Articles tagged with Viral Latency
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Researchers have uncovered a key reason why HIV remains difficult to cure, revealing that subtle variations in the Rev-RRE axis influence viral replication and latency reactivation. Understanding this regulatory system could help develop strategies to flush out the dormant virus and eliminate it for good.
A subset of CD4+ 'helper' T cells helps fight cytomegalovirus infection and reduces the chances of transmission. The late-rising T cells expand long after the initial response has died down, gathering in high numbers in the salivary gland.
Researchers from UTHealth Houston discovered that Epstein-Barr virus (EBV)-specific T-cells are present in high numbers in the cerebrospinal fluid of people with multiple sclerosis at its earliest stages. The study suggests that these cells may be contributing to the disease's pathogenesis.
A new molecular compound has been identified that can activate latent HIV-1 in cells, showing promise for HIV treatments. Researchers found that this compound, YSE028, can reactivate latently infected cells and induce cell death, potentially leading to a complete cure for HIV.
Researchers have found that microglial cells in the brain can serve as a stable viral reservoir for latent HIV. This discovery provides new insights into how to target and eradicate the virus, particularly in the brain or peripheral blood.
Researchers have identified a distinct latent reservoir of HIV-infected CD4+ T cells in the central nervous system (CNS), separate from the latent reservoir in blood and lymph tissue. This finding highlights a new challenge in creating a cure for HIV, as any curative therapy would need to activate both dormant reservoirs.
Researchers identified 7 key symptoms of long COVID, including heart issues and joint pain, in a study of 52,461 patients. The findings could help healthcare providers diagnose and treat the condition more effectively.
Researchers discovered host proteins APOBEC3 can aid HIV's latency, a major hurdle to cure research. The finding raises questions about the role of these proteins and potential ways to block their activity to inhibit viral persistence.
A recent study from Linköping University found that COVID-19 reactivated several latent viruses, including the Epstein-Barr virus, in people with chronic fatigue syndrome (ME/CFS). The study suggests that these reactivated viruses may contribute to the disease's symptoms and could potentially be used as a diagnostic tool.
A UCLA-led team has improved a method to kill HIV-infected cells, using natural killer cells to target and eliminate them. The approach could lead to reducing or eliminating the virus from infected individuals who rely on medication.
A new strategy for curing HIV targets latent viruses by blocking and excising the virus, offering hope for patients to be taken off daily treatments. The HOPE Collaboratory's approach uses genome editing technology to destroy latent HIV.
A team of researchers from the University of Illinois at Urbana-Champaign has identified five new chemicals that can promote latency in HIV, providing a potential solution to the disease. By screening over 1800 compounds, they discovered compounds that can suppress viral reactivation and reduce the risk of disease progression.
A research team at George Washington University is exploring the role of sex hormones in HIV latency and its impact on treatment efficacy. The study aims to develop more effective approaches to a cure for HIV, particularly for women and transgender patients who are disproportionately affected by the virus.
Researchers have discovered a region of viral protein LANA that is crucial for KSHV persistence in human cells, which could potentially be used to develop therapy for KSHV tumors. The study found that this LANA region interacts with p53 and other unacetylated proteins, allowing the virus to persist in tumor cells.
A new assay detects intact HIV latent proviruses at higher frequencies than previous methods, revealing a significant amount of intact virus in infected individuals; this finding is crucial for developing an HIV cure. The study provides a benchmark for assessing persistent proviral DNA and its composition.
Researchers discover that cytomegalovirus enters a dormant state by varying protein levels in viral particles, allowing the virus to survive and persist for life. This 'bet-hedging' strategy enables the virus to balance between infectiousness and latency.
A new study found that reactivated HSV in trigeminal nerves of laboratory mice kills off at least a portion of sensory neurons. Antiviral drugs like acyclovir can prevent this outcome, suggesting a potential strategy for preventing neurodegeneration related to HSV reactivation.
Researchers at Harvard Medical School have successfully used CRISPR-Cas9 gene editing to disrupt both latent and active herpes virus in human cells. The findings offer a model system for using gene editing in a localized way to disrupt active replication, but the challenge of delivering gene-editing therapy to neurons remains unsolved.
New research reveals that chromatin dynamics regulate the entire herpes virus genome's expression during infection. The discovery sheds light on the interplay between the virus and host cells, potentially leading to more effective treatments.
Researchers found that antiretroviral therapy alters the host environment to form most of the long-lived HIV reservoir. The study's findings suggest that treatment may contribute to the formation or stabilization of the latent viral reservoir.
Researchers can now measure hidden, inactive HIV in patients' cells using a new genetic technique developed by Howard Hughes Medical Institute. This allows scientists to track progress depleting the latent reservoir of HIV, a crucial step towards finding a cure.
Researchers found that HIV-infected cells can only reactivate in larger host cells, while smaller cells remain latent or silent. The study suggests a natural mechanism for viral reactivation and offers potential strategies for biasing viral decision-making through drug treatments.
Researchers discovered a way to manipulate the Tat gene circuit to activate latent HIV in cells, making them susceptible to immune system destruction or drug therapies. This could lead to a cure for HIV by targeting the latent reservoir.
A team of investigators from the University of Pittsburgh has identified compounds that block the reactivation of latent HIV-1 in a human cell line. The research, published in Antimicrobial Agents and Chemotherapy, found 12 kinase inhibitors that irreversibly blocked HIV-1 reactivation with minimal toxicity.
A new study published in Nature demonstrates that administering broadly neutralizing antibodies and immune-stimulating agents can delay viral rebound following ART discontinuation in monkeys. This two-pronged approach represents a potential strategy to target the latent reservoir, rendering infected cells more susceptible to elimination.
The University of North Carolina at Chapel Hill HIV Cure Center and Cell Microsystems will use the NIH grant to automate and streamline the measurement of the HIV reservoir. The team aims to accurately detect emergence of HIV after exposure to potential therapeutics and evaluate the efficacy of latency reversal therapies.
A new study reveals that the mechanical properties of viral DNA govern the direction of infection, with synchronous and random infections differing in their DNA's stiffness. Temperature and stress levels influence this process, with heat making DNA more flexible and potentially leading to lytic events.
Researchers found that estrogen receptor modulators increase the effectiveness of HIV latency reversal therapies. Exposure to estrogen limits the emergence of HIV from latency, suggesting a potential factor in future eradication therapies.
Researchers found that HIV uses alternative splicing to tune random noise, dictating its fate and function. This inefficient process could be targeted to create novel HIV cure strategies.
Researchers have found that only a small percentage of latently infected cells are reactivated by the 'shock and kill' approach, indicating a need for new treatment strategies. The study suggests exploring alternative approaches to control or eliminate non-reactivatable latent HIV genomes.
Researchers have discovered that human cytomegalovirus (HCMV) differentiates human hematopoietic progenitor cells into a long-lived, immunosuppressive monocyte subset for viral latency. This unique cell population is identified through specific surface proteins and can evade the T-cell immune response.
Researchers propose a mathematical model to investigate the effects of drug parameters and dosing schedules on HIV latent reservoirs and viral load dynamics. The study suggests that drugs with proper pharmacodynamic properties can potentially prevent or postpone establishment of viral infection.
Scientists from Scripps Research Institute have shown that a novel compound effectively suppresses HIV virus production in chronically infected cells and prevents viral rebound. The 'block-and-lock' approach blocks reactivation of the virus in cells and locks it into a durable state of latency.
A new synthetic molecule, SUW133, has been designed to reactivate dormant human immunodeficiency virus (HIV) in mice and lead to cell death. In a study published in PLOS Pathogens, researchers found that up to 25% of latently infected cells died within 24 hours after treatment.
EZH2/1 inhibitors, used in cancer clinical trials, have activity against a variety of viruses, including HSV. These compounds suppress viral gene expression and induce antiviral pathways.
Researchers at UNC Health Care have developed an assay to detect antigen production and immune effectors capable of clearing infected cells. Vorinostat reverses latent HIV infection, making it vulnerable to clearance and potentially paving the way for a cure for the millions living with the virus.
Researchers at UNC have shown that interval dosing of Vorinostat can reverse latent HIV and improve detection, paving the way for further research into clearing infection. The study's findings suggest that pairing a latency reversing agent with an antiviral immune therapy may be necessary to achieve a cure.
Researchers at Gladstone Institutes found that inhibiting SMYD2 enzyme can reactivate latent HIV, offering a potential therapeutic target for the 'shock and kill' approach. This breakthrough could lead to new strategies for eliminating HIV latency and developing more effective treatments.
Researchers at NIH's National Institute of Allergy and Infectious Diseases have identified a set of protein complexes that are recruited to viral genes to stimulate both initial infection and reactivation from latency. Environmental stresses also induce reactivation, providing new targets for the development of therapeutics.
Researchers found that rapamycin treatment reduced proinflammatory cytokine release and toxicity without decreasing HIV-1 reactivation in T cells. The treatment did not impair the immune system's ability to recognize infected T cells, making it a potential strategy for targeting latent HIV-1 reservoirs.
A researcher at Texas Tech University Health Sciences Center El Paso is on a mission to identify genes that enable HIV latentness. He plans to conduct genome-wide knockout screening to find specific genes that allow the virus to persist.
A new study published in Nature Medicine found that over 90% of latent HIV 'provirus' genomes are genetic duds, unable to replicate and cause disease. This challenges the current methods for measuring the size of the reservoir, highlighting a need for more accurate counting methods.
Researchers at the University of North Carolina and partner institutions have made significant strides in understanding HIV latency, a key obstacle to eradicating the virus. The team has developed effective strategies, including histone deacetylase inhibitors, to reverse latency and boost the immune system.
Scientists discover galectin-9 potently forces latent HIV out of hiding and poisons the virus, increasing APOBEC3G levels to destroy genetic code. This 'shock and kill' strategy holds promise for a cure, altering treatment approach to eliminate all viral traces from the body.
Researchers develop CRISPR/Cas9 guide RNA sequences targeting latent herpesvirus DNA in infected human cells, suppressing virus replication. Efficient elimination of EBV genomes was observed, while HCMV replication was impaired with simultaneous editing at multiple critical sites.
Human cells have evolved mechanisms to detect and respond to latent herpesvirus infections, but the virus has developed ways to evade these defenses. The study identifies a viral protein that blocks cellular proteins from reactivating the infection.
Researchers at NIH have developed a protein that awakens resting immune cells infected with HIV, facilitating their destruction. The protein, VRC07-αCD3, has shown promise in laboratory studies and animal trials, offering new hope for an HIV cure.
A clinical trial of romidepsin, an HDAC inhibitor, found that it can reverse HIV latency in individuals on long-term antiretroviral therapy. The treatment did not negatively affect T-cell function, and increased plasma HIV-1 RNA was detectable in five of six participants.
UC Davis researchers have identified a compound, PEP005, that activates latent HIV and increases activation by up to 15-fold when combined with JQ1. This breakthrough offers promising hope for an HIV cure. The study's findings suggest that PEP005 is already approved by the FDA and has great potential to advance into clinical studies.
Researchers have found two combination treatments that effectively reactivated latent HIV in cells, providing novel opportunities for advancing HIV eradication strategies. Ingenol-3-angelate and PEP005, combined with JQ1, showed a 7.5-fold increase in viral reactivation compared to PEP005 alone.
Researchers at Scripps Research Institute aim to suppress HIV in latently infected cells using a novel antiviral target and a molecule called didehydro-Cortistatin A. The new approach has the potential to reduce the size of the latent reservoir pool of HIV.
A new study published in mBio shows that Cortistatin A significantly inhibits viral replication and reduces residual virus levels in infected dormant cells, establishing a near-permanent state of latency.
Scientists have established a model for latent HIV infection of brain cells and identified various compounds that can affect latency. The study aims to develop new therapeutic approaches to silence the virus in brain cells, which could improve clinical care for HIV-1 patients.
Researchers have developed a multifaceted approach to identify drug combinations that reverse HIV-1 latency. Several 2-drug combinations were found to be able to reactivate HIV-1 without triggering an inflammatory response, and a model was created to correlate changes in viral RNA with virus secretion from T cells.
Scientists at the Gladstone Institutes found that HIV remains active as infected cells transition to rest, controlled by the virus's Tat protein. This independent control allows the virus to survive even if host cells are inactive, making it harder to cure the infection.
Researchers found that latent HIV likely resides in long-lived memory cells that help the immune system remember pathogens. The study suggests these cells are the source of the virus's hidden reserves, which could lead to a possible cure for HIV.
Researchers have developed a novel treatment approach for persistent viral infections like herpes by blocking the activity of host cell protein LSD1, reducing HSV infection, shedding, and recurrence. This epigenetic therapy shows promise as an antiviral strategy to control shedding and reactivation of latent virus.
Researchers have developed a multipronged strategy to eradicating the hidden reservoir of infected cells in the body. A 'shock-and-kill' approach involving inducers and virus-fighting antibodies shows promise for curing HIV-1 infection in humans.
Broadly neutralizing antibodies, combined with viral inducers, have been found to control HIV in mice by targeting latent reservoirs of infected cells. The approach, called "shock and kill," resulted in a 57% success rate in preventing viral rebound.
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.