Deciphering the molecular mechanisms of oyster resistance to Pacific Oyster Mortality Syndrome (POMS) disease induced by high temperatures

Abstract

Climate change and rising temperatures are frequently cited as key factors in the emergence of diseases. While the increase in temperature can alter host immunity, influence pathogen virulence, and change the geographic distribution of vectors and their associated pathogens, few studies have investigated the impact of temperature variations on the molecular mechanisms controlling disease permissiveness. The present study addresses this question on a panzootic and polymicrobial disease, the Pacific Oyster Mortality Syndrome (POMS). POMS, initiated by the herpesvirus OsHV-1 μVar, affects juveniles of Magallana gigas, which is the most widely cultured oyster species in the world. In our study, two full-sib families were exposed to the disease under permissive (23 °C) and non-permissive (30 °C) conditions. Using an integrative multi-omics approach, we demonstrate that high temperature has a dual effect on oysters (1) inducing a metabolic reprogramming, creating a sub-optimal metabolic environment for viral infection and thereby limiting POMS development, and (2) enhancing the host's antiviral immune capabilities, both at a baseline level and in response to infection. Overall, these responses triggered at elevated temperature improve oyster survival against POMS. Our study showed that temperature exerts complex effects on host-pathogen interactions; and molecular-level mechanistic approaches are crucial to thoroughly understand and accurately assess how temperature changes can influence epidemiological risk.