Abstract

Purpose: Immune reconstitution inflammatory syndrome is one of the main components of the pathogenesis of HIV infection. The severity of systemic inflammation and immune activation is an important prognostic indicator of disease progression. Aim of research: to determine the diagnostic significance of systemic inflammation markers in HIV-infected patients in depend of on the level of viral replication HIV. Methods & Materials: The study involved 224 HIV patients who were divided into three main groups according to the level of HIV replication. Patients with undetectable viremia or with a viral load (VL) less than 50 copies/ml (n = 82) were included in 1st group, with a defined patients with a level of HIV RNA concentration of more than 10 000 copies/ml (n = 74) were in 3rd group. All patients received HAART. The content of lipopolysaccharide-binding protein (LBP), procalcitonin and cytokines (TNF-α, IL-1β, IL-6, IL-8, IL-10, INF-γ, INF-α) were detected in the blood serum using a solid-phase enzyme-linked immunosorbent assay. The concentration of HIV RNA (viral load of HIV, copies/ml) was determined in blood plasma by the RT-PCR. Results: Significant increase in the level of LBP and cytokines IL-1β, TNF -α, IL-6, IL-8, IL-10, INF-γ, INF-α was found in groups of patients in comparison with healthy people. An average correlation was found between the level of HIV viral load and the LBP level in the blood in the groups of patients with a defined level of HIV viremia (2nd and 3rd). In patients with HIV infection with viremia, there are signs of more active systemic inflammation, accompanied by increased production of antiendotoxin proteins and cytokines (TNF-α, IL-10, INF-α and INF-γ), compared with patients with undetectable levels of viral load of HIV. Level of procalcitonin in all groups of patients had not any statistical deviation in comparison with its level in the healthy people. Conclusion: Full suppression of HIV replication is associated with lower levels of LBP, TNF-a, IL10, INF-α and INF-γ. Antiretroviral therapy can significantly reduce the severity of systemic inflammation in patients with HIV infection, but does not ensure the normalization of the concentration of antiendotoxin proteins and cytokine status.

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