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Herpes Simplex Virus-1 Fine-Tunes Host's Autophagic Response to Infection: A Comprehensive Analysis in Productive Infection Models.

Yakoub AM, Shukla D - PLoS ONE (2015)

Bottom Line: The autophagic response of the host cell was suggested to be regulated by HSV-1.We found that autophagy was slightly inhibited in one cell type, while in other cell types autophagy maintained its basal levels mostly unchanged during productive infection.This study refines the concept of HSV-1-mediated autophagy regulation to imply either inhibition, or prevention of activation, of the innate immune pathway.

View Article: PubMed Central - PubMed

Affiliation: Department of Microbiology and Immunology, University of Illinois, Chicago, IL United States of America, 60612; Department of Ophthalmology and Visual Sciences, University of Illinois Medical Center, Chicago, IL United States of America, 60612.

ABSTRACT
Herpes simplex virus-1 (HSV-1) infection causes severe conditions, with serious complications, including corneal blindness from uncontrolled ocular infections. An important cellular defense mechanism against HSV-1 infection is autophagy. The autophagic response of the host cell was suggested to be regulated by HSV-1. In this study, we performed a detailed analysis of autophagy in multiple HSV-1-targeted cell types, and under various infection conditions that recapitulate a productive infection model. We found that autophagy was slightly inhibited in one cell type, while in other cell types autophagy maintained its basal levels mostly unchanged during productive infection. This study refines the concept of HSV-1-mediated autophagy regulation to imply either inhibition, or prevention of activation, of the innate immune pathway.

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Analysis of Autophagy in HSV-1 Infection of Corneal Epithelial Cells.A. HCE cells were uninfected or infected with HSV-1 at the indicated MOIs. SQSTM1/p62 and LC3 were immunoblotted at 2 hpi. Quantification of band intensities was performed using digital band quantification software (ImageQunatTL; GE). B. Uninfected or infected HCE cells were immunoblotted at 8 hpi.
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pone.0124646.g004: Analysis of Autophagy in HSV-1 Infection of Corneal Epithelial Cells.A. HCE cells were uninfected or infected with HSV-1 at the indicated MOIs. SQSTM1/p62 and LC3 were immunoblotted at 2 hpi. Quantification of band intensities was performed using digital band quantification software (ImageQunatTL; GE). B. Uninfected or infected HCE cells were immunoblotted at 8 hpi.

Mentions: We then measured the effect of HSV-1 infection on autophagy in human corneal epithelial (HCE) cells, an important target of HSV-1 infection in vivo. The cells were infected with HSV-1 (KOS) at MOI of 0.1 or 1, and autophagy was monitored after 2 or 8 hpi. To assess autophagy, we measured, via immunoblotting, levels of LC3 and sequestosome1 (SQSTM1)/p62. Upon activation of the pathway, LC3-II levels increase while p62 is depleted due to its degradation by autophagy [17–19]. At all conditions, no significant changes in autophagy flux were observed, as monitored via LC3-II and p62 levels (Fig 4A and 4B).


Herpes Simplex Virus-1 Fine-Tunes Host's Autophagic Response to Infection: A Comprehensive Analysis in Productive Infection Models.

Yakoub AM, Shukla D - PLoS ONE (2015)

Analysis of Autophagy in HSV-1 Infection of Corneal Epithelial Cells.A. HCE cells were uninfected or infected with HSV-1 at the indicated MOIs. SQSTM1/p62 and LC3 were immunoblotted at 2 hpi. Quantification of band intensities was performed using digital band quantification software (ImageQunatTL; GE). B. Uninfected or infected HCE cells were immunoblotted at 8 hpi.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4403807&req=5

pone.0124646.g004: Analysis of Autophagy in HSV-1 Infection of Corneal Epithelial Cells.A. HCE cells were uninfected or infected with HSV-1 at the indicated MOIs. SQSTM1/p62 and LC3 were immunoblotted at 2 hpi. Quantification of band intensities was performed using digital band quantification software (ImageQunatTL; GE). B. Uninfected or infected HCE cells were immunoblotted at 8 hpi.
Mentions: We then measured the effect of HSV-1 infection on autophagy in human corneal epithelial (HCE) cells, an important target of HSV-1 infection in vivo. The cells were infected with HSV-1 (KOS) at MOI of 0.1 or 1, and autophagy was monitored after 2 or 8 hpi. To assess autophagy, we measured, via immunoblotting, levels of LC3 and sequestosome1 (SQSTM1)/p62. Upon activation of the pathway, LC3-II levels increase while p62 is depleted due to its degradation by autophagy [17–19]. At all conditions, no significant changes in autophagy flux were observed, as monitored via LC3-II and p62 levels (Fig 4A and 4B).

Bottom Line: The autophagic response of the host cell was suggested to be regulated by HSV-1.We found that autophagy was slightly inhibited in one cell type, while in other cell types autophagy maintained its basal levels mostly unchanged during productive infection.This study refines the concept of HSV-1-mediated autophagy regulation to imply either inhibition, or prevention of activation, of the innate immune pathway.

View Article: PubMed Central - PubMed

Affiliation: Department of Microbiology and Immunology, University of Illinois, Chicago, IL United States of America, 60612; Department of Ophthalmology and Visual Sciences, University of Illinois Medical Center, Chicago, IL United States of America, 60612.

ABSTRACT
Herpes simplex virus-1 (HSV-1) infection causes severe conditions, with serious complications, including corneal blindness from uncontrolled ocular infections. An important cellular defense mechanism against HSV-1 infection is autophagy. The autophagic response of the host cell was suggested to be regulated by HSV-1. In this study, we performed a detailed analysis of autophagy in multiple HSV-1-targeted cell types, and under various infection conditions that recapitulate a productive infection model. We found that autophagy was slightly inhibited in one cell type, while in other cell types autophagy maintained its basal levels mostly unchanged during productive infection. This study refines the concept of HSV-1-mediated autophagy regulation to imply either inhibition, or prevention of activation, of the innate immune pathway.

Show MeSH
Related in: MedlinePlus