Autophagy in Herpes Simplex and Varicella-Zoster Virus Infections

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Table of Contents

Abstract
Introduction
Methods
Results
Discussion
Reference List

Abstract

The article in question deals with the difference between autophagy found in herpes simplex virus (HSV) infection and varicella-zoster virus (VZV) infection. It is found that autophagy is proviral when it comes to VZV infection while HSV has genes that block autophagic flux. The experiments held have several implications as they reveal peculiarities of autophagy in similar types of infections. The researchers also stress that the methodology used is effective for autophagy measurement.

Introduction

Autophagy is one of the most important processes associated with a cell’s lifecycle. It is related to cell death, cell development, its survival, metabolism, immunity, as well as infection and aging (Chaabane et al., 2013). Therefore, this process is thoroughly studied in relation to various diseases and processes. For instance, researchers try to understand the way the process can be affected by the disposal of certain nanoscale materials (Stern, Adiseshaiah & Crist, 2012). Su, Yang, Xu, Chen and Yu (2015) explore the role autophagy plays in the development of metastasis.

The article in question written by Buckingham et al. (2015) explores the difference between autophagic flux associated with herpes simplex virus (HSV) infection and varicella-zoster virus (VZV) infection. Buckingham et al. (2015) note that numerous experiments show that autophagy occurs in cultured cells affected by VZV infection. The researchers conclude that autophagy is proviral during VZV while, in cells with HSV infection, it is significantly different.

Methods

Buckingham et al. (2015) explored autophagic flux in xenografts of human skin during the SCID VZV pathogenesis mouse model. The model presupposes the insertion of xenografts of human fetal skin under the skin of a mouse that is affected by SCID. After that, the researchers inoculated human cells with VZV infection. The xenografts are harvested on the 7^th, 14^th, and 21^st days after the inoculation. It was found that autophagy was significant in the infected cells. The researchers also examined autophagic flux in the infected cultured cells. Autophagy was significantly less apparent in the latter case.

Results

It is found that autophagy in VZV infected cells is very unstable and virions are often released, while in HSV virions are enclosed within infected cells only. Buckingham et al. (2015) conclude that inoculation of cells with virions will result in a lower level of autophagy. It is reported that the ratio of particle to PFU was 40,000:1 (Buckingham et al. 2015). The researchers report that VZV-related autophagy is associated with cell stress and that a more significant inoculum induces more significant autophagy.

Discussion

The researchers note that their experiment supports their hypothesis that autophagosome development is primary to autophagy inhibiting. Buckingham et al. (2015) state that the method used is highly effective and can be utilized for other experiments aimed at measuring autophagy. Buckingham et al. (2015) also stress that the experiments conducted show that VZV induces autophagy while a similar HSV infection has a different effect and often blocks autophagosome maturation. In other words, the researchers identified two genes in HSV inhibiting autophagy. These genes are US11 and ICP34.5. The researchers stress the significance of the experiment that justifies early phase autophagy in such diseases as Epstein-Barr virus infection.

Apart from that, the findings can be applied in research associated with other diseases and infections. Thus, it is possible to tie autophagic flux with metastasis development and the role US11 and ICP34.5 genes can play in this process.

Reference List

Buckingham, E.M., Carpenter, J.E., Jackson, W., Zerboni, L., Arvin, A.M., & Grose, C. (2015). Autophagic flux without a block differentiates varicella-zoster virus infection from herpes simplex virus infection. PNAS, 112(1), 256-261.

Chaabane, W., User, S.D., El-Gazzah, M., Jaksik, R., Sajjadi, E., Rzeszowska-Wolny, J., Łos, M.J. (2013). Autophagy, apoptosis, mitoptosis and necrosis: Interdependence between those pathways and effects on cancer. Arch Immunol Ther Exp, 61, 43-58.

Stern, S.T., Adiseshaiah, P.P., & Crist, R.M. (2012). Autophagy and lysosomal dysfunction as emerging mechanism of nanomaterial toxicity. Particle and Fibre Toxicology, 9, 1-20.

Su, Z., Yang, Z., Xu, Y., Chen, Y., & Yu, Q. (2015). Apoptosis, autophagy, necroptosis, and cancer metastasis. Molecular Cancer, 14 (48), 1-14.

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Autophagy in Herpes Simplex and Varicella-Zoster Virus Infections

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