MERS is an enveloped, (+) sense single stranded RNA virus. The genome is linear, and is about 30 kilobases long.
MERS is a classic example of the coronavirus particle we have grown accustomed to in the news. The icosahedral phage particle is surrounded by a "crown" of spike proteins, which allow the virus to bond with host cell membrane proteins and gain access to the cell.
MERS coronavirus enters the cells of human respiratory tract through an interaction between dipeptidyl peptidase IV (DPP4, left) cell surface protein and the C-domain of its own S1 spike protein. MERS using DPP4 to enter cells is problematic, because DPP4 is present on epithelial and endothelial cells of most human organs, which is why complications of the virus include multiorgan failure, which generally leads to death. (Ramunujan, 2014)
When MERS has depleted the available resources within the cell it has infected, it uses an interesting mechanism to release itself: triggering cell apoptosis by displacing protein kinase R–like endoplasmic reticulum kinase (PERK) from 78-kDa glucose-regulated protein (GRP78). This interjection in the proapoptotic communication pathway encourages the cell to apoptose sooner than it would naturally. (Chu, 2021) This spills out all of the copies of the virus that were made by the cell, and propagates the infection to surrounding tissues.