Highly pathogenic avian influenza H5N1 (HPAI H5N1) viruses can infect mammals, including humans, causing severe systemic disease with the inhibition of the immune system and a high mortality rate. In conditions of lymphoid tissue depletion, the liver plays an important role in host defence against viruses. The changes in mice liver infected with HPAI H5N1 virus A/goose/Krasnoozerskoye/627/05 have been studied. It has been shown that the virus persistence in the liver leads to the expression of proinflammatory cytokines (TNF-α, IL-6) and intracellular proteases (lysozyme, cathepsin D, and myeloperoxidase) by Kupffer cells. Defective antiviral response exacerbates destructive processes in the liver accelerating the development of liver failure. 1. Introduction Influenza takes a special place in the human infectious pathology because it has no equivalent in prevalence and incidence of diseases. The causative agent of the highly pathogenic avian influenza A/H5N1 (HPAI H5N1) is of particular interest. Its characteristic features are wide geographical distribution and high pathogenicity to humans causing the severe disease with high mortality in the absence of specific immunity in the human population [1–3]. There is a constant threat of a pandemic, due to the constant evolution of influenza viruses, the high population density in areas of active circulation of HPAI H5N1, its ability to direct transmission from birds to humans, and the possibility of reassortment with viruses adapted in the human population [4–6]. An infectious disease caused by HPAI H5N1 viruses occurs with damage to many organs and systems of the organism and severe symptoms of intoxication [7, 8]. When studying the distribution of HPAI H5N1 viruses in tissues of internal organs of infected animals in a number of studies, it was shown that they are able to replicate not only in the lung, but also in extrapulmonary organs including liver, kidney, spleen, and brain [9–11]. The incubation period typical for HPAI H5N1 is too brief for the occurrence of primary humoral response [12], and the initial period of the disease occurs with the inhibition of the interferon response and reduction of interferon in the blood [10]. At the same time, many researchers have reported significant depletion of lymphoid tissue as a result of massive apoptosis of lymphocytes under the infection [13, 14]. In this connection, a special role acquires nonspecific protection mechanisms of the organism, particularly cells of the mononuclear phagocyte system, a significant pool of which is concentrated in the lungs and
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