The virus consists of a thin protein envelope, a capsid, and inside of which are its genome, the genes. When the herpes virus infects a cell, amounts of genetic material are produced that replicate – thus taking up more and more space within the cell’s nucleus.
Alex Evilevitch, a researcher at Lund University, has for many years studied the mechanisms behind herpes infection and the physical properties of the virus. The amount of genetic material in the cell nucleus leads to what Alex Evilevitch describes as a mechanical load on the nuclear envelope and that the nuclear envelope risks rupturing.
The herpes virus only affects humans
The herpes simplex virus (HSV) is found all over the world and humans are the only host. The virus exists in two closely related forms, (HSV-1, HSV-2.). Both can cause rashes and sores, especially on the lips and genitals.
In herpes simplex infection, blisters appear on a specific area of the skin. When you become infected, the virus travels along the skin’s nerves to a ganglion where it can “rest” for many years. It can then be activated, for example, during stress, sun exposure and menstruation, and then travel to the skin or mucous membranes where it leads to new herpes blisters. The blisters usually appear in the same place each time.
Source: Swedish Public Health Agency
From the perspective and survival of the herpes virus, this scenario is not good at all. For the herpes virus, it is essential that the cell nucleus remains intact so that the chances of replication are maximized.
A better understanding of how the cell nucleus deals with the herpes virus
The area is largely unexplored. But with increased understanding of how cell nucleus mechanisms are affected by an infected herpes virus, we can understand how cell nuclei can withstand the stresses of the virus. Alex Ivlevich, who led the study at Lund University, explains that the mechanisms prevent early damage to the nuclear envelope and the DNA copying machines in the cell nucleus, which the virus uses to replicate itself.
The image shows a reconstruction of human herpes simplex virus type 1. Cross-section shows tightly stacked herpes DNA (green) in the virus capsid. Electron microscope image. Photo: Alex Evelvich.
The researchers came to this conclusion by examining how the cell nucleus is affected by the injection of human herpes simplex virus type 1 (HSV-1) DNA into the cell nucleus during herpes infection. Using a nuclear power microscope, the researchers examined the response of healthy cell nuclei to HSV-1 DNA, that is, how the cell adapts and changes at different stages of viral infection. It is a robust mechanical response aimed at maintaining nucleolar integrity and the function required for the spread of the herpes virus into the cell nucleus.
It is important to understand how the virus spreads in our cells
The nuclear mechanisms of the cell in response to viral infection have not been investigated before. Our observations of the cell’s mechanical adaptation allow the virus to use the cell’s DNA replication machinery to maximize its dissemination in the cell. Alex Evilevitch says understanding the general mechanisms that regulate the life cycle of a virus reveals new antiviral targets for treatment.
Such a biophysical approach to virus control is less susceptible to mutations and opens an important new strategy for treating viruses with high mutation rates or other preventive strategies, which are a major challenge in vaccine development.
Scientific material:
Expulsion of HSV-1 DNA into the nucleus results in significant mechanical shifts indicating mechanical protection of the integrity of the nucleusPNAS, February 21, 2022
Alex Evelvich Previous studies on the herpes virus:
call:
Alex Evilevitch, Research Group Leader, Senior Lecturer in the Department of Experimental Medical Sciences, Lund University, [email protected]
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