Samantha McInally1, Kristin Wall2, Tianwei Yu3, Rabindra Tirouvanziam4,5, William Kilembe6, Jill Gilmour7, Susan A Allen8, Eric Hunter9,10. 1. Emory Vaccine Center at Yerkes National Primate Research Center, Atlanta, GA, USA. 2. Rollins School of Public Health, Emory University, Atlanta, GA, USA. 3. School of Data Science, The Chinese University of Hong Kong, Shenzhen, Shenzhen, Guangdong Province, China. 4. Department of Pediatrics, Emory University School of Medicine, Atlanta, GA, USA. 5. Center of CF and Airways Disease Research, Children's Healthcare of Atlanta, Atlanta, GA, USA. 6. Zambia-Emory HIV Research Project, Lusaka, Zambia. 7. Faculty of Medicine, Imperial College, London, SW7 2AZ, UK. 8. Department of Pathology and Laboratory Medicine, Emory University, Atlanta, GA, USA. 9. Emory Vaccine Center at Yerkes National Primate Research Center, Atlanta, GA, USA. ehunte4@emory.edu. 10. Department of Pathology and Laboratory Medicine, Emory University, Atlanta, GA, USA. ehunte4@emory.edu.
Abstract
BACKGROUND: To determine if individuals, from HIV-1 serodiscordant couple cohorts from Rwanda and Zambia, who become HIV-positive have a distinct inflammatory biomarker profile compared to individuals who remain HIV-negative, we compared levels of biomarkers in plasma of HIV-negative individuals who either seroconverted (pre-infection) and became HIV-positive or remained HIV-negative (uninfected). RESULTS: We observed that individuals in the combined cohort, as well as those in the individual country cohorts, who later became HIV-1 infected had significantly higher baseline levels of multiple inflammatory cytokines/chemokines compared to individuals who remained HIV-negative. Genital inflammation/ulceration or schistosome infections were not associated with this elevated profile. Defined levels of ITAC and IL-7 were significant predictors of later HIV acquisition in ROC predictive analyses, whereas the classical Th1 and Th2 inflammatory cytokines such as IL-12 and interferon-γ or IL-4, IL-5 and Il-13 were not. CONCLUSIONS: Overall, the data show a significant association between increased plasma biomarkers linked to inflammation and immune activation and HIV acquisition and suggests that pre-existing conditions that increase systemic biomarkers represent a factor for increased risk of HIV infection.
BACKGROUND: To determine if individuals, from HIV-1 serodiscordant couple cohorts from Rwanda and Zambia, who become HIV-positive have a distinct inflammatory biomarker profile compared to individuals who remain HIV-negative, we compared levels of biomarkers in plasma of HIV-negative individuals who either seroconverted (pre-infection) and became HIV-positive or remained HIV-negative (uninfected). RESULTS: We observed that individuals in the combined cohort, as well as those in the individual country cohorts, who later became HIV-1 infected had significantly higher baseline levels of multiple inflammatory cytokines/chemokines compared to individuals who remained HIV-negative. Genital inflammation/ulceration or schistosome infections were not associated with this elevated profile. Defined levels of ITAC and IL-7 were significant predictors of later HIV acquisition in ROC predictive analyses, whereas the classical Th1 and Th2 inflammatory cytokines such as IL-12 and interferon-γ or IL-4, IL-5 and Il-13 were not. CONCLUSIONS: Overall, the data show a significant association between increased plasma biomarkers linked to inflammation and immune activation and HIV acquisition and suggests that pre-existing conditions that increase systemic biomarkers represent a factor for increased risk of HIV infection.
Entities:
Keywords:
Chemokines; Cytokines; HIV acquisition; HIV discordant couples; HIV pathogenesis
Authors: Lindi Masson; Jo-Ann S Passmore; Lenine J Liebenberg; Lise Werner; Cheryl Baxter; Kelly B Arnold; Carolyn Williamson; Francesca Little; Leila E Mansoor; Vivek Naranbhai; Douglas A Lauffenburger; Katharina Ronacher; Gerhard Walzl; Nigel J Garrett; Brent L Williams; Mara Couto-Rodriguez; Mady Hornig; W Ian Lipkin; Anneke Grobler; Quarraisha Abdool Karim; Salim S Abdool Karim Journal: Clin Infect Dis Date: 2015-04-21 Impact factor: 9.079
Authors: Melis N Anahtar; Elizabeth H Byrne; Kathleen E Doherty; Brittany A Bowman; Hidemi S Yamamoto; Magali Soumillon; Nikita Padavattan; Nasreen Ismail; Amber Moodley; Mary E Sabatini; Musie S Ghebremichael; Chad Nusbaum; Curtis Huttenhower; Herbert W Virgin; Thumbi Ndung'u; Krista L Dong; Bruce D Walker; Raina N Fichorova; Douglas S Kwon Journal: Immunity Date: 2015-05-19 Impact factor: 31.745
Authors: Juan J García; Antonio Cidoncha; María E Bote; María D Hinchado; Eduardo Ortega Journal: Ann Clin Biochem Date: 2013-10-08 Impact factor: 2.057
Authors: Daniela C Mónaco; Dario A Dilernia; Andrew Fiore-Gartland; Tianwei Yu; Jessica L Prince; Kristine K Dennis; Kai Qin; Malinda Schaefer; Daniel T Claiborne; William Kilembe; Jianming Tang; Matt A Price; Paul Farmer; Jill Gilmour; Anju Bansal; Susan Allen; Paul Goepfert; Eric Hunter Journal: J Exp Med Date: 2016-08-22 Impact factor: 14.307
Authors: Nallely Mora; William H Adams; Stephanie Kliethermes; Lara Dugas; Neelam Balasubramanian; Jasmin Sandhu; Helen Nde; Christina Small; Joanne Jose; Steven Scaglione; Jennifer E Layden Journal: BMC Infect Dis Date: 2016-06-13 Impact factor: 3.090