Herpes Structural Protein Deactivates Immune System to Gain Access to Brain
May 22, 2020 | Biotechnology
Reading time: 3 minutes
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An international team of scientists led by researchers from Aarhus University, University of Oxford, and the University of Gothenburg has discovered a molecular mechanism that helps Herpes simplex virus (HSV1) infect the brain. Herpes infections are initiated at mucosal surfaces where the virus infects epithelial cells. When HSV1 spreads from the peripheral nerves and into the central nervous system, it can infect the brain and cause herpes simplex encephalitis, a rare disease with high mortality if left untreated. In most cases, the innate immune system prevents HSV1 brain infection, but HSV1 is sometimes able to evade the brain’s defenses.
The new research study, published recently in the Journal of Experimental Medicine through an article entitled “HSV1 VP1-2 deubiquitinates STING to block type I interferon expression and promote brain infection,” could be integral in developing new therapies for treating this disease.
The stimulator of interferon genes (STING) protein plays an important role in immunity, and it is activated by a virus’s DNA during viral infection. STING initiates a cascade of cellular actions that help fight the invader. Those initial efforts include gene activation and production of cytokine proteins such as type I interferon (IFN) that boost the immune response.
“HSV1 has evolved multiple mechanisms to evade the host cells’ induction of type I IFN,” explained lead study investigator Chiranjeevi Bodda, PhD, an assistant professor at Aarhus University. “But how HSV1 evades the type I IFN response in the brain were not well understood.”
In the current study, the research team worked to identify proteins encoded in HSV1’s genome that promoted HSV1’s immune evasion in the brain. They infected mouse brain cells grown in culture with HSV1 mutants that were missing key genes, or whose gen... You can read the entire article in the Genetic Engineering and Biotechnology News (GEN) Blog.
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