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A method for quantifying mechanical properties of tissue following viral infection. PLoS One 2012;7(8):e42197

Date

08/08/2012

Pubmed ID

22870300

Pubmed Central ID

PMC3411685

DOI

10.1371/journal.pone.0042197

Scopus ID

2-s2.0-84864560232 (requires institutional sign-in at Scopus site)   6 Citations

Abstract

Viral infection and replication involves the reorganization of the actin network within the host cell. Actin plays a central role in the mechanical properties of cells. We have demonstrated a method to quantify changes in mechanical properties of fabricated model three-dimensional (3D) connective tissue following viral infection. Using this method, we have characterized the impact of infection by the human herpesvirus, cytomegalovirus (HCMV). HCMV is a member of the herpesvirus family and infects a variety of cell types including fibroblasts. In the body, fibroblasts are necessary for maintaining connective tissue and function by creating mechanical force. Using this 3D connective tissue model, we observed that infection disrupted the cell's ability to generate force and reduced the cumulative contractile force of the tissue. The addition of HCMV viral particles in the absence of both viral gene expression and DNA replication was sufficient to disrupt tissue function. We observed that alterations of the mechanical properties are, in part, due to a disruption of the underlying complex actin microfilament network established by the embedded fibroblasts. Finally, we were able to prevent HCMV-mediated disruption of tissue function by the addition of human immune globulin against HCMV. This study demonstrates a method to quantify the impact of viral infection on mechanical properties which are not evident using conventional cell culture systems.

Author List

Lam V, Bigley T, Terhune SS, Wakatsuki T

Author

Scott Terhune PhD Professor in the Microbiology and Immunology department at Medical College of Wisconsin




MESH terms used to index this publication - Major topics in bold

Cells, Cultured
Cytomegalovirus
Cytomegalovirus Infections
Fibroblasts
Humans