Molecular Pathway

MERS-CoV is understood to be antibody mediated, with the primary method of controlling the viral load sitting squarely on the shoulders of helper T-Cells. It is still unknown weather long-term antibodies are produced as a consequence of infection with MERS. 

Since infectious populations are highly dispersed, and the virus does not propagate well between humans, the virus meets a dead end within the humans that are infected with MERS. Because of this dispersion, understanding the long-term impact is still being investigated, but so far no chronic infections have been noted in survivors. (Mubarak, 2019)

Although the typical target for MERS-CoV is epithelial cells, any cell that presents a DPP4 receptor is able to be attacked by MERS. This means kidneys, liver, pancreas, and gastrointestinal systems are all at risk of infection from MERS-CoV. MERS-CoV is also capable of evading host immune response by enlisting host proteins to interfere with the TLR-3 signaling pathway, preventing its activation. (Mubarak, 2019)

As previously stated in Stucture and Classification, DPP4 receptors on the surfaces of cells. Although we know that recognition sites are host-specific, it is undetermined as of yet whether or not dromedary camels undergo similar molecular pathways as humans. We do know, however, that bactran camels do not suffer from infection with MERS, so again host specificty is preserved.  

The mode of action for disease symptoms are due to a combination of factors: Initiation of proapoptotic pathways due to enlistment of PERK which cause the infected cells to lyse, along with the production of enzymes that prevent recognition by T-cells. Although most concentrated in the airway of humans, a broad variety of organ systems have epithelial cells with DPP4 receptors, which makes the effects of the virus much more prolific than just the respiratory system. (Al-Qahtan, 2017)