Studies of Influenza A/H1N1 A/Tomsk/13/2010 Virus Topology during Development of Infectious Process in Mammals

Abstract

Influenza A/H1N1 A/Tomsk/13/2010 virus registered in Siberia in 2010 proved to be an extremely pathogenic strain. Dynamic study of the topology of this influenza virus strain in the lungs, liver, kidneys, lymph nodes, and great vessels of infected mice was carried out. Influenza A virus was detected by immunohistochemical methods in cells of different histogenesis in all the studied organs throughout the observation period (days 1-30 postinfection), which indicated effective replication and long persistence of influenza A/H1N1 A/Tomsk/13/2010 virus in mammalian cells.

Death Mechanisms of Pulmonary Alveolocytes in Mice Infected with Influenza Viruses A/H1N1/California/04/2009 and A/H5N1/Goose/Krasnoozerskoye/627/05

“…The scale of the overall apoptotic and necrotic destructive processes was significantly greater in A/H5N1-infected mice than in A/H1N1-infected ones. Hence, the necrotic processes in influenza are implemented via cytodestructive effects of the viruses; they are stimulated by hypoxia, ischemia, and thrombosis of the blood vessels resulting from enhanced tropicity of influenza viruses to endotheliocytes [4,9]. Seemingly, the apoptotic death of the cells is induced by hypoxia; its development depends on the number and activation degree of macrophages in the infiltrates and their up-regulated secretion of nitric oxide, proteases [1,2,4], and apoptosis-inducing factors, which is characteristic of mitochondrial pathway; moreover, apoptosis can be triggered from cell membrane via the plasmalemmal receptor pathway.…”

Pancreatic toxicity of influenza A/H1N1-California virus infection in mice at the background of hyperglycemia induced by streptozotocin administration

“…Его антиген выявлен у мышей в клетках органов через 30 сут после инфицирования, что свидетельствовало об успешной репликации и пролонгированной персистенции вируса в организме; в то же время доказательств активной репликации в ПЖ, в частности, у хорьков, интраназально привитых вирусом гриппа H1N1 1918, не найдено; при ретроспективном анализе (пандемия 2009 г.) выявлено, что повышенный уровень глюкозы в плазме является независимым предиктором тяжести индуцированной H1N1 пневмонии, а не результатом прямого повреждения β-клеток ПЖ [7][8][9]. Тем не менее при создании 84 клонов мышиных моноклональных антител против H1N1 показано, что два клона специфически перекрестно реагировали с α-клетками панкреатических островков человека [10]; также обнаружено, что линия клеток ПЖ (инсулиномы) мыши может поддерживать репликацию вируса гриппа A/H1N1/PR8 [11].…”

Influenza A virus infection induces liver injury in mice

“…A case reported that a 3-year-old boy infected with the H5N1 avian influenza virus died of Reye's syndrome and respiratory distress syndrome [5]. A novel pandemic 2009 influenza A ⁄ H1N1 different from the seasonal influenza infection induced hepatocellular injury with increased serum aminotransaminase levels [6,7]. When humans are infected with H7N9, hypoxic and fatty changes in the liver tissue have been observed [8,9].…”