“BRAIN-ONLY” FORM OF DOLPHIN MORBILLIVIRUS INFECTION IN STRIPED DOLPHINS (STENELLA COERULEOALBA): PATHOGENETIC INSIGHTS

Dolphin Morbillivirus (DMV), a highly pathogenic agent, can give rise to peculiar, “brain-only” forms of infection (BOFDI), in which evidence of viral antigen and/or genome can be found exclusively in the brain tissue from striped dolphins (Stenella coeruleoalba)1-4 and, far less commonly, from bottlenose dolphins (Tursiops truncatus)4. These BOFDIs show morphopathological and neuropathogenetic similarities with subacute sclerosing panencephalitis and old dog encephalitis, which are known to occur in Measles Virus (MeV)-infected patients and in Canine Distemper Virus (CDV)-infected dogs, respectively5. We investigated in the brain tissue of 3 BOFDI-affected, male striped dolphins, 2 adults and 1 newborn, the expression levels of 5-lipoxygenase (5-LOX), along with the ultrastructural damage and the neuronal and non-neuronal cell populations colonized by the viral pathogen. The expression levels of 5-LOX, which were evaluated by means of Western Blot (WB) analysis, were significantly (P ≤ 0.05) higher in the brain parenchyma of the 3 aforementioned cetaceans, when compared with those of 3 additional striped dolphins showing no direct nor indirect evidence of DMV infection. Furthermore, alongside with a number of nuclear (chromatin) and cytoplasmic (mitochondrial) ultrastructural changes, double labeling-indirect immunofluorescence (DL-IIF) microscopy revealed different degrees of viral colonization of calbindin (CALB)-immunoreactive (IR) and nitric oxide synthase (NOS)-IR neurons, but not of (GFAP-IR) astrocytes, within the brain tissue from the two DMV-affected adults as compared to the DMV-affected newborn. Albeit preliminary, this is the first study addressing the ultrastructural pathology and the neuropathogenesis of BOFDI, with special emphasis on the neuronal and non-neuronal cell populations colonized by DMV in the striped dolphin’s brain. Further studies aimed at characterizing the virus- and the host-related factors involved in BOFDI pathogenesis are warranted