2017
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Immune Escape via a Transient Gene Expression Program Enables Productive Replication of a Latent Pathogen
Abstract: SUMMARY How type I/II interferons prevent periodic reemergence of latent pathogens in tissues of diverse cell-types remains unknown. Using homogenous neuron cultures latently-infected with herpes simplex virus-1, we show that extrinsic type I or II interferon act directly on neurons to induce unique gene expression signatures and inhibit the reactivation-specific burst of viral genome-wide transcription called Phase I. Surprisingly, interferons suppressed reactivation only during a limited period early in Phas⦠Show more
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ββ¦When analyzing host gene expression after treatment with our diverse set of drugs, we observed recurrent downregulation of the host innate immune response pathway. In agreement with our previous findings ( Shnayder et al., 2020 ), this indicates that viral gene expression during latent infection does have functional consequences and suggests a constant arms race between viral mRNA or viral protein expression and expression of host innate immune response genes during infection and latency ( Linderman et al., 2017 ). In summary, our findings suggest that herpesvirus temporal gene expression cascade is dictated by a more intricate set of dependencies than was previously appreciated and that as envisioned for many years, the trademark of gene expression during HCMV latency is the unique repression of IE genes.β¦β
Section: Discussionsupporting
confidence: 92%
Exaggerated anticipatory anxiety is common in social anxiety disorder (SAD).
Neuroimaging studies have revealed altered neural activity in response to social stimuli in SAD, but fewer studies have examined neural activity during anticipation of feared social stimuli in SAD.
The current study examined the time course and magnitude of activity in threat processing brain regions during speech anticipation in socially anxious individuals and healthy controls (HC).
Method Participants (SAD n = 58; HC n = 16) underwent functional magnetic resonance imaging (fMRI) during which they completed a 90s control anticipation task and 90s speech anticipation task.
ββ¦When analyzing host gene expression after treatment with our diverse set of drugs, we observed recurrent downregulation of the host innate immune response pathway. In agreement with our previous findings ( Shnayder et al., 2020 ), this indicates that viral gene expression during latent infection does have functional consequences and suggests a constant arms race between viral mRNA or viral protein expression and expression of host innate immune response genes during infection and latency ( Linderman et al., 2017 ). In summary, our findings suggest that herpesvirus temporal gene expression cascade is dictated by a more intricate set of dependencies than was previously appreciated and that as envisioned for many years, the trademark of gene expression during HCMV latency is the unique repression of IE genes.β¦β
Section: Discussionsupporting
confidence: 92%
Exaggerated anticipatory anxiety is common in social anxiety disorder (SAD).
Neuroimaging studies have revealed altered neural activity in response to social stimuli in SAD, but fewer studies have examined neural activity during anticipation of feared social stimuli in SAD.
The current study examined the time course and magnitude of activity in threat processing brain regions during speech anticipation in socially anxious individuals and healthy controls (HC).
Method Participants (SAD n = 58; HC n = 16) underwent functional magnetic resonance imaging (fMRI) during which they completed a 90s control anticipation task and 90s speech anticipation task.
ββ¦When analyzing host gene expression due to treatment with our diverse set of drugs, we observed recurrent down regulation of the host innate immune response pathway. In agreement with our previous findings 61 , this indicates that viral gene expression during latent infection does have functional consequences and suggests a constant arms race between viral mRNA or viral protein expression and expression of host innate immune response genes during infection and latency 62 . In summary, our findings suggest that herpesvirus temporal gene expression cascade is dictated by a more intricate set of dependencies than was previously appreciated and that as envisioned for many years, the trademark of gene expression during HCMV latency is the unique repression of IE genes.β¦β
Section: Discussionsupporting
confidence: 92%
Exaggerated anticipatory anxiety is common in social anxiety disorder (SAD).
Neuroimaging studies have revealed altered neural activity in response to social stimuli in SAD, but fewer studies have examined neural activity during anticipation of feared social stimuli in SAD.
The current study examined the time course and magnitude of activity in threat processing brain regions during speech anticipation in socially anxious individuals and healthy controls (HC).
Method Participants (SAD n = 58; HC n = 16) underwent functional magnetic resonance imaging (fMRI) during which they completed a 90s control anticipation task and 90s speech anticipation task.
ββ¦We conclude that the absence of CD28 and CTLA4 is a crucial regulator of immune responses leading to higher IFN-Ξ± and IFN-Ξ² expression during latency, which results in delayed reactivation. Consistent with our results, exogenous IFN-Ξ² and IFN-Ξ³ have been shown to transiently suppress HSV reactivation in a neuron intrinsic manner ( 56 ), and the expression of many genes with known roles in antiviral defenses and IFN signaling (e.g., Mx1/2, STAT1/2, ISG15, IFIT2, IRF1/7/9, Daxx, PKR, TAP1, and USP18) is downregulated in three knockout mice strains used in our study ( Table 2 ). Our finding that greater expression of IFN-Ξ² and IFN-Ξ³ in CD28 β/β and CD28 β/β CTLA4 β/β mice corresponds to reduced reactivation is consistent with the results of the above-mentioned study.β¦β
Section: Discussionsupporting
confidence: 91%
Exaggerated anticipatory anxiety is common in social anxiety disorder (SAD).
Neuroimaging studies have revealed altered neural activity in response to social stimuli in SAD, but fewer studies have examined neural activity during anticipation of feared social stimuli in SAD.
The current study examined the time course and magnitude of activity in threat processing brain regions during speech anticipation in socially anxious individuals and healthy controls (HC).
Method Participants (SAD n = 58; HC n = 16) underwent functional magnetic resonance imaging (fMRI) during which they completed a 90s control anticipation task and 90s speech anticipation task.
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