<unk>  is caused by the<unk>  virus (OROV) that belongs to the Peribunyaviridae family of arboviruses. This virus is a single-stranded, negative sense RNA virus which is the cause of this disease. There are no specific ultrastructural studies of the<unk>  virus in human tissues that have been recorded to this date. It is likely that this viral agent shares similar morphological characteristics with other members of the Orthobunyavirus genus. Members of the Orthobunyavirus genus have a three part, single-stranded, negative sense RNA genome of small (S), medium (M) and large (L) RNA segments. These segments function to encode nucleocapsids, glycoproteins and the RNA polymerase in that sequential order. Through phylogenetic analysis of nucleocapsid genes in different<unk>  virus strains, it has been revealed that there are three unique genotypes (I, II, III) that are currently spreading through Central and South America. Genomic Reassortment Genetic reassortment is said to be one of the most important mechanisms in explaining the viral biodiversity in orthobunyaviruses. This occurs when two genetically related viruses infect the same cell at the same time forming a progeny virus and this virus holds various components of genetic L, M and S segments from the two parental viruses. In reassortment, the S and L segments are the ones that are usually exchanged between species further, the S segment, that is coded by the nucleocapsid protein, and the L polymerase function together to create a replication of the viral genome. Due to this, one segment will restrict the molecular evolution of another segment and this is said to be inherited as a pair. On the contrary, the M segment codes for viral glycoproteins and these could be more prone to mutations due to a higher selective pressure in their coding region because these proteins are major host range determinants. Pathogenesis There is not a significant amount of information about regarding the natural pathogenesis of OROV infections because there have been no recorded fatalities to date. It is known that within 2–4 days from the initial onset of systematic symptoms in humans, the presence of this virus is detected in the blood. In some cases this virus has also been recovered from the cerebrospinal fluid, but the route of invasion to the central nervous system remains unclear. To further understand the pathogenesis of how this virus manifests in the body experimental studies using murine models have been performed. Murine Models BALB/c neonate mice were treated with this virus subcutaneously and presented clinical symptoms five days after inoculation. The mice revealed a high concentration of the replicating virus in the brain along with inflammation of the meninges and apoptosis of neurons without encephalitis, which is inflammation of the brain due to an infection. These findings confirmed the neurotropism of this virus, which means that this virus is capable of infecting nerve cells. Immunohistochemistry was used to reveal how this virus had access to the central nervous system. The findings indicated that the OROV infection starts from the posterior parts of the brain and progresses toward the forebrain. The<unk>  virus spreads through the neural routes during early stages of the infection, reaching the spinal cord and traveling upward to the brain through brainstem with little inflammation. As the infection progresses, the virus crosses the blood-brain barrier and spreads to the brain parenchyma leading to<unk> e manifestations of encephalitis. Damage to the brain parenchyma can result in the loss of cognitive ability or death.
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