Abstract

In HIV-positive patients, hepatitis C virus (HCV) coinfection is associated with the development of se-vere 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 resto-ration of CD4+ T-cell counts during therapy are limited. The aim of this work was to characterize system-ic 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 (eotax-in, 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.

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