek; William Jimbo; Tebogo Madidimalo; Joseph Makhema; Max Essex; Roger L Shapiro Journal: J Infect Dis Date: 2012-10-12 Impact factor: 5.226
Authors: Paul K Drain; Roland Kupka; Gernard I Msamanga; Willy Urassa; Ferdinand Mugusi; Wafaie W Fawzi Journal: AIDS Date: 2007-10-01 Impact factor: 4.177
Authors: Li Liu; Shefali Oza; Daniel Hogan; Jamie Perin; Igor Rudan; Joy E Lawn; Simon Cousens; Colin Mathers; Robert E Black Journal: Lancet Date: 2014-09-30 Impact factor: 79.321
Authors: Adaora A Adimora; Elizabeth Topper Golub; Seble G Kassaye; Aadia Rana; Daniel Westreich; Anandi N Sheth; Jennifer Webster Cyriaque; Carrigan Parish; Deborah Konkle-Parker; Deborah L Jones; Mirjam-Colette Kempf; Igho Ofotokun; Ruth M Kanthula; Jessica Donohue; Patricia Raccamarich; Tina Tisdale; Catalina Ramirez; Lari Warren-Jeanpiere; Phyllis C Tien; Maria L Alcaide Journal: JMIR Res Protoc Date: 2021-12-20
Authors: Ethan K Gough; Thaddeus J Edens; Hyun Min Geum; Iman Baharmand; Sandeep K Gill; Ruairi C Robertson; Kuda Mutasa; Robert Ntozini; Laura E Smith; Bernard Chasekwa; Florence D Majo; Naume V Tavengwa; Batsirai Mutasa; Freddy Francis; Lynnea Carr; Joice Tome; Rebecca J Stoltzfus; Lawrence H Moulton; Andrew J Prendergast; Jean H Humphrey; Amee R Manges; Shine Trial Team Journal: EBioMedicine Date: 2021-06-15 Impact factor: 8.143