Cellular and humoral factors of innate antiviral immunity

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Abstract

The study presents new data on the biological effects of well-known cellular and humoral factors that ensure the functioning of innate immunity. Four mechanisms induced by viruses, which lead to the destruction of inhibitory proteins and trigger the transcription of interferon genes, are described. The paper also presented the order of synthesis of species of interferons and other pro-inflammatory cytokines in the development of an antiviral immune response. This is of great importance because viruses have significantly different resistance to the biological effects of interferons. Interferon lambda played a role in the development of innate immune reactions against many viruses, and the effectiveness of the functioning of the mechanisms of the innate and adaptive immunity in viral infections was evaluated, depending on the state of the stat l, 4, 6 genes and genes of interferon regulators. An interferon-independent variant of the innate immune response in viral infections that occurs a few hours after infection and is associated with chemokine CXCL10 has been described. Data on the most important role of the ubiquitin-proteasome cleavage pathway of proteins and the complement system in the implementation of antiviral effects of innate immunity are also presented. The uniqueness of the microbicidal effects of natural killers, which are realized only in cells that reduced the expression of major histocompatibility complex I molecules, has been established. In addition, natural killers can recognize and do not attack target cells carrying antigens of HLA-E, the sublocus of the major histocompatibility complex I molecules. The natural killers were found to acquire the properties of memory cells. This is facilitated by interleukins 12 and 18. The extracellular neutrophil traps of neutrophils showed microbicidal effects against many viruses. The congenital lymphoid cells have multifaceted effects on the development of an antiviral immune response.

About the authors

Alexander V. Moskalev

Military Medical Academy of S.M. Kirov

Author for correspondence.
Email: alexmav195223@yandex.ru
ORCID iD: 0000-0002-3403-3850
SPIN-code: 8227-2647

doctor of medical sciences, professor

Russian Federation, Saint Petersburg

Boris Yu. Gumilevsky

Military Medical Academy of S.M. Kirov

Email: alexmav195223@yandex.ru
SPIN-code: 3428-7704
Scopus Author ID: 6602391269
ResearcherId: J-1841-2017

doctor of medical sciences, professor

Russian Federation, Saint Petersburg

Andrey V. Apchel

Military Medical Academy of S.M. Kirov; A.I. Herzen Russian State Pedagogical University of the Ministry of Education and Science of the Russian Federation

Email: alexmav195223@yandex.ru
ORCID iD: 0000-0001-7658-4856
SPIN-code: 4978-0785
Scopus Author ID: 6507529350
ResearcherId: Е-8190-2019

doctor of medical sciences, professor

Russian Federation, Saint Petersburg; Saint Petersburg

Vasiliy N. Tsygan

Military Medical Academy of S.M. Kirov

Email: alexmav195223@yandex.ru
ORCID iD: 0000-0003-1199-0911
SPIN-code: 7215-6206

doctor of medical sciences, professor

Russian Federation, Saint Petersburg

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2. Fig. 1. Type I interferon (IFN) synthesis, secretion, receptor binding, and signal transduction: а — simplified schematic of type I IFN synthesis and paracrine signaling, which results in the synthesis of IFN-stimulated genes. PRR, pattern recognition receptor. b — A complex, but integrated, depiction of the detection/alarm system that leads to IFN synthesis. Viruses or viral components are bound by TLRs that trigger downstream signaling cascades, leading to the production of type I IFNs (α and β) and NF-KB-regulated proteins. Type I IFNs are released from the cells and can then bind to IFN receptors on the surfaces of adjacent cells to stimulate synthesis of IFN-responsive genes

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Copyright (c) 2022 Moskalev A.V., Gumilevsky B.Y., Apchel A.V., Tsygan V.N.

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