Mushroom virus X disease: host molecular and innate immune responses upon stress induced by aerosolised pathogens, toxins and virulence light

Abstract

The mushroom virus X (MVX) patch disease is currently of international interest. Often the disease is observed with barren patches beside healthy looking mushrooms, arrested pins, premature opening, brown, off-colour and distortions in shape. In molecular terms, ~26 disparate MVX linked dsRNAs ranging from 20.2Kb to 640bp have been detected, some in unencapsidated forms, and linked to stress (e.g. browning symptoms). Using molecular and chemical methods other stress factors including microbe (pathogen) associated molecular patterns (MAMPs) characterised by bacterial lipopolysaccharide, lipoproteins and fungal ribotoxic secondary metabolites tricothecenes prevalent in mushroom growing substrate constituents or in aerosolised tunnel environments were detected.  It was investigated that when the host innate immune responses when challenged with stress components / MAMPs which invariably include dsRNAs via calibration of signal recognition systems (e.g G-Proteins/ cAMP), the sentinel protein kinases (PKs) that recognize and respond to various external stimuli during hosts’ growth, development and pathogenesis. RT-PCR assays of trichothecenes and MVXdsRNAs in combination increased PK expressions. The visual correlation between the MVX associated browning patches and the emergent zones of hosts’ immune responses exhibited and the aerosolised ‘mycotoxin’ particulate grids in the indoor tunnel environments were examined. Preliminary data obtained indicated that the sporadic lighting differences in tunnels could result in the ‘light activation of histidine kinases’ which are key environmental sensing molecular components of Pseudomonas syringae that triggers virulence on its host and its contribution to browning related illness of mushrooms is discussed. We have isolated and cloned miRNAs from MVX infected Agaricus bisporus possessing consensus hairpin structural identities of bacterial infection response (BiR) related microRNA associated with Toll Like Receptor (TLR) family in other eukaryotes, which are the primary evolutionary conserved sensors of pathogen-associated molecular patterns (PAMPs), that are known to trigger host inflammatory and immune responses. Our preliminary data suggest that host cells or their surface colonising pathogens could co-opt for suppressing their own replication, evade immune elimination and establish a ‘persistent chronic infection’, culminating into a host-viral pathogen perception-deception cycles.