Quinlan Richert1, Adriana Trajtman2, Luisa Arroyave3, Julia Toews4, Marissa Becker5, Ken Kasper6, Paul McLaren7, Zulma Rueda8, Yoav Keynan9. 1. Department of Medical Microbiology, University of Manitoba, Winnipeg, Canada. Electronic address: umricheq@myumanitoba.ca. 2. Department of Medical Microbiology, University of Manitoba, Winnipeg, Canada. Electronic address: Adriana.trajtman@umanitoba.ca. 3. Facultad de Medicina, Universidad Pontificia Bolivariana, Medellin, Colombia. Electronic address: luisa16_fer@hotmail.com. 4. University of British Columbia, Department of Biochemistry, Canada. Electronic address: juliatoews10@gmail.com. 5. Department of Medical Microbiology, University of Manitoba, Winnipeg, Canada; Department of Internal Medicine, University of Manitoba, Winnipeg, Canada; Community Health Sciences, University of Manitoba, Winnipeg, Canada. Electronic address: Marissa.Becker@umanitoba.ca. 6. Department of Medical Microbiology, University of Manitoba, Winnipeg, Canada; Department of Internal Medicine, University of Manitoba, Winnipeg, Canada. Electronic address: kkasper@exchange.hsc.mb.ca. 7. Department of Medical Microbiology, University of Manitoba, Winnipeg, Canada. Electronic address: Paul.mclaren@umanitoba.ca. 8. Facultad de Medicina, Universidad Pontificia Bolivariana, Medellin, Colombia. Electronic address: zulmaruedav@gmail.com. 9. Department of Medical Microbiology, University of Manitoba, Winnipeg, Canada; Department of Internal Medicine, University of Manitoba, Winnipeg, Canada; Community Health Sciences, University of Manitoba, Winnipeg, Canada. Electronic address: keynany@yahoo.com.
Abstract
INTRODUCTION: Despite the life-prolonging effects of Highly Active Antiretroviral Therapy (HAART), persons with HIV are still prone to higher rates of non-AIDS related morbidity (such as heart, kidney, and liver disease) than the general public. This is likely due to chronic immune activation and inflammation that persists in HIV-positive persons despite virological suppression. What remains undetermined, however, is whether a link exists between chronic inflammation/immune activation and suboptimal immune recovery on HAART. The hypothesis of the present study is that higher levels of systemic subclinical inflammation and immune activation are linked with suboptimal immune recovery on HAART. METHODS: Fifteen eligible patients from the Manitoba HIV program were enrolled and followed for up to two years; blood samples were drawn at 4 timepoints each, and concentrations of 21 proinflammatory markers were measured. Patients were grouped according to CD4:CD8 recovery at viral suppression, and the inflammatory profiles of the two groups were compared. RESULTS AND CONCLUSIONS: APRIL and BAFF are higher in those with poor recovery at the point of viral suppression, but were also higher in this group at the onset of therapy and through the three additional follow-up visits. TNF-R1, CD163, and Osteopontin, were also in higher concentrations at the outset of therapy and beyond. These five molecules could thus see potential use in the future as biomarkers of likely poor immune recovery. Future work should focus on replicating these findings with larger cohorts. Copyright Â
INTRODUCTION: Despite the life-prolonging effects of Highly Active Antiretroviral Therapy (HAART), persons with HIV are still prone to higher rates of non-AIDS related morbidity (such as heart, kidney, and liver disease) than the general public. This is likely due to chronic immune activation and inflammation that persists in HIV-positive persons despite virological suppression. What remains undetermined, however, is whether a link exists between chronic inflammation/immune activation and suboptimal immune recovery on HAART. The hypothesis of the present study is that higher levels of systemic subclinical inflammation and immune activation are linked with suboptimal immune recovery on HAART. METHODS: Fifteen eligible patients from the Manitoba HIV program were enrolled and followed for up to two years; blood samples were drawn at 4 timepoints each, and concentrations of 21 proinflammatory markers were measured. Patients were grouped according to CD4:CD8 recovery at viral suppression, and the inflammatory profiles of the two groups were compared. RESULTS AND CONCLUSIONS: APRIL and BAFF are higher in those with poor recovery at the point of viral suppression, but were also higher in this group at the onset of therapy and through the three additional follow-up visits. TNF-R1, CD163, and Osteopontin, were also in higher concentrations at the outset of therapy and beyond. These five molecules could thus see potential use in the future as biomarkers of likely poor immune recovery. Future work should focus on replicating these findings with larger cohorts. Copyright Â
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