VSV drives CD8 T cell-mediated tumour regression through infection of both cancer and non-cancer cells.

Oncolytic viruses (OV) are designed to selectively infect and kill cancer cells, while simultaneously eliciting antitumour immunity. The mechanism is expected to originate from infected cancer cells. However, recent reports of tumour regression unaccompanied by cancer cell infection suggest a more complex mechanism of action.

Utilising the intrinsic fluorescence of pomalidomide for imaging applications.

Optimisation of protein degraders requires balancing multiple factors including potency, cell permeability and solubility. Here we show that the fluorescence of pomalidomide can be used in high-throughput screening assays to rapidly assess cellular penetration of degrader candidates. In addition, this technique can be paired with endocytosis inhibitors to gain insight into potential mechanisms of candidates entering a target cell.

Safety Assessment of Maxim. Water Extract: General Toxicity Studies in Sprague-Dawley Rats and Beagle Dogs With Re-evaluation of Genotoxic Potentials.

Maxim., commonly known as Manchurian stripe maple, is a deciduous tree belonging to the family of Aceraceae and has been traditionally used in folk medicine for its remedial effects in liver diseases and traumatic bleedings. With a growing body of experimental evidence for its pharmacological efficacies, such as neuroprotective, hepatoprotective, antioxidant, and anti-inflammatory activities, has gradually gained popularity as a health supplement and functional food.

Visualizing Oncolytic Virus-Host Interactions in Live Mice Using Intravital Microscopy.

Oncolytic virus (OV) therapy is an emerging cancer treatment that uses replicating viruses to infect and kill tumor cells and incite anticancer immunity. While the approach shows promise, it currently fails most patients, indicating strategies to improve OV activity are needed. Developing these will require greater understanding of OV biology, particularly in the context of OV delivery and clearance, the infection process within a complex tumor microenvironment, and the modulation of anticancer immunity.

Author Correction: Smac mimetics and oncolytic viruses synergize in driving anticancer T-cell responses through complementary mechanisms.

The originally published version of this article contained an error in the spelling of the author Pankaj Tailor, which was incorrectly given as Pankaj Taylor. This has now been corrected in both the PDF and HTML versions of the article.

Smac mimetics and oncolytic viruses synergize in driving anticancer T-cell responses through complementary mechanisms.

Second mitochondrial activator of caspase (Smac)-mimetic compounds and oncolytic viruses were developed to kill cancer cells directly. However, Smac-mimetic compound and oncolytic virus therapies also modulate host immune responses in ways we hypothesized would complement one another in promoting anticancer T-cell immunity. We show that Smac-mimetic compound and oncolytic virus therapies synergize in driving CD8 T-cell responses toward tumors through distinct activities.

Coxsackievirus B3 regulates T-cell infiltration into the heart by lymphocyte function-associated antigen-1 activation via the cAMP/Rap1 axis.

Coxsackievirus B3 (CVB3) infection can trigger myocarditis and can ultimately lead to dilated cardiomyopathy. It is known that CVB3-induced T-cell infiltration into cardiac tissues is one of the pathological factors causing cardiomyocyte injury by inflammation. However, the underlying mechanism for this remains unclear.

Induction of innate immune response following infectious bronchitis corona virus infection in the respiratory tract of chickens.

Infectious bronchitis virus (IBV) replicates in the epithelial cells of trachea and lungs of chicken, however the mechanism of generation of innate immune response against IBV infection in these tissues has not been fully characterized. Our objective was to study innate responses induced early following IBV infection in chickens. Initiation of the transcription of selected innate immune genes such as TLR3, TLR7, MyD88, IL-1β and IFN-β, as well as recruitment of macrophages, were evident following an initial down regulation of some of the observed genes (TLR3, IL-1β, and IFN-γ) in trachea and lung.

Induction of Toll-like receptor 4 signaling in avian macrophages inhibits infectious laryngotracheitis virus replication in a nitric oxide dependent way.

LPS is one of the pathogen associated molecular patterns that activates Toll-like receptor 4 (TLR4) signaling pathway eliciting antiviral host responses in mammals although information on such responses in avian species is scarce. Our objectives were to characterize the LPS induced innate responses particularly the expression of LPS receptors (TLR4, CD14) in avian macrophages and observe whether TLR4 mediated induction of NO can elicit antiviral response against infectious laryngotracheitis virus (ILTV) replication. We found that LPS was capable of inducing the expression of TLR4, CD14 and NO production but not the type 1 interferons in an avian macrophage cell line, MQ-NCSU.

A mechanism of immunoreceptor tyrosine-based activation motif (ITAM)-like sequences in the capsid protein VP2 in viral growth and pathogenesis of Coxsackievirus B3.

Coxsackievirus B3 (CVB3) is an RNA virus that mainly causes myocarditis. We have reported previously that immunoreceptor tyrosine-based activation motif (ITAM)-like sequences are contained in the capsid protein VP2 of CVB3. The substitution of two tyrosines for phenylalanines in the ITAM-like region causes attenuation of CVB3, possibly via defective viral assembly.

Application of attenuated coxsackievirus B3 as a viral vector system for vaccines and gene therapy.

Coxsackievirus B3 (CVB3) contains a single-stranded plus-strand RNA genome and belongs to the genus Enterovirus in the family Picornaviridae. For decades, many studies have shown that enteroviruses are potential viral vectors. Of these viruses, polioviruses and coxsackieviruses have predominantly been investigated.

Characterization of attenuated coxsackievirus B3 strains and prospects of their application as live-attenuated vaccines.

Coxsackievirus strain CVB3 is widespread in the human population and causes myocarditis or pancreatitis. However, despite its clinical impact, there is no commercially available and clinically applicable prophylactic vaccine. This study examines the characteristics of attenuated CVB3 strains developed so far and their application as live-attenuated CVB3 vaccines, and discusses problems to be overcome in the development of live-attenuated vaccines.

Systematic analysis of attenuated Coxsackievirus expressing a foreign gene as a viral vaccine vector.

Recombinant viruses expressing foreign antigens may provide a convenient vaccine vector capable of inducing preventative immunity. In this study, we explored the capacity of highly attenuated Coxsackievirus B3 (CVB3) to act as a recombinant vector to deliver foreign genes into experimental animals for the purpose of vaccination. The infectious cDNA of highly attenuated CVB3, YYFF, which has been reported previously (Vaccine 27:1974), was used to construct a recombinant YYFF cDNA (YYFF-HCV) by inserting a truncated form of hepatitis C virus (HCV) envelope protein E2 as an antigenic marker immediately upstream from the gene encoding the VP4 capsid protein.

Systemic analysis of a novel coxsackievirus gene delivery system in a mouse model.

In order to systemically investigate the possibility of using coxsackievirus B3 (CVB3) to deliver foreign genes in vivo, a recombinant strain of CVB3 encoding the renilla gene (CVB3- renilla) was constructed. The recombinant CVB3 resulted in extensive and transient expression of the renilla protein within mouse organs, especially the pancreas. The level of expression was generally dependent upon the viral titer present.

Attenuation of coxsackievirus B3 by VP2 mutation and its application as a vaccine against virus-induced myocarditis and pancreatitis.

Coxsackievirus B3 (CVB3) is a common agent of viral myocarditis, a major cause of sudden cardiac death, and ultimately dilated cardiomyopathy. However, there is no vaccine in clinical use. In this study, we identified the conserved amino acid sequences in the C-terminal region of the VP2 of the coxsackievirus B group and some echoviruses.

Recombinant lentivirus-delivered short hairpin RNAs targeted to conserved coxsackievirus sequences protect against viral myocarditis and improve survival rate in an animal model.

Coxsackieviruses are important human pathogens that induce myocarditis and pancreatitis. However, there are no vaccines or therapeutic reagents for their clinical treatment. Although RNA interference (RNAi)-based approaches to the prevention of viral production have been developed recently, limitations to the in vivo delivery systems and variations in the viral target sequences still hamper the strategy.

Production of cross-reactive peptide antibodies against viral capsid proteins of human enterovirus B to apply diagnostic reagent.

The coxsackievirus group B (CVB) of the genus Enterovirus and the species human enterovirus B is a nonenveloped virus containing a single-stranded positive-sense RNA genome. Coxsackievirus has icosahedral symmetry and four capsid proteins, VP1, VP2, VP3, and VP4. Specific antibodies against each viral protein are prerequisites for various studies.