A new study has revealed herpes simplex virus (HSV) encephalitis brain inflammation as an effect produced by CXCL1 signalling to neutrophils and a follow up protein block demonstrates in less severe disease.
This new research to target CXCL1 signalling protein is a possible therapeutic approach that could reduce and lower the level of brain damage and death due to herpes simplex virus, the most common cause of viral encephalitis globally.
HSV popularly implicated for cold sores symptoms, is also implicated in inflammations of the brain which leads to extensive brain damage that is fatal in most cases, even with rapid anti-viral therapy. Encephalitis due to HSV is rapid and survivors are left with brain injuries due to the inflammation and damage caused by the virus and immune cells gaining access to the brain after evading the blood-brain barrier.
Inflammation due to HSV encephalitis is caused by neutrophils, a type of immune cell that circulates in the blood. The signaling protein required for recruitment of these immune cells to the brain from the blood stream is a new target for HSV therapies.
It is also important to determine the roles of specific immune cells and the factors that enable their crossing of the blood-brain barrier which is protective, as new therapies to target them can be formulated.
Although mouse models have been used to demonstrate that neutrophils are required to increase the permeability of the blood-brain barrier and further intensified the damage to the brain in HSV encephalitis monocytic immune cells were determined as protectors against HSV and were not required in the control of the virus.
CXCL1 was implicated as the signaling protein required for recruitment of neutrophils the immune cells into the brain where they caused maximum damage. The belief is that blocking this protein will prevent the recruitment of neutrophils thus mitigating and eliminating the potential damage caused by neutrophils.
CXCL1 is now a new target for therapies in HSV encephalitis. This is because such a therapy can prevent the influx of neutrophils without limiting the roles of protective immune cells.