Abalone herpesvirus (AbHV) infection of cultured abalones Haliotis diversicolor supertexta induced acute high mortality in 2003. Years later, sporadic mortality was noted for an extended period of months, resulting in high cumulative mortality. Moribund abalones were analyzed using PCR, in situ hybridization, and histopathology, because thus far no viral particles have been observed by transmission electron microscopy. PCR using 20 primer sets, specifically designed from sequences of acute AbHV infection, failed to amplify any products from abalones suffering from chronic mortality. Subsequently, a 1406-bp sequence was amplified from chronic moribund abalones, and this sequence showed a 92% (553 bp/602 bp) homology with the gene of an AbHV Taiwan isolate (NCBI serial no. KF537536.1), suggestive of an AbHV pathotype. Histopathology of AbHV pathotype infection showed hemocyte infiltration in the lamina propia of the digestive tract, and hemocytes of various stages were evident, as well as the loss of seminal tubules in the gonad. In situ hybridization revealed that in AbHV infection, positive signals were restricted to the neural ganglia, while in AbHV pathotype infection, positive signals were observed only in the hemocytes. It appeared that the tropism of AbHV shifted from mainly neurotropic in AbHV infection to mainly hemocytotropic in abalone suffering from chronic mortality. Abalone shriveling syndrome-associated virus co-infection was detected in some of AbHV pathotype infection events. Further studies are needed to better understand the pathogenesis of AbHV pathotype affecting H. diversicolor in Taiwan.
Induction of acidic fibroblast growth factor and full-length platelet-derived growth factor expression in human cardiac allografts. Analysis by PCR, in situ hybridization, and immunohistochemistry.