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Transcriptomic Profiling Reveals Intense Host-Pathogen Dispute Compromising Homeostasis during Acute Rift Valley

Erick Bermúdez-Méndez1,2,3,4, Paolo Angelino3,4,5, Lucien van Keulen6

  • 1Department of Virology and Molecular Biology, Wageningen Bioveterinary Research, Lelystad, The Netherlands.

Journal of Virology
|June 12, 2023
PubMed
Summary
This summary is machine-generated.

Rift Valley fever virus (RVFV) infection in lambs impairs liver function by downregulating metabolic enzymes. Elevated LRP1 expression may influence RVFV tissue tropism, offering insights into pathogenesis.

Keywords:
RNA-seqRift Valley fever virushost-pathogen interactionspathogenesis

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Area of Science:

  • Virology and Pathogenesis
  • Host-Pathogen Interactions
  • Molecular Biology

Background:

  • Rift Valley fever virus (RVFV) is a mosquito-borne pathogen causing severe disease in animals and humans, posing a significant public health threat.
  • The molecular mechanisms of RVFV pathogenesis *in vivo*, particularly host factor involvement, remain incompletely understood despite known *in vitro* interferon responses.
  • Natural RVFV infections are acute, with rapid viremia followed by decline, necessitating a deeper understanding of host responses in natural hosts.

Purpose of the Study:

  • To investigate the *in vivo* host transcriptional profiles in response to RVFV infection in lambs.
  • To identify host factors and gene regulation networks involved in RVFV pathogenesis.
  • To elucidate the molecular basis of RVFV tissue tropism and organ dysfunction.

Main Methods:

  • RNA sequencing (RNA-seq) technology was employed to analyze host gene expression in liver and spleen tissues of RVFV-infected lambs.
  • Transcriptional profiles were compared between infected and control groups to identify differentially expressed genes and pathways.
  • Specific host factors, such as LRP1, were investigated for their potential role in RVFV tropism and pathogenesis.

Main Results:

  • Interferon (IFN)-mediated pathways were confirmed to be robustly activated during RVFV infection.
  • Hepatocellular necrosis was associated with a significant downregulation of metabolic enzymes, leading to compromised liver function and homeostasis.
  • Elevated basal expression of Low-density lipoprotein receptor-related protein 1 (LRP1) in the liver was linked to RVFV tissue tropism.

Conclusions:

  • RVFV infection severely impacts liver function through downregulation of essential metabolic enzymes.
  • The study provides insights into the *in vivo* host response, highlighting the role of IFN pathways and metabolic dysregulation.
  • Basal LRP1 expression levels may be a key determinant of RVFV's tissue tropism, advancing our understanding of its pathogenesis.