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Hepatitis C Virus Cure in Human Immunodeficiency Virus Coinfection Dampens Inflammation and Improves Cognition
Bing Sun1, Linda Abadjian2, Alexander Monto3,4
1Department of Laboratory Medicine, San Francisco Veterans Affairs Medical Center, San Francisco, California, USA.
Insights
Curing Hepatitis C Virus (HCV) in individuals with HIV/HCV coinfection reduces inflammation and improves cognitive function, particularly in visual learning and memory. This suggests both viruses contribute to cognitive impairment.
Area of Science:
- Immunology
- Virology
- Neuroscience
Background:
- Chronic inflammation in HIV/HCV coinfection is linked to cognitive impairment.
- Direct-acting antiviral therapies offer a potential to reduce inflammation and improve cognition.
Purpose of the Study:
- To determine if achieving sustained viral response (SVR) to HCV therapy decreases chronic inflammation and improves cognition in HIV/HCV coinfected individuals.
- To compare inflammatory markers and cognitive function before and after HCV treatment.
Main Methods:
- Longitudinal study of four groups: HCV-monoinfected, HIV/HCV-coinfected, HIV-monoinfected, and healthy controls.
- Measurement of monocyte activation, gene expression, exosome microRNA (miRNA), plasma inflammation markers, and cognitive impairment.
- Assessment before and after HCV therapy in relevant groups.
Main Results:
- HCV cure reduced plasma markers (soluble CD163, neopterin) and blood CD16+ monocytes in coinfection.
- Cognitive function, measured by the global deficit score, improved by 25% in coinfected individuals post-treatment.
- HCV SVR decreased specific monocyte interferon genes in both mono- and coinfected groups.
Conclusions:
- HCV cure in coinfection normalizes monocyte activation to levels seen in HIV monoinfection.
- Cognitive impairment significantly improves with HCV cure, suggesting contributions from both HIV and HCV.
- HCV cure enhances cognitive function, especially in the visual learning/memory domain.
Background:
Chronic inflammation in human immunodeficiency virus (HIV)/hepatitis C virus (HCV) coinfection increases cognitive impairment. With newer, direct-acting antiviral therapies for HCV, our objective was to determine whether chronic inflammation would be decreased and cognition improved with HCV sustained viral response (SVR) in coinfection.
Methods:
We studied 4 groups longitudinally: 7 HCV-monoinfected and 12 HIV/HCV-coinfected persons before and after treatment for HCV, 12 HIV-monoinfected persons, and 9 healthy controls. We measured monocyte activation and gene expression, monocyte-derived exosome micro-ribonucleic acid (miRNA) expression, plasma inflammation, and cognitive impairment before and after therapy.
Results:
Plasma soluble CD163 and neopterin were decreased in HCV mono- and coinfected persons. Blood CD16+ monocytes were decreased in coinfection after HCV treatment. Global deficit score improved 25% in coinfection with the visual learning/memory domain the most improved. Hepatitis C virus SVR decreased monocyte interferon genes MX1, IFI27, and CD169 in coinfection and MX1, LGALS3BP, and TNFAIP6 in HCV monoinfection. Monocyte exosomes from coinfected persons increased in microRNA (miR)-19a, miR-221, and miR-223, all of which were associated with decreasing inflammation and nuclear factor-κB activation.
Conclusions:
Hepatitis C virus cure in coinfection brings monocyte activation to levels of HIV alone. Cognitive impairment is significantly improved with cure but not better than HIV infection alone, which strong suggests that cognitive impairment was driven by both HIV and HCV.SummaryHCV cure in HIV coinfection improves monocyte and plasma activation markers and increases cognitive function in the visual learning/memory domain.
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