Dual Transcriptomic Analysis Reveals a Delayed Antiviral Response of against Haliotid Herpesvirus-1.

Viruses

Key Laboratory of Maricultural Organism Disease Control, Ministry of Agriculture, Qingdao KeyLaboratory of Mariculture Epidemiology and Biosecurity, Yellow Sea Fisheries Research Institute,Chinese Academy of Fishery Sciences, Qingdao 266071, China.

Published: April 2019

AI Article Synopsis

  • Haliotid herpesvirus-1 (HaHV-1) is a newly discovered herpesvirus that causes severe neurological disease in abalone species.
  • A comprehensive study used RNA sequencing to analyze transcriptomic changes in abalone at different time points post HaHV-1 injection, revealing 448 million raw reads generated and assembled into a significant number of unigenes.
  • Findings indicate that while the virus shows heightened activity at 24 hours post-infection, the host's immune response is not triggered until 60 hours, suggesting HaHV-1 may have evolved methods to dodge early immune detection.

Article Abstract

Haliotid herpesvirus-1 (HaHV-1) is the first identified gastropod herpesvirus, causing a highly lethal neurologic disease of abalone species. The genome of HaHV-1 has been sequenced, but the functions of the putative genes and their roles during infection are still poorly understood. In the present study, transcriptomic profiles of at 0, 24 and 60 h post injection (hpi) with HaHV-1 were characterized through high-throughput RNA sequencing. A total of 448 M raw reads were obtained and assembled into 2.08 × 10 unigenes with a mean length of 1486 bp and an N50 of 2455 bp. Although we detected increased HaHV-1 DNA loads and active viral expression at 24 hpi, this evidence was not linked to significant changes of host transcriptomic profiles between 0 and 24 hpi, whereas a rich immune-related gene set was over-expressed at 60 hpi. These results indicate that, at least at the beginning of HaHV-1 infection, the virus can replicate with no activation of the host immune response. We propose that HaHV-1 may evolve more effective strategies to modulate the host immune response and hide during replication, so that it could evade the immune surveillance at the early stage of infection.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6520846PMC
http://dx.doi.org/10.3390/v11040383DOI Listing

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