Publications by authors named "Baca Chan"
Article Synopsis
- Spillover from wild animals threatens human health, with few successful global solutions, one of which is the use of oral vaccines for rabies in certain regions.
- There's interest in developing 'transmissible' vaccines that can spread immunity among wildlife, but they raise environmental concerns due to potential release of genetically modified viruses.
- The study proposes a method to control the stability of these vaccines' genetic material, allowing for better management and fine-tuning of their lifespan in wild animal populations through specific genetic adjustments.
Article Synopsis
- Researchers focused on cytomegaloviruses (CMVs) in Natal multimammate mice, a species found in sub-Saharan Africa and linked to zoonotic diseases like Lassa virus (LASV).
- They isolated infectious CMVs from these mice and sequenced multiple genomes, identifying three distinct CMV types (MnatCMV1, MnatCMV2, and MnatCMV3) and discovering cases of coinfection.
- The findings help understand CMV diversity and are aimed at developing a vaccine based on MnatCMVs to combat LASV in its animal reservoir.
Article Synopsis
- Engineering microbes to carry foreign genes is common, but these added genes often diminish over time, posing challenges for long-term applications.
- To prolong the stability of these genes, it’s essential to manage the speed of genetic mutations and the selection pressure against them.
- A new method allows researchers to estimate how quickly these transgenes are lost and predicts their persistence based on mutation rates and selection strength, facilitated by an interactive web application called MuSe.
Article Synopsis
- Researchers explored the m15 locus of murine cytomegalovirus (MCMV) and its role in modulating natural killer (NK) cell immunity, revealing complex transcription patterns that were previously unrecognized.
- They found that five overlapping transcripts are produced from the m15 region rather than the previously understood separate m14, m15, and m16 genes.
- Disruption of all five transcripts decreased the virus's ability to spread and replicate in salivary glands, leading to stronger NK cell responses, while NK cell depletion restored viral growth, highlighting the importance of these transcripts in immune evasion.
Article Synopsis
- The study successfully cloned a low-passage strain of murine cytomegalovirus (MCMV) known as G4 as a bacterial artificial chromosome (BAC), enabling better manipulation and understanding of the virus.
- Unlike lab strains, G4 can replicate effectively in C57BL/6 mice due to a specific gene modification (m157) that alters its interaction with natural killer (NK) cells.
- Through next-generation sequencing, researchers discovered a mutation affecting salivary gland tropism and identified a novel spliced gene (sgg1.1) whose restoration improved the virus's ability to infect salivary glands, offering new insights into the virus's biology.
Article Synopsis
- The study investigates how the human cytomegalovirus (HCMV) evades the immune response that is activated through type I interferon (IFN) signaling, focusing on the role of the UL35 protein.
- It was discovered that UL35 inhibits the activation of IFN transcription triggered by DNA and RNA sensors, with experiments showing that cells expressing UL35 have a reduced IFN response compared to those infected with a version of HCMV lacking UL35.
- The research also highlights that UL35 interacts with the signaling factor TBK1 and demonstrates that while UL35 is modified by O-GlcNAc transferase, this modification is not essential for its function in suppressing the immune response.
Article Synopsis
- Protein tyrosine phosphatase 1B (PTP1B) is known to negatively regulate leptin and insulin signaling, and mice without PTP1B are resistant to obesity and diabetes.
- Recent findings suggest PTP1B has a new function related to its presence on the endoplasmic reticulum membrane, rather than just its phosphatase activity.
- PTP1B-deficient immune cells produced lower amounts of type I interferon (IFN) when activated, indicating that PTP1B plays a role in enhancing the secretion of antiviral cytokines.
Article Synopsis
- The host immune system continuously fights off microorganisms, utilizing pattern recognition receptors (PRRs) to quickly identify and respond to pathogens, primarily through the production of type I interferons (IFN).
- Type I IFN are important proteins that trigger a variety of IFN-stimulated genes (ISGs), although many of these genes remain uncharacterized and their effects can vary depending on the virus.
- In particular, herpesviruses are being closely studied for their ability to evade or manipulate ISGs, revealing a complex relationship that influences how the immune system defends against viral infections.
Coevolution pays off: Herpesviruses have the license to escape the DNA sensing pathway.
Med Microbiol Immunol
August 2019
Article Synopsis
- Early detection of viral infections by pattern recognition receptors (PRR) is vital for activating a strong immune response, particularly through cytosolic DNA sensors that trigger type I interferon production via the STING protein.
- Herpesviruses, large DNA viruses, have developed numerous strategies to evade and manipulate host immune responses, specifically targeting the DNA sensing and STING pathways.
- This review will highlight the mechanisms of DNA sensing and the sophisticated ways herpesviruses adapt to influence crucial aspects of the innate immune response.
Article Synopsis
- Cytomegaloviruses (CMVs), particularly murine CMV (MCMV), manipulate the immune system, specifically targeting the type I interferon (IFN) response through the protein m152.
- M152 binds to the stimulator of interferon genes (STING), delaying its movement to the Golgi, which is essential for activating the antiviral IFN signaling.
- While m152 inhibits STING's ability to trigger IFN-related responses, it does not impact its role in activating NF-κB signaling, allowing MCMV to benefit from early viral replication while counteracting the host's antiviral defenses.
Article Synopsis
- Murine gammaherpesvirus 68 (MHV68) is a model for studying human gammaherpesviruses, specifically Epstein-Barr virus and Kaposi's sarcoma-associated herpesvirus, focusing on the immune responses to infection.* -
- The research identified that UNC93B, TLR7, and TLR9 are crucial for plasmacytoid dendritic cells' (pDC) ability to recognize and respond to MHV68 through the production of alpha interferon (IFN-α), with TLR9 overshadowing the effect of TLR7.* -
- The study also revealed that UNC93B deficiency leads to increased viral replication and reactivation of MHV68 in various organs,
Article Synopsis
- * M35 significantly suppresses the induction of the IFNβ promoter and the proinflammatory cytokine response downstream of Toll-like receptors (TLR), primarily targeting NF-κB-mediated transcription.
- * Deletion of the M35 gene from MCMV leads to increased type I IFN production and lower viral loads during infection, highlighting its critical role in the virus's ability to evade the immune response.
Article Synopsis
- LANA, a protein from Kaposi sarcoma herpesvirus, is primarily found in the nucleus and is crucial for maintaining the virus's latent state by supporting the replication of its DNA.
- There are shorter versions of LANA that exist in the cytoplasm, but their roles weren't clearly understood until recent research identified that they interact with cGAS, a protein involved in the immune response against DNA viruses.
- The study suggests that these cytoplasmic LANA isoforms can inhibit cGAS's activity, which may help the virus switch from a dormant to an active state during replication, revealing a new function for LANA beyond its role in latency.
Article Synopsis
- - Multi-strain infections, where multiple genetically distinct strains of pathogens coexist, can significantly impact disease severity and pathogen dynamics, particularly in cases like human cytomegalovirus (HCMV).
- - Research using mice showed that competition occurs between co-infecting strains of mouse cytomegalovirus (MCMV), influenced by the presence of natural killer (NK) cells and the specific strain characteristics, leading to the exclusion of certain strains from the host.
- - The study highlights how this within-host competition affects the shedding of viral strains, potentially preventing less virulent strains from spreading, which is essential for understanding disease transmission dynamics.