Pathology

The importance of immune evasion in the pathogenesis of rabies virus

“…RABV not only impacts on innate immune signaling within infected cells, but also has developed mechanisms to suppress broader adaptive inflammatory responses. In the CNS, despite high levels of viral replication in naturally infected humans and animals, a lack of significant infiltration by inflammatory immune cells is a hallmark of pathogenic infection [ 59 ]. Several lines of evidence indicate key roles in pathogenesis [ 2 , 74 ].…”

“…Pathogenesis is dependent on virus reaching the CNS (reviewed in [ 26 ]) where replication and neural network-dependent spread induce severe neurological symptoms including agitation, spasms and paralysis, preceding a lethal outcome [ 25 ]. Despite this, it has been long appreciated that pathological changes in the CNS are generally mild, with infected humans/animals lacking significant inflammation or neural cell death [ 59 ]. Thus, RABV appears to have evolved neuro-protective capacity involving mechanisms to evade host immunity, thereby replicating in neurons without inducing strong immune responses.…”

Overexpression of MAP2 and NF-H Associated with Dendritic Pathology in the Spinal Cord of Mice Infected with Rabies Virus

“…Rabies is an illness caused by a virus that primarily affects the central nervous system. The virus almost exclusively affects neurons, resulting in notable neurological changes without any apparent morphological changes in the affected nervous tissue [ 6 ]. Even neuronal death from apoptosis is not considered important in the pathology.…”

“…In addition to its exclusive neurotropic feature, rabies differs from other viruses because it does not induce viremia and has the highest mortality of any known infectious disease (more than Ebola, for example) [ 6 ]. Another characteristic of rabies is its apparently late effect on different pathophysiological parameters; the electroencephalogram pattern is preserved unchanged for almost the entire duration of the disease and collapses only a few hours before the disease in both humans and animal models.…”

“…Generally, dendritic pathology is linked to the loss of MAP2 [ 16 ]. These results suggest that the degeneration of neuronal processes due to the disruption of cytoskeletal integrity from rabies viral infection is a component of neural dysfunction [ 6 ].…”