Open Access. Powered by Scholars. Published by Universities.®
- Discipline
-
- Immunology and Infectious Disease (5)
- Immunology of Infectious Disease (4)
- Medicine and Health Sciences (4)
- Biochemistry, Biophysics, and Structural Biology (3)
- Cancer Biology (3)
-
- Cell and Developmental Biology (3)
- Cell Biology (2)
- Diseases (2)
- Immunity (2)
- Molecular Biology (2)
- Virus Diseases (2)
- Biochemistry (1)
- Biology (1)
- Chemicals and Drugs (1)
- Genetics and Genomics (1)
- Laboratory and Basic Science Research (1)
- Molecular Genetics (1)
- Molecular and Cellular Neuroscience (1)
- Nervous System Diseases (1)
- Neuroscience and Neurobiology (1)
- Nucleic Acids, Nucleotides, and Nucleosides (1)
- Other Immunology and Infectious Disease (1)
- Pathogenic Microbiology (1)
- Respiratory Tract Diseases (1)
- Keyword
-
- Adenovirus (3)
- Autophagic Cell Death (2)
- Autophagy (2)
- GCN2 (2)
- Antigen presentation (1)
-
- Astrocyte (1)
- Autohpagy (1)
- Cell Death (1)
- Chromatin (1)
- Coronavirus (1)
- Epigenetics (1)
- Epithelium (1)
- Glioma (1)
- HERV-K (1)
- Human breast cancer (1)
- Immune response (1)
- Influenza (1)
- Innate immunity (1)
- JNK (1)
- Melanoma (1)
- NADPH oxidase (1)
- Neurodegeneration (1)
- P53 (1)
- Pancreatic cancer (1)
- Pattern recognition receptors (1)
- Pneumonia (1)
- Reactive Oxygen Sepcies (1)
- Retrovirus (1)
- SARS-CoV-2 (1)
- ShRNA (1)
Articles 1 - 8 of 8
Full-Text Articles in Virology
Expanding Inducible Epithelial Resistance Against Pneumonia: Novel Virus, Novel Receptor, Michael Longmire
Expanding Inducible Epithelial Resistance Against Pneumonia: Novel Virus, Novel Receptor, Michael Longmire
Dissertations and Theses (Open Access)
Pneumonia is the leading infectious cause of death worldwide and presents a continuing risk among immunocompromised patients. Our work has been focused for many years on the phenomenon of inducible epithelial resistance, where activation of the innate immune response in the airway epithelium is necessary and sufficient to produce a pathogen-killing but self-protective environment to prevent severe disease. Inducible resistance is pathogen-agnostic and has been demonstrated against an array of respiratory infections. We achieve this using a combination of pattern recognition receptor agonists – Pam2CSK4 and ODN M362 being the current formulation – which produce synergistic levels of pathogen reduction …
Molecular Mechanisms Behind Sars-Cov-2 Induced Host Genome Restructuring, Erin Simpson
Molecular Mechanisms Behind Sars-Cov-2 Induced Host Genome Restructuring, Erin Simpson
Dissertations and Theses (Open Access)
Severe Acute Respiratory Syndrome Coronavirus -2 (SARS-CoV-2) has caused unprecedented morbidity and mortality worldwide. There are two pathophysiological hallmarks associated with severe patient outcomes after SARS-CoV-2 acute infection, namely delayed/weakened interferon production and overactive inflammatory responses. Our previous work has shown that these altered immune responses are due, at least in part, to significant alterations in 3D genome organization and epigenetic landscape following SARS-CoV-2 infection that are distinct from and more severe than changes caused by other viral infections or immune stimulants. While these changes at the chromatin level are important for understanding the immune dysregulation seen in some cases …
The Effect Of Activation Induced Cytidine Deaminase Phosphorylation And Herpes Virus Uracil Dna Glycosylase On Antibody Diversification, Marc Macaluso
The Effect Of Activation Induced Cytidine Deaminase Phosphorylation And Herpes Virus Uracil Dna Glycosylase On Antibody Diversification, Marc Macaluso
Dissertations and Theses (Open Access)
Activation-induced cytidine deaminase (AID) is a mutagenic enzyme that is expressed in mammalian B-cells and initiates the antibody diversification processes of somatic hypermuntation (SHM) and isotype class switch recombination (CSR). AID is targeted to the immunoglobulin gene locus where it deaminates cytosines to generate uracil residues in DNA. This generates guanine-uracil (U:G) mismatch lesion which are recognized by uracil DNA glycosylase (UNG), a DNA repair enzyme that removes uracil from DNA and triggers downstream repair of the lesion. While UNG is a ubiquitously expressed DNA repair enzyme, its recognition and removal of AID introduced uracils is essential in both SHM …
Characterization Of The Role(S) Of Env Protein Of Human Endogenous Retrovirus-K In Multiple Human Cancers, Ming Li
Dissertations and Theses (Open Access)
Human endogenous retroviruses (HERVs) are remnants from ancient retroviral infections, and most of them are inactive in normal tissues. One family of HERV, HERV-K, is found to be associated with multiple human cancers including breast cancer, pancreatic cancer and melanoma, but the causal relationship between HERV-K and cancer is still unclear. Increased expression of HERV-K in melanoma cells correlates with malignant transformation, while a serological response to HERV-K in breast cancer or melanoma patients correlates with survival probability. However, the mechanism behind these observations remains obscure. Our laboratory reported that anti-HERV-K envelope (Env) protein antibodies show antitumor potential in targeting …
C-Jun N-Terminal Kinases Regulate Adenovirus-Mediated Autophagy And Antigen Presentation, Sarah R. Klein
C-Jun N-Terminal Kinases Regulate Adenovirus-Mediated Autophagy And Antigen Presentation, Sarah R. Klein
Dissertations and Theses (Open Access)
Targeted immunotherapy with recombinant, oncolytic adenoviruses is under investigation for the treatment of cancer. Evidence indicates adenoviruses induce autophagy that is required for oncolysis, but the molecular regulation of autophagy in infected cells remains under investigation. Our data suggested the canonical pathway regulating starvation-induced autophagy was not implemented in adenovirus-induced autophagy; however, adenovirus infection triggered phosphorylation of c-Jun N-terminal kinases (JNK) that was essential for autophagy. Adenoviral replication within the host cell elicited JNK pathway activation leading to B cell lymphoma-2 (Bcl-2) phosphorylation. JNK-dependent Bcl-2 phosphorylation stimulated the dissociation of Bcl-2/beclin 1 heterodimers, enabling beclin 1 to initiate autophagy. Moreover, …
Upregulation Of Reactive Oxygen Species During The Retrovirus Life Cycle And Their Roles In A Mutant Of Moloney Murine Leukemia Virus, Ts1-Mediated Neurodegeneration, Soo Jin Kim
Dissertations and Theses (Open Access)
Viral invasion of the central nervous system (CNS) and development of neurological symptoms is a characteristic of many retroviruses. The mechanism by which retrovirus infection causes neurological dysfunction has yet to be fully elucidated. Given the complexity of the retrovirus-mediated neuropathogenesis, studies using small animal models are extremely valuable. Our laboratory has used a mutant moloney murine leukemia retrovirus, ts1-mediated neurodegneration. We hypothesize that astrocytes play an important role in ts1-induced neurodegeneration since they are retroviral reservoirs and supporting cells for neurons. It has been shown that ts1 is able to infect astrocytes in vivo and in …
Mechanisms Of Adenovirus-Mediated Autophagy, Erin White
Mechanisms Of Adenovirus-Mediated Autophagy, Erin White
Dissertations and Theses (Open Access)
A patient diagnosed with a glioma, generally, has an average of 14 months year to live after implementation of conventional therapies such as surgery, chemotherapy, and radiation. Glioblastomas are highly lethal because of their aggressive nature and resistance to conventional therapies and apoptosis. Thus other avenues of cell death urgently need to be explored. Autophagy, which is also known as programmed cell death type II, has recently been identified as an alternative mechanism to kill apoptosis- resistant cancer cells. Traditionally, researchers have studied how cells undergo autophagy during viral infection as an immune response mechanism, but recently researchers have discovered …
Mechanisms Of Adenovirus-Mediated Autophagy, Erin White
Mechanisms Of Adenovirus-Mediated Autophagy, Erin White
Dissertations and Theses (Open Access)
A patient diagnosed with a glioma, generally, has an average of 14 months year to live after implementation of conventional therapies such as surgery, chemotherapy, and radiation. Glioblastomas are highly lethal because of their aggressive nature and resistance to conventional therapies and apoptosis. Thus other avenues of cell death urgently need to be explored. Autophagy, which is also known as programmed cell death type II, has recently been identified as an alternative mechanism to kill apoptosis- resistant cancer cells. Traditionally, researchers have studied how cells undergo autophagy during viral infection as an immune response mechanism, but recently researchers have discovered …