Articles tagged with Host Cells
Researchers have discovered that certain RNA viruses, including Poliovirus and Hepatitis C virus, copy themselves by seizing a cellular enzyme to create replication factories enriched in phosphatidylinositol-4-phosphate (PI4P) lipids. This process enables the viruses to attract and stimulate the enzymes needed for replication.
Researchers have discovered the molecular signals used by Toxoplasma gondii to control cell behavior, paving the way for new treatments and vaccines. By disabling these signals, scientists can liberate cells from parasite takeover, potentially improving immune responses and treatment outcomes.
A new switch has been discovered that enables Salmonella bacteria to sabotage host cells, allowing it to replicate and establish an infection. This finding could lead to the development of drugs to combat Salmonella-related diseases.
Wolf-Watz recognized for seminal work on Yersinia host-pathogen interaction and international collaborations that advanced microbiological sciences. His proposal of type III protein secretion systems as unique injectors of proteins into host cells has been critical to understanding host-pathogen interactions.
A new study by Imperial College London discovered a virus called vaccinia spreading four times more quickly than previously believed. The virus uses a novel mechanism to spread rapidly between cells, making it harder to target with antiviral drugs.
Researchers at Salk Institute identify viral protein ICP0 that shuts down host cell's DNA damage response, enabling HSV to infect cells. By removing specific ubiquitin marks, ICP0 allows the virus to take over and multiply.
Researchers discovered that the Ebola virus uses a protein called VP35 to mask its RNA, evading the host cell's immune response. This unique mechanism makes Ebola highly deadly and difficult to treat.
Researchers discover unique structure in viral protein Rev, allowing it to penetrate nucleus and nucleoli. This finding opens new avenues for studying the relationship between protein localization and host cell impact.
A phase I/II study at Johns Hopkins Medicine has shown that mini stem cell transplantation can safely reverse severe sickle cell disease in nine out of ten patients. The procedure, which uses intravenous transplants of blood-forming stem cells from healthy donors, promotes the coexistence of host and donor cells.
Researchers at Tufts University have discovered how the parasite Trypanosoma cruzi prolongs its life in human host cells by activating anti-apoptotic molecules, enabling it to evade death. This study provides new insights into the mechanisms behind Chagas' disease.
Structural biologists reveal how internalin B dimer activates human receptor Met, allowing Listeria to infect cells. The discovery may lead to therapeutics for improved wound healing and treatment of listeriosis.
Research at Yale University reveals that an overactive immune response, rather than declining immunity, is to blame for increased susceptibility to viral infections among the elderly. In a study involving infected mice, inhibiting interleuken 17 prevented liver damage and death in aged cohorts.
The HIV Nef protein inhibits cell mobility in immune cells, disrupting their ability to establish contact and combat the virus. This mechanism may lead to the malfunction of B-lymphocytes in AIDS patients.
Researchers have designed probiotics that can bind toxins in the gut, preventing them from interacting with host intestinal cells. These receptor-mimic probiotics offer a promising treatment for diseases such as cholera and traveller's diarrhoea, and may also be used to prevent outbreaks following natural disasters.
Researchers designed synthetic protein-like mimics that interrupt HIV's interaction with host cell proteins, blocking infection. The novel molecules, dubbed 'foldamers,' are highly resistant to degradation and have potent antiviral activity.
Researchers developed a blood mRNA expression signature that accurately identified influenza infection and distinguished between viral and bacterial infections. This breakthrough may lead to the creation of a blood test for diagnosing respiratory infections and predicting treatment outcomes.
Researchers have discovered a new type of cellular defense mechanism that acts against DNA sequences present in high copy numbers, even if they have not integrated into the genome. Small RNA molecules play a central role in this process, which is also found in Drosophila and potentially in mammals.
Montana State University researchers study Sulfolobus turreted icosahedral virus (STIV) and its effects on host cells. The virus forms pyramid-like projections on the surface of infected cells, releasing progeny in a previously unknown manner.
Researchers at USC have identified a critical molecular mechanism that allows the influenza virus to evade the body's immune response system. The study reveals that the virus targets the ubiquitin ligase TRIM25, inhibiting its ability to activate RIG-I and trigger an alarm signal.
Researchers at the University of Oregon have developed a new method to isolate RNA from specific cells using a chemically modified gene from Toxoplasma gondii. This approach allows for precise study of gene expression and cellular differences, opening up new avenues for research in development, neurobiology, and disease studies.
Researchers create first 3D model of dengue virus replication, providing insight into the process and offering new approaches for developing measures to prevent or treat dengue fever. The study provides crucial information for developing therapy against this infectious disease.
Researchers have determined key structural features of the mimivirus, a giant virus large enough to be seen with a light microscope. The findings reveal a starfish-shaped structure that covers a special vertex where the genetic material leaves the virus to infect its host.
Researchers have identified 39 interaction partners of bacterial toxins, revealing how these toxins manipulate human host cell signaling pathways. This breakthrough could lead to the development of new treatments targeting the underlying mechanisms disrupted by bacterial toxins.
Researchers at the University of Pennsylvania School of Medicine have found a way to change one cell type into another by flooding it with specific messenger RNAs from another cell type. This approach, called Transcriptome induced phenotype remodeling (TIPeR), offers the possibility for a new type of cell-based therapy for neurodegener...
Researchers at the University of Pennsylvania have found a new way to combat malaria by trapping parasites inside host cells. They identified an enzyme called calpain-1, which parasites use to break out of infected cells, and developed a method to block it, leaving parasites trapped.
Researchers at HZI have identified a molecular signal pathway that enables E. coli bacteria to adhere to host cells and form pedestals, allowing them to reproduce on the cell surface without being flushed from the intestine. The discovery sheds light on how pathogenic bacteria develop complex processes in the host.
Researchers have detailed the molecular structure of Clostridium difficile's protective 'jacket', a surface layer that helps the pathogen colonize human gut cells and cause illness. Understanding this structure could lead to new treatments, including targeted drugs and vaccines, to combat the deadly superbug.
UAB researchers have developed a new method to produce and study HPV-18, which could lead to a better understanding of how the virus functions and causes diseases. The new approach allows for the reproduction of the entire infection cycle of HPV-18 in primary human skin cells, providing opportunities to understand its molecular mechani...
Researchers at EMBL have discovered a promising drug target in influenza virus, specifically the PA subunit responsible for cleaving host RNA caps. This finding provides new insights into the cap snatching mechanism that allows the virus to hijack human cells and multiply.
Researchers at Purdue and Stony Brook universities have determined the precise atomic-scale structure of the poliovirus attached to key receptor molecules in human host cells. The study provides a detailed analysis of how a virus can enter its host cell, shedding light on infection processes.
Scientists have identified a crucial role for sulfonation in HIV replication, finding that inhibiting this pathway can compromise viral gene expression and render host cells resistant to infection. This discovery provides a promising new target for HIV/AIDS therapy.
Researchers James Eberwine and Aaron Gitler at the University of Pennsylvania School of Medicine have been awarded prestigious NIH awards to investigate RNA-based therapeutics and mechanisms of neurodegenerative diseases. Their research aims to develop novel individualized therapeutics and understand protein folding and misfolding in y...
Researchers developed a method to preserve and visualize SARS-coronavirus replication complexes, revealing the dependence on modified host membranes for viral replication. The study provides insights into the interplay between viral proteins and host membranes, opening doors for new antiviral strategies.
Researchers found that multiple viral genomes can increase overall viral gene expression, leading to a nonlinear effect on gene networks controlling cell fate. This can result in the host cell entering a latent state rather than immediately being killed by the virus.
A team of researchers has developed a method to separate parasitic organisms from their host cells using fluorescent proteins, allowing for more detailed studies. The approach yielded the identification of 509 proteins in the parasites, providing valuable characteristics such as fatty acid degrading enzymes.
Scientists discovered that Cryptococcus yeast cells hide inside macrophages and use them as vehicles to travel through the body before attacking and spreading. This new escape mechanism allows the yeast cells to evade antifungal drugs and the immune system, making fatal infections harder to treat.
Researchers found that V para hijacks host cell processes to trigger rapid autophagy, leading to cell death within three hours. The study highlights the importance of understanding this pathogen's molecular mechanisms to develop effective treatments.
A study found that sesame seed extract and konjac gum can bind to E. coli and Salmonella bacteria, potentially preventing them from entering host cells. This natural approach may offer protection against gastro-intestinal infections or reduce symptom severity.
A study published in PLOS Pathogens identifies over 120 viral proteins that disrupt key cellular processes, including gene expression and antiviral responses. Herpesviruses employ multiple strategies to manipulate the host cell nucleus, particularly through disruption of PML bodies.
New research reveals that viruses can travel around infected cells by hitching a ride on microtubules, which are microscopic tubes forming part of the cell cytoskeleton. This transport system allows virus DNA to be integrated into the host genome, improving our knowledge of how the virus replicates in host cells.
Researchers at EMBL and CNRS identified the key protein domain responsible for binding to host RNA molecules, allowing the virus to multiply. The PB2 cap-binding site is a promising target for designing mimics of the cap that would inhibit viral replication.
Biologists at Purdue University have determined the structural changes that enable dengue virus to mature and become infectious. The researchers found that the changing acidity plays a vital role in this process, allowing the virus to fuse with cell membranes and infect new host cells.
Researchers have identified a new defense mechanism in the intestine that protects against pathogenic bacteria, which could lead to targeted treatments for diseases like Crohn's disease. The Caspase-12 protein regulates this mechanism, limiting defensin production and triggering an inflammatory reaction.
Researchers from the University of Wisconsin-Madison have developed a system to genetically disarm the Ebola virus by removing its VP30 gene. This allows for safe study of the pathogen in specialized cells, enabling the development of countermeasures such as vaccines and antiviral compounds.
Epstein-Barr virus uses LMP1 to activate TRADD, a critical signaling molecule. Without TRADD, LMP1 loses its ability to induce apoptosis, allowing uncontrolled cell growth and cancer formation.
The Crimean Congo hemorrhagic fever virus uses protein 'knives' to cut bonds between cellular proteins, evading the immune system's defense. This allows the virus to replicate and spread, leading to high mortality rates. The discovery provides insight into why the virus is so virulent.
Research identifies a previously unknown enzymatic mechanism used by pathogens to disrupt the host immune response, promoting pathogenicity through manipulation of a common signaling pathway. This discovery may lead to new strategies for fighting bacterial infections and developing more effective antibiotics.
Researchers developed a hairpin-shaped molecule that imitates the spatial structure of an important viral protein, preventing the discharge of viral RNA from the cell nucleus. This breakthrough could lead to the development of a new class of HIV treatment drugs.
The University of Utah has been awarded a five-year, $19.2 million NIH grant to establish an HIV research center focusing on the structural biology of the virus. This research aims to understand how HIV takes control of host cells and develop new treatments.
Researchers identified a new strategy that KSHV uses to replicate its viral genome, allowing it to evade the immune system. By eliminating viral protein production, they found that KSHV DNA can autonomously recruit cellular replication machinery proteins.
Researchers found that HIV fusion peptide dramatically decreases energy needed to bend a cell membrane, making it easier for the virus to infect immune cells. This discovery will aid in future computer simulations and drug discovery efforts.
Researchers discovered that herpes viruses trick mouse cells into activating the DNA damage response, allowing them to replicate more efficiently. Blocking this activation significantly reduces viral replication rates, providing a promising target for antiviral therapy.
Yersinia pathogen uses effector protein YpkA to target Gaq, a messenger protein that transmits alarm signals into the host cell. This study identifies a novel molecular target for preventing disease and fighting antibiotic-resistant strains.
Biologists used simple equations to describe the motion of Listeria monocytogenes, reproducing all observed shapes with just two variables. The equations can help identify bacterial mutants and rule out mechanisms driving the motion.
Researchers have determined the atomic structure of a key protein that helps toxoplasmosis parasites invade human cells. The protein binds to specific sugars on host cell surfaces, allowing the parasite to stick and enter cells.
Danish researchers have shed light on how viruses, like HIV and bird flu, trick human cells into producing proteins needed for replication. They developed optical tweezers to investigate the mechanical unfolding of pseudoknots, a crucial step in virus replication.
Researchers discovered a single Toxoplasma protein, ROP16, that travels to the host cell nucleus and blocks normal responses to invasion. This finding has wide-ranging implications for diseases caused by other parasites, including malaria.
A new study has identified a key player in HIV-1's nuclear import process, revealing that host cell tRNA molecules facilitate the entry of the virus's reverse transcription complex into the nucleus. This finding sheds light on the complex mechanisms by which HIV-1 integrates its genetic material into host cells.
Researchers at Rockefeller University have uncovered the mechanism by which Yersinia proteins disrupt host cell structure, killing their hosts. A mutation that impairs this process significantly reduces the bacteria's virulence, offering a potential target for new antibiotics.
Researchers found that HIV's Vpr protein disables host immunity by interacting with PARP-1 through the glucocorticoid receptor. This discovery provides potential novel approaches for designing new drugs to combat AIDS and inflammatory disorders.