Limited exposure of ligand-receptor complexes to proteinase has been used to detect receptor-induced conformational changes in several proteins, including avian sarcoma/leucosis virus (ALV) envelope protein complexed with its receptor Tva and spike protein of mouse hepatitis virus complexed with soluble receptor, CEACAM1a [21], [22], [22].
For example, C57BL/6 (B6) mice infected with mouse hepatitis virus (JHM strain, JHMV) develop severe encephalitis, with death occurring within 7 days.
We analysed brain lesions of Lewis rats infected with mouse hepatitis virus leading to a complex immune response including CD8+ T cells [ 18, 70] and specific anti-viral antibodies [ 51, 88, 97].
In in vivo studies, however, Carbajal et al. [ 10] reported that CXCR4, but not CXCR7, plays a role in the migration and differentiation of OPCs in a model of chronic demyelination within the spinal cord after primary infection with mouse hepatitis virus (MHV) [ 11].
The results are also consistent with the reports that demyelination induced by mouse hepatitis virus (MHV) is associated with both T cell types [21].
The M protein was also shown to interact with the mouse hepatitis virus (MHV) nucleocapsid consisting of the genomic-size mRNA 1 and N protein in a pre-Golgi compartment, probably at the ER membrane.
A similar situation occurs on the mouse CEACAM1a (MHVR1a) N-terminal domain, in which Ile-41 appears to engage with the mouse hepatitis virus spike protein.
Infection with neuroadapted mouse hepatitis virus strain JHM was also reported to exacerbate AD-like pathology in a transgenic mouse AD model [ 219].
60 Interestingly, following respiratory infection in the lungs of aged mice with either mouse hepatitis virus-1, respiratory syncytial virus, influenza A virus, or severe acute respiratory syndrome coronavirus, elevated expression of prostaglandin D2 correlated with reduced homing of lung DCs to regional lymph nodes and T cell activation.
A possibly causative role of HCoV-OC43 in determining chronic brain damage is further supported by the fact that chronic demyelinisation of mouse CNS can be induced by infection with another CoV, mouse hepatitis virus (MHV), which belongs to the same antigenic group as HCoV-OC43 and has structural similarities with it (39 ).
