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Cross-species analysis of transcriptomic response to alphaherpesvirus infection in human, bovine and equine cells

ABSTRACT: Comparative transcriptomics offers a powerful approach to elucidate host–virus interactions across related pathogens, yet systematic evaluations across spe-cies-matched cellular systems remain limited. Here, we performed a cross-species RNA-sequencing analysis of respective species’ cells infected with three alphaherpesviruses - herpes simplex virus 1 (HSV-1), bovine al-phaherpesvirus 1 (BHV-1), and equid alphaherpesvirus 1 (EHV-1) - to dissect conserved and virus-specific transcriptional responses. We show that certain orthologous genes and orthologous pathways are differentially regulated upon infection among the three species like pathways related to translation rRNA processing and TNF-alpha signaling. We find that the earliest sampled timepoint of infection, 2 hours post infection (hpi), shows the most commonly enriched pathways among the three species compared to later timepoints. At 6h and 9h post infection, BHV-1- and EHV-1-infections have more in common with each other in terms of enriched pathways than with HSV-1 infections. Moreover, we provide a comprehensive analysis of temporal viral gene expression for all three herpesviruses. Together, these findings provide a comparative framework for understanding alphaherpesvirus–host interactions and reveal both conserved core responses and species-specific transcriptional signatures. This work estab-lishes a foundation for identifying broadly acting antiviral targets as well as vi-rus-specific vulnerabilities that may inform host-directed therapies and cross-species disease management.

ORGANISM(S): Bos taurus Equus caballus Homo sapiens

PROVIDER: GSE314009 | GEO | 2026/01/14

REPOSITORIES: GEO

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Project description:The overall goal of the study was to use in vivo data combined with functional genomics to define gene expression signatures representative of a spectrum of HSV CNS infections. Innate immune deficiencies result in a spectrum of severe clinical outcomes following infection. In particular, there is a strong association between loss of the signal transducer and activator of transcription (Stat) pathway, breach of the blood-brain barrier (BBB), and virus-induced neuropathology. The gene signatures that characterize resistance, disease, and mortality in the virus-infected nervous system have not been defined. Herpes simplex virus type 1 (HSV-1) is commonly associated with encephalitis in humans, and humans and mice lacking Stat1 display increased susceptibility to HSV central nervous system (CNS) infections. In this study, two HSV-1 strains were used, KOS (wild type [WT]), and Δvhs, an avirulent recombinant lacking the virion host shutoff (vhs) function. In addition, two mouse strains were used: strain 129 (control) and a Stat1-deficient (Stat1(-/-)) strain. Using combinations of these virus and mouse strains, we established a model of infection resulting in three different outcomes: viral clearance without neurological disease (Δvhs infection of control mice), neurological disease followed by viral clearance (Δvhs infection of Stat1(-/-) mice and WT infection of control mice), or neurological disease followed by death (WT infection of Stat1(-/-) mice). Through the use of functional genomics on the infected brain stem and liver, we determined gene signatures that were representative of the three infection outcomes. Gender matched, 6- to 8- week old immunocompetent, control 129S6 and 129S6 Stat1 knockout mice were infected corneally with 2x10^6 PFU of either wild type HSV-1, a vhs-null HSV virus, or mock-infected. Brain stems and liver of individual mice were isolated at days 1, 3, 5 and 7 post-inoculation for microarray analysis. For microarray analysis, samples were collected from n=2 animals (1 male, 1 female) per mouse strain and virus strain for each time point. Equal masses of tissue were pooled from two mock-infected mice per time point and run on microarray.

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Cross-species analysis of transcriptomic response to alphaherpesvirus infection in human, bovine and equine cells

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