High temperature induces transcriptomic changes inCrassostrea gigasthat hinders progress of Ostreid herpesvirus (OsHV-1) and promotes survival

Abstract

Among all the environmental factors, seawater temperature plays a decisive role in triggering marine diseases. Like fever in vertebrates, high seawater temperature could modulate the host response to the pathogens in ectothermic animals. In France, massive mortality of Pacific oysters Crassostrea gigas caused by the ostreid herpesvirus 1 (OsHV-1) is markedly reduced when temperatures exceed 24°C in the field. In the present study we assess how high temperature influences the host response to the pathogen by comparing transcriptomes (RNA-sequencing) during the course of experimental infection at 21°C (reference) and 29°C. We show that high temperature induced host physiological processes that are unfavorable to the viral infection. Temperature influenced the expression of transcripts related to the immune process and increased the transcription of genes related to apoptotic process, synaptic signaling, and protein processes at 29°C. Concomitantly, the expression of genes associated to catabolism, metabolites transport, macromolecules synthesis and cell growth remained low since the first stage of infection at 29°C. Moreover, viral entry into the host might have been limited at 29°C by changes in extracellular matrix composition and protein abundance. Overall, these results provide new insights into how environmental factors modulate the host-pathogen interactions.

Viral Decoys: The Only Two Herpesviruses Infecting Invertebrates Evolved Different Transcriptional Strategies to Deflect Post-Transcriptional Editing

“…Alternatively, the different temperatures (18 • C for abalone and 15 • C for clam) we applied during infections could lead to differential infection dynamics [44,45]. These temperatures were, however, chosen to resemble the environmental conditions for which mortalities were observed, and are similar to the temperature threshold necessary for OsHV-1 to cause disease in oysters (16 • C) [46], whereas only much higher temperatures (24 • C) were shown to limit the progression of OsHV-1 infection [47]. It is therefore unlikely that infection dynamics during mortalities in both hosts differ substantially from our experimental infections.…”

Comparative Proteomics of Ostreid Herpesvirus 1 and Pacific Oyster Interactions With Two Families Exhibiting Contrasted Susceptibility to Viral Infection

“…To infect oysters, authors performed experimental injections of OsHV-1 in the adductor muscle of Pacific oysters, an experimental approach developed by Schikorski et al. ( 11 ) which is routinely used to evaluate in vivo interactions between C. gigas and OsHV-1 ( 33 , 39 – 41 ). Infection by injection provides a better synchronization of the viral infection compared to natural infections.…”

“…In the context of viral infection, ubiquitin-related proteins coordinate an effective antiviral immune response by regulating efficient antiviral signaling pathways such as the RIG-I-like, Toll-like or interferon-like pathways ( 80 ). Several studies showed that genes related to the ubiquitination process increased during the first hours of infection (6 and 12 hpi) with a higher expression in more resistant compared to more susceptible Pacific oysters ( 20 , 41 , 79 ). In our study ubiquitin-related proteins were highly modulated in the more resistant Pacific oysters, while few of them were modulated in the more susceptible Pacific oysters.…”

The Pacific Oyster Mortality Syndrome, a Polymicrobial and Multifactorial Disease: State of Knowledge and Future Directions

“…bacterial virulence or oyster physiology) could be influenced by high temperatures and thereby affect POMS permissiveness. Although the effect of high temperatures on bacterial virulence remains to be investigated, a recent work demonstrated that oyster immunity is modulated, and apoptotic processes induced, by high temperatures, which could explain the observed decrease of permissiveness ( 11 ).…”