A virus is unable to survive without a host, which begs the questions whether viruses are living or nonliving organisms. Viruses are composed of protein shells that harbour genetic material waiting to be replicated by the host organism. These “beings” (because some may feel conflicted if I were to call them an organism) have fascinating survival cycles, each unique, with many elusive aspects to be investigated. The latest viral craze is MERS-CoV.
Middle East respiratory syndrome coronavirus (MERS-CoV) is a novel virus that was first reported in Saudi Arabia in 2012, with symptoms that resemble severe acute respiratory syndrome (SARS). The virus has spread to several other countries including the US with the most recent largest outbreak in South Korea in 2015. Fortunately, no cases have been detected in Canada. The symptoms that parallel SARS include lymphopenia, a condition of having very low levels of white blood cells crucial in the human immune system. However, due to its ability to infect broad tissue types and coincidentally, our body’s abundant expression of the virus’ receptor DPP4 (MERS-CoV receptor dipeptidyl peptidase 4), the pathogenicity and fatality rate is significantly higher than SARS. Previous studies have shown that MERS-CoV can interject at several alternate points in the human immune system leading to strong pathogenesis, naming the virus one of the latest threat to the global health.
Chu and colleagues1 have recently elucidated that the virus was most efficiently infecting human T cells in peripheral blood of the circulatory system, spleen and tonsils. T cell is a type of white blood cells, i.e. lymphocyte, which plays numerous roles in our immune system as defenders against pathogens. One of the major roles of T cells involves flagging virus-infected cells in order to induce programmed cell death of the infected cells, i.e. apoptosis - which could be thought of as cell suicide for sick cells. Interestingly, when T cells were infected with MERS-CoV, the virus was inducing the apoptosis of the T cells, thus inhibiting T cells from performing their role of flagging virus-infected cells. When the investigators compared the ability of MERS-CoV to infect different types of immune cells, T cells were predominantly infected amongst others. This was due to the abundance of surface DPP4 expression which correlated with higher efficiency of infection. This pattern of infection was shown to be distinct from SARS, as the SARS virus could not enter or induce apoptosis in T cells. An animal study using marmoset monkeys also supported the findings that MERS-CoV is able to reach the spleen to infect T cells.
Chu and colleagues1 investigated the pathogenesis of MER-CoV, which has been closely compared to the SARS virus as they both belong to the same family of viruses, causing similar symptoms. However the authors were able to demonstrate that MER-CoV is, indeed, an upgraded version of SARS with distinct and stronger pathogenesis that involves infection and apoptosis of T cells making these novel “beings” the next lethal viral threat.
 Chu, H. et al. Middle East Respiratory Syndrome Coronavirus Efficiently Infects Human Primary T Lymphocytes and Activates the Extrinsic and Intrinsic Apoptosis Pathways. J. Infect. Dis. 213, jiv380 (2015).