A MECHANISM OF VIRAL INFECTION OF RESIDENT MACROPHAGES BY AN AGENT OF HEMORRHAGIC
FEVER WITH RENAL SYNDROME: ULTRASTRUCTURAL ASPECTS
N. G. Plekhova,1 L. M. Somova-Isachkova, R. A. Slonova, G. G. Kompanets, E. V. Pustovalov, E. I. Drobot
Research Institute of Epidemiology and Microbiology, Siberian Branch of RAMS, Vladivostok, Russia;
1 e-mail: pl_nat@ hotmail.com
Monocytes/macrophages are one of the first cells subjected to the infectious effect of viruses. The present paper analyses for the first time the ultrastructural
changes in macrophages caused by an agent of hemorrhagic fever with renal syndrome (HERS) - hantavirus (HV). After a local fusion with the host cell plasmalemma and its
adsorption on the cell surface, the HV penetrates through the macrophage membrane. This process occurred without destruction of cell plasmalemma. HV viral particles were
observed within the macrophage cytoplasm mostly on the smooth granular endoplasmic reticulum vesicles. Viroplasts were defined in macrophages after a 2 h incubation, with
synthesis of viral nucleoproteins and primary covers being observed on the surface of viroplasts. Viral particles left macrophages in the process of budding on the phagocyte surface.
Thereby HV, similar to other enveloped viruses, realizes entrance and egress from the target cell without damaging its plasmalemma. This accounts for the viral ability to reproduce
in macrophages for a long time without any cytopathological effect. Consequently, in the absence of obvious destuction changes, mononuclear phagocytes can serve as a long-term
storage of viruses, and thus being involved in HV dissemination during HERS.
Key words: ultrastructure, monocytes/macrophages, hantavirus
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