In a new study, researchers have discovered a function in a pro-inflammatory protein that could play an important part in improving current and future therapeutics for the herpes virus.
The research was conducted by a team at the University of Arizona College of Medicine-Phoenix.
The study examined whether the protein IL-36g is an essential component of the immune response to a herpes infection, or if other mechanisms can compensate for the lack of IL-36g.
Despite the widespread use of antiviral medications to treat genital herpes, more than 260 million women worldwide are living with this lifelong infection and transmitting it to new individuals daily.
After the initial genital herpes simplex virus 2 (HSV-2) infection in the vaginal epithelium, the virus spreads through the nervous system, where it establishes latency.
The virus goes into “hiding,” where it persists for a lifetime and periodically reactivates, causing lesions.
Cytokines, proteins essential to the immune system, coordinate the response to pathogens and allow for cell-to-cell communication. IL-36g is a pro-inflammatory cytokine identified 20 years ago.
Over the years, researchers have shown that it exhibits an important function in chronic inflammatory diseases, but only recently have scientists studied its role in infectious diseases such as herpes.
The team is the first group to detect IL-36g in the female reproductive tract and have been extending this work to evaluate the extent that this molecule can protect against, or contribute to, genital infection.
They found that after intravaginal HSV-2 infection, the virus was able to spread systemically throughout the nervous system and to the brain in those lacking IL-36g, whereas our control group, which had the gene intact, was significantly more protected against HSV-2 spread in the nervous system.
They confirmed that IL-36g is limiting the spread of the virus from the genital tract to the nervous system.
The precise mechanism in which IL-36g protects against neuroinvasion is unknown but is an exciting and important area of future research.
In addition, researchers concluded IL-36g played a critical role in recruiting neutrophils, a type of white blood cell that protects against invading pathogens.
Melissa Herbst-Kralovetz, Ph.D. is the senior and corresponding author of the study.
The study is published in the Journal of Immunology.
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