The second cleavage occurs at the Golgi apparatus, where GP1-GP2, having been trafficked to the Golgi, is cleaved into separate mature viral glycoproteins, GP1 and GP2 (with cleavage mediated by SK1-/PS1 or MTBPS1). The spikes present on the virion envelope are dictated by tetramer formation of GP-1 and GP-2.When LCMV attacks a cell, the process of replication starts by attachment of the virus to host receptors through its surface glycoproteins. It is then endocytosed into a vesicle inside the host cell and creates a fusion of the virus and vesicle membranes. The ribonucleocapsid is then released in the cytoplasm. The RNA-dependent, RNA-polymerase brought along with the virus initially binds to a promoter on the L and S segments and begins transcription from negative-stranded to a positive-stranded mRNA. The formation of a strong hairpin sequence at the end of each gene terminates transcription. The mRNA strands are capped by the RNA-dependent, RNA-polymerase in the cytoplasm and are then subsequently translated into the four proteins essential for LCMV assembly. The ribonucleocapsid interacts with the Z matrix protein and buds on the cell membrane, releasing the virion out from the infected cell. The first arenavirus, Lymphocytic choriomeningitis mammarenavirus (LCMV), was isolated in 1933 by Charles Armstrong during a study of an epidemic in St. Louis.
Morbidity and mortality rates vary with the species of animal and its age at infection, as well as the strain of the virus and route of exposure. Neonatally and congenitally infected mice remain asymptomatic for many months, but the onset of glomerulonephritis reduces overall life expectancy. The morbidity rate in naturally infected post-neonatal mice is unknown; however, subclinical disease may be the most common form, as few natural outbreaks have been reported. In hamsters, approximately half of all congenitally infected animals clear the virus when they are approximately three months old and remain healthy; the remaining animals develop chronic disease. Hamsters infected as adults usually remain asymptomatic. Callitrichid hepatitis is reported to be highly fatal in naturally infected marmosets and tamarins in zoos. Since 1980, 12 outbreaks with 57 deaths have been reported in the U.S. In experimentally infected rhesusmacaques, three of four animals became fatally ill when inoculation was by the intravenous route. In contrast, inoculation by the intragastric route usually led to asymptomatic infections, with occasional disease and few deaths. In pets
Pet rodents are not known to be natural reservoirs for lymphocytic choriomeningitis virus. However, pets can become vectors if they are exposed to wild house mice in a breeding facility, pet store, or home. Such infections are rare. To date, (January 2017) documented infections in humans have occurred only after introduction to infected mice, guinea pigs, and hamsters, with the majority of cases transmitted by mice.