The Comparative Pathology of Experimental Venezuelan Equine Encephalomyelitis Infection in Different Animal Hosts

Experimental encephalitis following peripheral inoculation of West Nile virus in mice of different ages

“…The occurrence of subclinical CNS infection following extraneural inoculation with highly virulent arboviruses is probably a relatively common laboratory phenomenon, since findings similar to ours have been reported for a number of arboviruses: louping-ill (Doherty, 1969), Langat (Thind & Price, 1969a;Webb et al 1968), Japanese encephalitis (Huang & Wong, 1963) and Venezuelan equine encephalitis (Gleiser, Gochenour, Berge & Tigertt, 1961). These descriptive studies of pathogenesis indicate that virus invasion of the CNS occurs later during abortive infection than it does during lethal infection.…”

Encephalitic Development in Alphaviral Infection

“…The mouse model mimics both human and equine disease with mice developing neurotropic disease characterized by lethal encephalitis and lymphotropism following a biphasic disease course (Gardner, et al, 2008;Gleiser, et al, 1962;Steele, et al, 1998). Following peripheral routes of infection, mice display human like disease with progression from infection of the lymphoid tissue and ultimate destruction of CNS tissues.…”

“…Like the majority of symptomatic human infections, infection in NHP represents an acute biphasic, nonspecific febrile disease with infection of lymphoid organs (Danes, et al, 1973;Gleiser, et al, 1962;Monath, et al, 1974a;Nalca, et al, 2003b;Pratt, et al, 1998;Reed, et al, 2007;Verlinde, 1968;Victor, et al, 1956) . In a comprehensive study with rhesus macaques infected IP, animals developed a transient viremia and biphasic fever, but otherwise displayed no clinical signs of disease with complete resolution of pathologies by five weeks PI.…”

“…Lymphoid depletion occurred rapidly by two days post-infection with extensive lymphoid necrosis, later followed by lymphoid hyperplasia as the animals recovered from infection. Lesions in the brain characterized by perivascular cuffs associated with lymphocytes and gliosis were also apparent and developed around six days post-infection starting at the olfactory bulb and spread caudally throughout the brain (Danes, et al, 1973;Gleiser, et al, 1961;1962;Monath, et al, 1974b;Pratt, et al, 1998;Reed, et al, 2007;Verlinde, 1968;Victor, et al, 1956). A range of CNS involvement presents depending on strain of virus utilized and route of inoculation with IN and IC inoculation being particularly severe.…”

“…In cynomolgus macaques similar findings were reported except in the case of IN or aerosol infection where CNS damage is more severe and, in the case of IC infection, lethal (Danes, et al, 1973;Monath, et al, 1974b;Pratt, et al, 1998;Reed, et al, 2007;Steele & Twenhafel, 2010;Verlinde, 1968;Victor, et al, 1956). Thus, IN inoculation results in disease ranging from simply clinical signs of encephalitis and subsequent recovery to fulminant lethal encephalitis (Gleiser, et al, 1962;Steele & Twenhafel, 2010).…”