[Influenza viruses and atherosclerosis: the role of atherosclerotic plaques in prolonging the persistent form of influenza infection]. / Virusy grippa i ateroskleroz: rol' ateroskleroticheskikh bliashek v podderzhanii persistentnoi formy grippoznoi infektsii.

It was established that viral particles, like low-density lipoproteins (LDLP), when subjected to some modification changes, lost their ability to be internalized by tissue somatic cells and acquired tropism to macrophage cells. The data, obtained by us by using the polymerase chain reaction (PCR) method, made it possible to assert that atherosclerotic plaques, isolated from vessels of patients with ischemic heart disease (IHD) who underwent coronary bypass, contained RNA of the A(HINI) and AH3N3) influenza viruses. Whereas, the vessel portions, undamaged by atherosclerosis, did not contain any genetic substances of influenza viruses. It was for the first time that an experimentally supported understanding was expressed on that the atherosclerotic plaques serve as a "reservoir" for influenza viruses. It is also suggested that the mentioned plaques can be the carriers of influenza viruses for a long time, thus, prolonging the persistent form of influenza infection in the human body.

[Reticuloendothelial system and persistence of influenza virus in the body]. / Retikuloéndotelial'naia sistema i persistentsiia virusa grippa v organizme.

The method of in situ transcription was used to detect influenza virus genome in the organs of infected mice. Virus-specific RNA was found in the alveolar macrophages 5 months after infection, this confirming the capacity of the virus to persist in vivo in these cells for a long time. Evidence in favor of influenza virus modification in an infected host body is presented, which fact dramatically affects virus interactions with macrophages. Problems in the development of acute and persistent infections and influenza virus persistence in reticuloendothelial cells are discussed.