Capsid Reinforcement of Herpes Simplex Virus Triggered by DNA Packaging

Roos, Wouter H.; Radtke, Kerstin; Kniesmeijer, Edward; Geertsema, Hylkje; Sodeik, Beate; Wuite, Gijs J.L.

doi:10.1016/j.bpj.2008.12.2165

Cited by 1 publication

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“…Viruses are striking examples of biomolecular aggregates where recent studies of their individual mechanical properties have provided interesting insights into their physical functionality. Among others, these studies have unveiled the structural role that the DNA may play either reinforcing the shell or exerting pressure on the viral walls, [3][4][5][6], the influence of defects on their stiffness [7], the existence of mechanical pre-stress [8,9], or the dependence of the mechanical properties on the conformational changes required for the infectivity [10,11].…”

Section: Introductionmentioning

confidence: 99%

Interplay between the mechanics of bacteriophage fibers and the strength of virus-host links

et al. 2014

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Viral fibers play a central role in many virus infection mechanisms since they recognize the corresponding host and establish a mechanical link to its surface. Specifically, bacteriophages have to anchor to bacteria through the fibers surrounding the tail before starting the viral DNA translocation into the host. The protein gene product (gp) 37 from bacteriophage T4 long tail fibers forms a fibrous parallel homotrimer located at the distal end of the long tail fibers. Biochemical data indicate that, at least, three of these fibers are required for initial host cell interaction but do not reveal why three and no other numbers are required. By using atomic force microscopy, we obtained high-resolution images of gp37 fibers adsorbed on a mica substrate in buffer conditions and probed their local mechanical properties. Our experiments of radial indentation at the nanometer scale provided a radial stiffness of ∼ 0.08 N/m and a breaking force of ∼ 120 pN. In addition, we performed finite element analysis and determined a Young's modulus of ∼ 20 MPa. From these mechanical parameters, we hypothesize that three viral fibers provide enough mechanical strength to prevent a T4 virus from being detached from the bacteria by the viral particle Brownian motion, delivering a biophysical justification for the previous biochemical data.

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