Key Receptor Identified for Tick-Borne Encephalitis Virus, Paving Way for New treatments
Table of Contents
- 1. Key Receptor Identified for Tick-Borne Encephalitis Virus, Paving Way for New treatments
- 2. Unlocking the infection Process
- 3. The Role of LRP8
- 4. Promising Results in Animal Studies
- 5. Global Implications and Future Research
- 6. Understanding Flaviviruses and Their Impact
- 7. Frequently Asked Questions About TBEV and its Receptor
- 8. what conformational changes in viral envelope proteins are triggered by the decrease in internal pH during TBEV entry?
- 9. Mechanisms of Cellular Entry Uncovered in Tick-Borne Encephalitis Virus Study
- 10. Understanding Tick-Borne Encephalitis Virus (TBEV) Infection
- 11. Key Cellular Receptors Involved in TBEV Entry
- 12. The Endocytic Pathways of TBEV
- 13. Post-Endocytic Events: Membrane Fusion and viral Release
- 14. The Role of Lipid rafts in TBEV Entry
BRONX, N.Y. – September 24, 2025 – A major breakthrough in understanding the tick-borne encephalitis virus (TBEV) has been announced today. Researchers have successfully identified the specific protein on human cells that the virus utilizes to initiate infection. This discovery, published in the prestigious journal Nature, is expected to accelerate the growth of targeted antiviral drugs and improve treatments for this perhaps devastating neurological disease.
Unlocking the infection Process
The research, a collaborative effort by scientists at Albert Einstein College of Medicine, Karolinska Institutet, and the United States Army medical Research Institute of Infectious Diseases (USAMRIID), marks the first time a crucial host-cell protein receptor has been identified for any flavivirus. Flaviviruses are a family of viruses responsible for a range of serious illnesses including dengue fever, Zika virus, and yellow fever. According to the Centers for Disease Control and Prevention, the incidence of vector-borne diseases, including those transmitted by ticks, has more than doubled in the U.S. from 2004 to 2016.
“By conclusively demonstrating that TBEV requires a specific protein receptor to infect human cells, we open the field to discovering receptors for othre flaviviruses and devising therapies for the devastating infections they cause,” explained Dr. Kartik Chandran,Professor of Microbiology & Immunology at Albert Einstein College of Medicine.
The Role of LRP8
The team’s investigation centered on identifying the “unlock” that TBEV uses to enter human cells. Through a meticulous process of analyzing thousands of cell variants, they pinpointed LRP8 – a low-density lipoprotein receptor – as the key. LRP8 is predominantly found on the surface of cells and plays a crucial role in neurological development and function, especially in the brain and at the blood-brain barrier.
Further research confirmed that TBEV’s envelope protein E specifically binds to LRP8, enabling the virus to gain entry and infect cells. This binding process is essential for the virus’s ability to spread and cause neurological damage.
Promising Results in Animal Studies
Researchers at USAMRIID conducted experiments on mice to validate the role of LRP8 in live organisms. Mice treated with a “decoy receptor” designed to block TBEV from binding to LRP8 showed remarkable resistance to a highly virulent strain of the virus. Nineteen out of twenty treated mice displayed no symptoms of infection, compared to all untreated mice succumbing to the disease.
“It was really exciting to see that LRP8 is crucial for TBEV to efficiently infect the brain,” stated Dr. Andrew Herbert, branch chief of viral immunology at USAMRIID.
Global Implications and Future Research
TBEV is currently endemic in Northern, Central, and Eastern europe, as well as Central and East Asia, causing over 10,000 clinical cases annually. However, the geographic range of the ticks carrying the virus is expanding, increasing the risk of infection in new areas. While vaccines are available, access remains limited, particularly in lower-income countries. Effective antiviral treatments are currently unavailable.
Researchers emphasize that further studies are needed to fully understand the intricacies of the LRP8-TBEV interaction and explore its potential for therapeutic intervention. Investigations will also focus on whether similar proteins are involved in the virus’s lifecycle within ticks.
| Virus | Geographic Distribution | Key Finding |
|---|---|---|
| Tick-Borne Encephalitis Virus (TBEV) | europe, Asia | LRP8 identified as key receptor for cell entry. |
| Dengue Virus | Tropical and Subtropical Regions | Belongs to the same flavivirus family, potential for similar receptor discovery. |
| Zika Virus | worldwide | Also a flavivirus; research may benefit from TBEV findings. |
Did You Know? Ticks can transmit several different pathogens alongside TBEV, highlighting the importance of preventative measures like tick checks and protective clothing.
Pro Tip: Regularly update your knowledge on emerging infectious diseases and recommended preventative measures through credible sources like the world Health organization (WHO) and the CDC.
What steps can be taken to prevent the spread of TBEV in newly affected areas? How will this discovery impact the development of broad-spectrum antiviral therapies for flaviviruses?
Understanding Flaviviruses and Their Impact
Flaviviruses represent a notable global health threat, causing a wide range of illnesses with varying degrees of severity. These viruses are primarily transmitted by mosquitoes and ticks, making vector control a crucial aspect of prevention. Understanding the mechanisms by wich these viruses infect cells is essential for developing effective treatments and vaccines. Ongoing research continues to shed light on the complexities of flavivirus infections, paving the way for innovative approaches to combat these diseases.
Frequently Asked Questions About TBEV and its Receptor
- What is tick-borne encephalitis virus (TBEV)? TBEV is a virus transmitted by ticks that can cause inflammation of the brain and spinal cord.
- What is the LRP8 receptor? LRP8 is a protein found on human cells that TBEV uses to enter and infect those cells.
- How was the LRP8 receptor identified? Researchers used a screening process involving thousands of cell variants to identify the gene responsible for TBEV infection.
- Is there a treatment for TBEV infection? Currently,there are no specific antiviral treatments for TBEV,but vaccines are available in some regions.
- What are the symptoms of TBEV infection? symptoms can vary but often include fever, headache, and neurological complications like meningitis or encephalitis.
- How can I protect myself from TBEV? Preventative measures include avoiding tick bites through the use of protective clothing, insect repellent, and thorough tick checks.
- Will this discovery help with other flaviviruses? Identifying the LRP8 receptor provides a crucial starting point for research into receptors used by other viruses in the flavivirus family.
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Mechanisms of Cellular Entry Uncovered in Tick-Borne Encephalitis Virus Study
Understanding Tick-Borne Encephalitis Virus (TBEV) Infection
Tick-borne encephalitis (TBE) is a viral disease affecting the central nervous system,transmitted to humans via tick bites.The causative agent, Tick-borne encephalitis virus (TBEV), belongs to the Flaviviridae family, alongside viruses like West Nile virus and Zika virus. Recent research has significantly advanced our understanding of how TBEV gains entry into host cells – a crucial step in initiating infection. This knowledge is vital for developing targeted antiviral therapies and preventative measures against TBE. Understanding TBEV pathogenesis begins with understanding cellular entry.
Key Cellular Receptors Involved in TBEV Entry
for a virus to infect a cell, it must first bind to specific receptors on the cell surface. Several receptors have been identified as playing a role in TBEV entry, though the exact mechanisms are still being elucidated.
* CD155 (PVR): This is considered a primary receptor for TBEV.CD155 is a member of the nectin family and is widely expressed on various cell types, including neurons, glial cells, and immune cells. Binding of TBEV to CD155 initiates the viral entry process. Studies show variations in CD155 expression can influence TBEV susceptibility in different individuals.
* Heparan Sulfate Proteoglycans (HSPGs): HSPGs act as attachment factors,facilitating initial virus binding to the cell surface before engagement with CD155.They don’t mediate entry on thier own but enhance the efficiency of infection. Viral attachment factors like HSPGs are frequently enough overlooked but play a critical role.
* Other Potential Receptors: Research suggests other receptors, like AXL and possibly others within the nectin family, may contribute to TBEV entry, particularly in specific cell types or under certain conditions. Further investigation is ongoing to fully characterize their roles.
The Endocytic Pathways of TBEV
once TBEV binds to cell surface receptors, it enters the cell via endocytosis – a process where the cell membrane invaginates and engulfs the virus.Several endocytic pathways are utilized by TBEV:
* Clathrin-Mediated endocytosis (CME): this is a major pathway for TBEV entry into many cell types. CME involves the formation of clathrin-coated pits, which bud off from the cell membrane, internalizing the virus within vesicles. Inhibiting CME can significantly reduce TBEV infection rates.
* Caveolae-Mediated Endocytosis: Caveolae are small invaginations of the cell membrane rich in cholesterol and caveolin proteins. TBEV can utilize caveolae for entry, particularly in certain cell types like endothelial cells.
* Macropinocytosis: This pathway involves the non-selective uptake of extracellular fluid and solutes. While less prominent than CME and caveolae-mediated endocytosis,macropinocytosis can contribute to TBEV entry,especially under conditions where other pathways are inhibited.
Following endocytosis, the virus-containing vesicles must undergo membrane fusion to release the viral genome into the cytoplasm. This process is pH-dependent.
- pH Drop: As the endosome matures, its internal pH decreases. This acidic surroundings triggers conformational changes in the viral envelope proteins.
- Fusion Peptide Activation: The acidic pH activates the fusion peptide of the TBEV envelope protein, enabling it to insert into the endosomal membrane.
- Membrane Fusion: The viral and endosomal membranes fuse, releasing the viral RNA genome into the cytoplasm.
- Replication: Once inside the cytoplasm, the viral RNA is translated and replicated, leading to the production of new viral particles. These particles are then assembled and released from the cell to infect other cells. Understanding viral replication cycle is key to developing antiviral strategies.
The Role of Lipid rafts in TBEV Entry
Lipid rafts are specialized microdomains within the cell membrane enriched in cholesterol and sphingolipids. they serve as platforms for organizing signaling molecules and facilitating viral entry.
* TBEV Clustering: Lipid rafts promote the clustering of TBEV particles on the cell surface, enhancing their interaction with receptors like CD155.
* Endocytosis Regulation: Lipid rafts are involved in regulating the efficiency of endocytosis, influencing the rate at which TBEV enters cells.
* Membrane Fusion: Lipid rafts may also play a role in facilitating membrane fusion, contributing to the release of the viral genome into the cytoplasm. Disrupting lipid raft