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Correlates of Elevated Interleukin-6 and C-Reactive Protein in Persons With or at High Risk for HCV and HIV Infections

Salter, Megan L. PhD*,†; Lau, Bryan PhD*; Mehta, Shruti H. PhD*; Go, Vivian F. PhD*; Leng, Sean MD; Kirk, Gregory D. MD, PhD*,§

JAIDS Journal of Acquired Immune Deficiency Syndromes: 15 December 2013 - Volume 64 - Issue 5 - p 488–495
doi: 10.1097/QAI.0b013e3182a7ee2e
Epidemiology and Prevention

Background: HIV and hepatitis C virus (HCV) infections may increase interleukin-6 (IL-6) and C-reactive protein (CRP). However, relationships between inflammatory biomarkers, chronic viral infections, clinical factors, and behavioral factors remain poorly understood.

Methods: Using linear regression, we modeled cross-sectional associations between loge IL-6 or loge CRP levels and HCV, HIV, injection drug use, and comorbidity among 1191 injection drug users.

Results: Mean age was 47 years, 46.0% reported currently injecting drugs, 59.0% were HCV monoinfected, and 27% were HCV/HIV coinfected. In multivariable models, higher loge IL-6 was associated with HCV monoinfection [β = 0.191, 95% confidence interval (CI): 0.043 to 0.339] and HCV/HIV coinfection (β = 0.394, 95% CI: 0.214 to 0.574). In contrast, HCV monoinfection (β = −0.523, 95% CI: −0.275 to −0.789) and HCV/HIV coinfection (β = −0.554 95% CI: −0.260 to −0.847) were associated with lower CRP. Lower CRP with HCV infection was independent of liver fibrosis severity, synthetic function, or liver injury markers; CRP decreased with higher HCV RNA. Increased injection intensity was associated with higher IL-6 (P = 0.003) and CRP (P < 0.001); increasing comorbidity (P < 0.001) and older age (P = 0.028) were associated with higher IL-6; older age was associated with higher CRP among HCV-uninfected participants (P = 0.021).

Conclusion: HIV and HCV infections contribute to chronic inflammation; however, reduced CRP possibly occurs through HCV-mediated mechanisms. Findings highlight potentially modifiable contributors to inflammation.

*Department of Epidemiology, Johns Hopkins University School of Public Health, Baltimore, MD;

Johns Hopkins University Center on Aging and Health, Baltimore, MD;

Divisions of Geriatric Medicine; and

§Infectious Diseases, Johns Hopkins University School of Medicine, Baltimore, MD.

Correspondence to: Megan L. Salter, PhD, Johns Hopkins Center on Aging and Health, 2024 E. Monument Street, Suite 2-704, Baltimore, MD 21205 (e-mail: msalter@jhsph.edu).

The authors have conflicts of interest to disclose.

Supported by the National Institutes of Health (grants RC1-AI-086053, R01-DA-04334, R01-DA-12568, R01-HL-90483, R01-DA-16078, and K01-AI071754) and the American Cancer Society (MRSG-07-284-01-CCE to G.D.K.)

All authors contributed to the conception and design or acquisition of data or analysis and interpretation of the data, drafting the article or revising it critically for important intellectual content, and final approval of the version to be published.

Supplemental digital content is available for this article. Direct URL citations appear in the printed text and are provided in the HTML and PDF versions of this article on the journal's Web site (www.jaids.com).

Received April 19, 2013

Accepted July 23, 2013

© 2013 by Lippincott Williams & Wilkins