Systemic inflammation in HIV/HCV coinfected patients with discordant response to antiretroviral therapy

Article Sidebar

pdf (Русский)
Published: Nov 8, 2021
DOI: https://doi.org/10.17072/1994-9952-2021-2-141-146
Keywords:
HIV/HCV coinfection systemic inflammation proinflammatory cytokines anti-inflammatory cytokines enzyme-linked immunosorbent assay multiplex assay

Main Article Content

Evgeniya Saidakova
Institute of Ecology and Genetics of Microorganisms UB RAS
https://orcid.org/0000-0002-4342-5362
Larisa Korolevskaya
Institute of Ecology and Genetics of Microorganisms UB RAS
https://orcid.org/0000-0001-9840-7578
Violetta Vlasova
Institute of Ecology and Genetics of Microorganisms UB RAS
https://orcid.org/0000-0002-1656-7277

Abstract

In HIV-positive patients, hepatitis C virus (HCV) coinfection is associated with the development of severe systemic inflammation and an increased risk of a discordant response to highly active antiretroviral therapy in which supressed viral replication doesn’t lead to effective CD4+ T-cell regeneration. At the same time, the data on the systemic inflammation in HIV/HCV coinfected patients with ineffective restoration of CD4+ T-cell counts during therapy are limited. The aim of this work was to characterize systemic inflammation in HIV/HCV coinfected patients with a discordant response to treatment. We studied three groups: 1) HIV/HCV coinfected subjects with a discordant response to therapy (CD4+ T-cells less than 350/ul); 2) HIV/HCV coinfected patients with a standard response to therapy (CD4+ T-lymphocytes over 350/ul); 3) voluntary blood donors without HIV and HCV infections. Systemic inflammation indices were assessed by the content of proinflammatory and anti-inflammatory cytokines in blood plasma (eotaxin, IL-1β, IL-4, IL-5, IL-10, IL-13, MCP-1, MIP-1α, MIP-1β, IP-10 , TNFα, TGF-β1, TGF-β2), the levels of which were analyzed by multiplex and enzyme-linked immunosorbent assays. As a result it was shown that in HIV/HCV coinfected patients, therapeutically uncontrolled hepatitis C leads to the development of pronounced systemic inflammation, which is only slightly aggravated by a discordant response to highly active antiretroviral therapy.

Article Details

How to Cite
Saidakova Е. В., Korolevskaya Л. Б., & Vlasova В. В. (2021). Systemic inflammation in HIV/HCV coinfected patients with discordant response to antiretroviral therapy. Bulletin of Perm University. Biology, (2), 141–146. https://doi.org/10.17072/1994-9952-2021-2-141-146
Issue
No. 2 (2021): Bulletin of Perm University. Biology
Section
Иммунология

License agreement

 

Author Biographies

Evgeniya Saidakova , Institute of Ecology and Genetics of Microorganisms UB RAS

Candidate of biology, senior researcher

Larisa Korolevskaya , Institute of Ecology and Genetics of Microorganisms UB RAS

Candidate of medicine, researcher

Violetta Vlasova , Institute of Ecology and Genetics of Microorganisms UB RAS

Laboratory assistant

References

Жердева А.И. и др. Клинико-эпидемиологическая характеристика ВИЧ-инфекции в Хабаровском крае: хронические вирусные гепатиты, туберкулез и другие оппортунистические заболевания // Дальневосточный журнал инфекционной патологии. 2008. № 12. С. 87‒94.

Саттарова Г.Ж. Исследования ВИЧ положительных сывороток на наличие маркеров гепатита В и С // Наука и новые технологии. 2014. № 3. С. 84‒85.

Шмагель Н.Г., Шмагель К.В., Черешнев В.А. Клинические аспекты неэффективности высокоактивной антиретровирусной терапии // Инфекционные болезни. 2011. Т. 9, № 1. С. 5‒10.

Autran B. et al. Restoration of the immune system with anti-retroviral therapy // Immunology Letters. 1999. Vol. 66. P. 207‒211.

Borges A.H. et al. Predicting risk of cancer during HIV infection: the role of inflammatory and coagulation biomarkers // AIDS. 2013. Vol. 27. P. 1433‒1441.

Brenchley J.M. et al. Microbial translocation is a cause of systemic immune activation in chronic HIV infection // Nature medicine. 2006. Vol. 12. P. 1365‒1371.

Chen T.Y. et al. Meta-analysis: increased mortality associated with hepatitis C in HIV-infected persons is unrelated to HIV disease progression // Clinical Infectious Diseases. 2009. Vol. 49. P. 1605‒1615.

Commins S.P., Borish L., Steinke J.W. Immunologic messenger molecules: cytokines, interferons, and chemokines // Journal of Allergy and Clinical Im-munology. 2010. Vol. 125. P. S53‒72.

de Oca Arjona M.M. et al. Bacterial translocation in HIV-infected patients with HCV cirrhosis: implication in hemodynamic alterations and mortality // Journal of Acquired Immune Deficiency Syndrome. 2011. Vol. 56. P. 420‒427.

Duprez D.A. et al. Inflammation, coagulation and car-diovascular disease in HIV-infected individuals // PLoS One. 2012. Vol. 7. P. e44454.

Gutierrez F. et al. Patients' characteristics and clinical implications of suboptimal CD4 T-cell gains after 1 year of successful antiretroviral therapy // Cur-rent HIV Research. 2008. Vol. 6. P. 100‒107.

Hammerich L., Tacke F. Interleukins in chronic liver disease: lessons learned from experimental mouse models // Clinical and Experimental Gastroenterol-ogy. 2014. Vol. 7. P. 297‒306.

Martinez-Esparza M. et al. Inflammatory status in human hepatic cirrhosis // World Journal of Gastroenterology. 2015. Vol. 21. P. 11522‒11541.

Netea M.G. et al. A guiding map for inflammation // Nature Immunology. 2017. Vol. 18. P. 826‒831.

Raffetti E. et al. Systemic inflammation-based scores and mortality for all causes in HIV-infected patients: a MASTER cohort study // BMC Infectious Diseases. 2017. Vol. 17. P. 193.

Tenorio A.R. et al. Soluble markers of inflammation and coagulation but not T-cell activation predict non-AIDS-defining morbid events during suppres-sive antiretroviral treatment // The Journal of Infectious Diseases. 2014. Vol. 210. P. 1248‒1259.

Tien P.C. et al. Inflammation and mortality in HIV-infected adults: analysis of the FRAM study cohort // Journal of Acquired Immune Deficiency Syndromes. 2010. Vol. 55. P. 316‒322.