The Junín virus virion is enveloped with a variable diameter of between 50 and 300nm. The surface of the particle encompasses a layer of T-shaped glycoprotein extensions, extending upto 10nm from the envelope, which are important for mediating attachment and entry into host cells.

The Junín virus genome comprises two single stranded RNA molecules, each encoding two different genes in an ambisense orientation. The two segments are termed ‘short (S)’ and ‘long (L)’ due to their respective lengths. The short segment (around 3400 nucleotides in length) encodes the nucleocapsid protein and the glycoprotein precursor (GPC). The GPC is subsequently cleaved to form two viral glycoproteins, GP1 and GP2 which ultimately form the T-shaped glycoprotein spike which extends from the viral envelope. [1]. The long segment (around 7200 nucleotides in length) encodes the viral polymerase and a zinc binding protein.

A member of the genus Arenavirus, Junín virus characteristically causes Argentine hemorrhagic fever (AHF). AHF leads to major alterations within the vascular, neurological and immune systems and has a mortality rate of between 20 and 30%[2]. Symptoms of the disease are conjunctivitis, purpura, petechia and occasional sepsis. The symptoms of the disease are relatively indistinct and may therefore be mistaken for a different condition.

Since the discovery of the Junín virus in 1958, the geographical distribution of the pathogen, although still confined to Argentina, has risen. At the time of discovery, Junín virus was confined to an area of around 15,000km². At the beginning of 2000, the distribution had risen to around 150,000km².[3]. The natural hosts of Junín virus are rodents, particularly Mus musculus, Calomys spp and Akodon azarae. Direct rodent to human transmission only transpires when contact is made with excrement of an infected rodent. This commonly occurs via ingestion of contaminated food or water, inhalation of particles within urine or via direct contact of broken skin with rodent excrement.