Viral Membrane Channels: Role and Function in the Virus Life Cycle

Sze, Ching Wooen; Tan, Yee-Joo

In poliovirus, 2B and 3A viroporins can inhibit the cellular protein secretion pathway by disassembling the Golgi complex or by blocking the ER-Golgi trafficking, which results in the accumulation of membrane vesicles in the cytoplasm [33, 34] . By interfering with the secretory pathway, poliovirus thwarts the host immune response against viral infection by shutting off the nascent MHC class I trafficking as well as down-regulating cytokine release [103, 104] . Similarly, Coxsackievirus 2B protein can also inhibit protein trafficking through the Golgi complex by forming pores in the ER membrane, leading to efflux of Ca 2+ ion from this compartment into the cytosol [38] . Alterations in the ion gradients are known to impact the membrane vesicle fusion and transport events [105] [106] [107] [108] . On the other hand, release of ER calcium into the cytosol can also trigger an immune response via the activation of inflammasomes as well as autophagy, two of the mechanisms developed by the host to clear off viral infection. However, viruses have evolved to hijack these protective mechanisms to benefit their own replication. These will be discussed in the next section.