LCMV Case Study

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Lymphocytic Choriomeningitis virus (LCMV) belongs to the Old World arenavirus family of enveloped viruses (Buchmeier et al., 2007). LCMV in particular has served as model organism from many significant studies in the field of immunology such as the Nobel Prize winning study of the Major Histocompatibility Complex (MHC) by Zinkernagel and Doherty (1975). LCMV’s natural reservoirs are the common household rodents (Traub, 1936). Household mice have shown to attain persistent asymptomatic LCMV infections (Oldstone and Dixon, 1976). This persistence of a chronic infection is vital to the evolution of the virus. As a result, LCMV has undergone co-evolution by horizontal and vertical transmission (Welsh et al., 2010).

LCMV’s genome consists of a
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Rojek et al. investigated this phenomenon by infecting Human embryonic kidney (HEK293T) cells with the LCVM immunosuppressive Clone 13 (cl-13) which binds to the α-DG receptor with high affinity and the New World arenavirus Pichinde which does not bind to the α-DG receptor as control (2007). Fig 1.0(A) shows the percentage of infected cells for each of the multiplicity of infections (MOIs) through immunofluorescence staining for the conserved epitope of the viral GP. Fig 1.0(B) shows that a Laminin Overlay Assay (LOA) detected that the quantity of the glycosylated α-DG decreases as the MOI for LCMV increases while the western blot shows that cytosolic β-DG remains constant. In addition there is no change observed in the quantity of glycosylated α-DG and cytosolic β-DG for the HEK293T cells infected with the increase of the MOI of the Pichinde virus. Fig 1.0(C) shows the results of a flow cytometry for the changes in the glycosylated α-DG for the LCMV and Pichinde virus at the different MOIs. These results are in accordance with those from Fig 1.0(B). Lastly, to test the down regulation in α-DG, HEK293T cells and human lung epithelial (A549) cells were infected with either LCMV cl-13 or Pichinde. Those flow cytometry results showed that there was a decrease in the glycosylated α-DG in both HEK293T and A549, whereas a minor change in core α-DG for the LCMV infection. Contrastingly, there was not change observed in quantity of glycosylated and core α-DG in both cell types infected with Pichinde virus (Rojek et al., 2007). Therefore, Rojek et al. concluded that LCMV infection causes down-regulation of glycosylated

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