Format

Send to

Choose Destination
Cytoskeleton (Hoboken). 2016 Aug;73(8):396-417. doi: 10.1002/cm.21308. Epub 2016 May 30.

Remodeling of the fibroblast cytoskeletal architecture during the replication cycle of Ectromelia virus: A morphological in vitro study in a murine cell line.

Author information

1
Division of Immunology, Department of Preclinical Sciences, Faculty of Veterinary Medicine, Warsaw University of Life Sciences-SGGW, Warsaw, Poland.
2
Molecular Biology Unit, Mossakowski Medical Research Centre, Polish Academy of Sciences, Warsaw, Poland.
3
Laboratory of Bioenergetics and Biomembranes, Department of Biochemistry, Nencki Institute of Experimental Biology, Warsaw, Poland.
4
Department of Biomedical Sciences, Ross University School of Veterinary Medicine, St. Kitts, West Indies.
5
Analytical Centre, Warsaw University of Life Sciences-SGGW, Warsaw, Poland.

Abstract

Ectromelia virus (ECTV, the causative agent of mousepox), which represents the same genus as variola virus (VARV, the agent responsible for smallpox in humans), has served for years as a model virus for studying mechanisms of poxvirus-induced disease. Despite increasing knowledge on the interaction between ECTV and its natural host-the mouse-surprisingly, still little is known about the cell biology of ECTV infection. Because pathogen interaction with the cytoskeleton is still a growing area of research in the virus-host cell interplay, the aim of the present study was to evaluate the consequences of ECTV infection on the cytoskeleton in a murine fibroblast cell line. The viral effect on the cytoskeleton was reflected by changes in migration of the cells and rearrangement of the architecture of tubulin, vimentin, and actin filaments. The virus-induced cytoskeletal rearrangements observed in these studies contributed to the efficient cell-to-cell spread of infection, which is an important feature of ECTV virulence. Additionally, during later stages of infection L929 cells produced two main types of actin-based cellular protrusions: short (actin tails and "dendrites") and long (cytoplasmic corridors). Due to diversity of filopodial extensions induced by the virus, we suggest that ECTV represents a valuable new model for studying processes and pathways that regulate the formation of cytoskeleton-based cellular structures.

KEYWORDS:

actin; tubulin; vimentin; viral spread

PMID:
27169394
DOI:
10.1002/cm.21308
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Wiley
Loading ...
Support Center