Articles tagged with Viral Latency
A new study shows that specific immune system signals repel a common parasite but also cause a dormant herpes virus to become active again in mice. The findings highlight complex interactions between infectious agents and the immune system, which can lead to unexpected consequences.
A team of scientists at the Gladstone Institutes has identified a new way to make latent HIV reveal itself by increasing its gene expression noise. This approach, known as the 'shock and kill' method, holds great promise for treating latent HIV infection.
Scientists at Johns Hopkins report that compounds designed to 'wake up' dormant HIV reservoirs have failed to work in laboratory tests of infected cells taken directly from patients. The failure challenges the idea that a single latency-reversing agent can uncover the hidden virus.
Researchers at Gladstone Institutes have discovered molecular signals that activate latent HIV, offering a potential strategy to purge viral infections and develop a cure. The study suggests using calcineurin, prostratin, and NF-κB proteins to activate the dormant virus.
A new study published in Cell suggests that the latent reservoir of HIV-infected patients is significantly larger than previously estimated, making it a major barrier to cure. The findings highlight limitations of current treatment strategies and could lead to the development of more effective interventions.
Mathematical analysis reveals that viral blips occur naturally due to infection rate saturation, not external triggers. Models propose a 5-dimensional immunological model that can generate blips, applicable to various viral diseases and autoimmune disorders.
Researchers discover that JQ1 can reactivate latent HIV by activating the virus in the presence of potent therapy, making it vulnerable to current treatments. The study also found potent suppression of inflammatory genes, suggesting its potential effectiveness against other inflammatory conditions.
Scientists at Gladstone Institutes have developed a method to precisely track the life cycle of individual cells infected with HIV, targeting 'HIV latency'. This breakthrough could help advance the discovery of a cure for AIDS by understanding and interrupting the dormant virus.
Researchers at Stanford University have created a collection of compounds called bryologs that can activate latent HIV reservoirs with equal or greater potency than the original substance. The discovery holds promise as a practical way to flush out dormant viruses, offering hope for a cure for AIDS patients.
AIDS experts at Johns Hopkins have developed a vaccination strategy that boosts other immune system T cells and prepares them to attack HIV before reactivating it. The approach aims to eliminate latent HIV virus from infected T cells, which has proven difficult to eradicate.
Scientists discovered an effective way to eliminate a persistent form of HIV-1 through vaccination strategy. The research found that heightened immune response prior to virus reactivation facilitates the elimination of latent viral reservoir, paving the way for true eradication.
Researchers have identified a protein produced by HIV-1 that drives infected cells out of dormancy and into the cell cycle. This finding sheds light on how HIV reactivates after entering a dormant state and may lead to new treatments for people with HIV infection.
Dr. Verdin's research aims to develop a new single cell technology to examine HIV latency, with the goal of devising novel strategies to eliminate latent HIV infection or restrict its pool to a size that can be controlled by the immune system.
New research identifies the source of 'noise' in HIV gene expression, finding that transcriptional bursting generates exceptionally high levels of noise. This finding suggests that latency may be fundamental to the HIV life cycle.
Researchers at Helmholtz Munich identify the BZLF1 protein as a crucial factor in EBV's life cycle, enabling viral activation and gene expression. The study reveals a novel mechanism for virus detection and reactivation, providing insights into EBV's role in tumor growth.
Researchers at Gladstone Institutes have found a key factor controlling HIV latency, which could lead to new strategies for clearing the virus. The discovery involves DNA methylation and a host protein called MBD2, and offers hope for future therapies to reactivate latent HIV.
Researchers have identified a viral protein, VP16, as the molecular key that prompts herpes simplex virus to exit latency and cause recurrent disease. The study provides a molecular target for designing improved HSV vaccines and treatments, which could also be used in cancer therapy.
Researchers at Thomas Jefferson University found that HIV recruits cellular miRNA to control viral RNA translation, allowing the virus to remain dormant. Manipulating miRNA's inhibitory effect on HIV may lead to new treatment strategies against the virus.
Activation of DNA damage response in early stages of Kaposi's sarcoma development functions as an anti-cancer barrier also in virus-induced malignancies. The study found that viral oncogene-induced DNA damage response is activated in Kaposi's sarcoma tumorigenesis, leading to growth arrest or apoptosis.
Researchers found that mice with chronic herpes virus infections can resist certain bacterial infections, suggesting potential benefits from latent viral infections. The study suggests that human immune systems have evolved to benefit from these chronic infections, which could impact vaccine development and disease research.
A new study proposes that HIV regulates latency by introducing a resistor into its main transcriptional activator, Tat. The model suggests that this simple switch acts as a 'feedback resistor' to prevent stray transcription and maintain dormancy.
A research team led by Professor Nigel W. Fraser discovered that herpes simplex virus-1 (HSV-1) produces an miRNA molecule encoded by the LAT gene. This miRNA works through RNA interference to prevent normal cell death, maintaining latent infection for life. The study offers a new target for treatment against latent infections.
A new approach using valproic acid has shown promise in reducing latent HIV infection by 75% in three out of four patients. The researchers suggest that a staged treatment process, starting with standard antiretroviral regimens and then targeting latent viral infection with HDAC inhibitors, could lead to the cure of HIV.
Random fluctuations in gene expression can influence HIV latency, suggesting that a cell's fate is determined by chance rather than predetermined mechanisms. The researchers' model suggests that targeting chemical modifications required for Tat's function could lead to new treatments.
Researchers have identified IL-7 as a potent and strain-specific inducer of latent HIV-1 cellular reservoirs in individuals on virally suppressive HAART. The growth factor stimulates HIV-1 activation from resting T cells, suggesting new approaches for HIV treatment.
Researchers at Thomas Jefferson University have discovered that interleukin-7 (IL-7) can stimulate latent HIV viruses, making them vulnerable to drugs and the immune system. The new technique may lead to improved treatments for HIV infection and could be a step towards complete viral eradication.
A team of scientists has developed a laboratory system to study the virus in its latent stage, discovering genes that may give it stealth capabilities. This could lead to the development of new drugs to clear the virus from infected individuals.
Researchers at The Wistar Institute discovered that the Epstein-Barr virus (EBV) uses a telomere-like system to survive within its host cells. This finding has significant implications for treating EBV-associated cancers, as inhibiting this mechanism could potentially inhibit tumor cell growth.
Researchers have successfully developed an immunotoxin that kills over 99% of latent HIV-infected cells using a monoclonal antibody and ricin. The treatment targets CD45RO molecules found on the surface of memory T cells, which are difficult to target due to their low abundance.
New data show that latent pools of infected cells are established early in HIV infection, even with treatment. Dr. Fauci discusses potential strategies to diminish latent pools by stimulating latently infected cells with antibodies or cytokines.