Pathophysiological roles and therapeutic potential of voltage-gated ion channels (VGICs) in pain associated with herpesvirus infection

Abstract

Herpesvirus is ranked as one of the grand old members of all pathogens. Of all the viruses in the superfamily, Herpes simplex virus type 1 (HSV-1) is considered as a model virus for a variety of reasons. In a permissive non-neuronal cell culture, HSV-1 concludes the entire life cycle in approximately 18-20 h, encoding approximately 90 unique transcriptional units. In latency, the robust viral gene expression is suppressed in neurons by a group of noncoding RNA. Historically the lesions caused by the virus can date back to centuries ago. As a neurotropic pathogen, HSV-1 is associated with painful oral lesions, severe keratitis and lethal encephalitis. Transmission of pain signals is dependent on the generation and propagation of action potential in sensory neurons. T-type Ca 2+ channels serve as a preamplifier of action potential generation. Voltage-gated Na + channels are the main components for action potential production. This review summarizes not only the voltage-gated ion channels in neuropathic disorders but also provides the new insights into HSV-1 induced pain.

Herpes simplex keratitis: A brief clinical overview

“…HSK has been associated with cornea denervation, although a certain degree of cornea nerve regeneration occurs a lot of the nerves do not come back to normal[ 301 ]. Sensory neuronal voltage-gated ion channels were associated with pain propagation in HSV-1 infection[ 302 ]. Further investigations are needed to probe a possible association between HSK and limbal stem cell deficiency as a sequel[ 303 ].…”