Publications by authors named "Carolina B Lopez"

A challenge in viral vaccine development is to produce vaccines that generate both neutralizing antibodies to prevent infection and cytotoxic CD8 T-cells that target conserved viral proteins and can eliminate infected cells to control virus spread. mRNA technology offers an opportunity to design vaccines based on conserved CD8-targeting epitopes, but achieving robust antigen-specific CD8 T-cells remains a challenge. Here, we tested the viral-derived oligonucleotide DDO268 as an adjuvant in the context of a model influenza A virus (IAV) nucleoprotein (NP) mRNA vaccine in C57BL/6 mice.

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This study reports the identification of Langya virus Korea (LayV KOR) during the surveillance of shrews in the Republic of Korea. LayV KOR represents the first identification of LayV outside of China, exhibiting approximately 80% and 95.5% homologies at nucleotide and amino acid levels.

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A challenge in viral vaccine development is to produce vaccines that generate both neutralizing antibodies to prevent infection and cytotoxic CD8 T-cells that target conserved viral proteins and can eliminate infected cells to control virus spread. mRNA vaccines offer an opportunity to design vaccines based on conserved CD8-targeting epitopes, but achieving robust antigen-specific CD8 T-cells remains a challenge. Here we tested the viral-derived oligonucleotide DDO268 as an adjuvant in the context of a model influenza A virus (IAV) nucleoprotein (NP) mRNA vaccine in C57BL/6 mice.

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Background: The discovery of viruses in small mammalian populations, particularly rodents, has expanded the family Paramyxoviridae. The overlap in habitats between rodents and humans increases the risk of zoonotic events, underscoring the importance of active surveillance. Rodent species, such as Apodemus agrarius, are natural hosts for Paramyxoviridae in the Republic of Korea (ROK).

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Common respiratory viruses, including the human parainfluenza viruses, threaten human health seasonally and associate with the development of chronic lung diseases. Evidence suggests that these viruses can persist, but the sources of viral products in vivo and their impact on chronic respiratory diseases remain unknown. Using the murine parainfluenza virus Sendai, we demonstrate that viral protein and RNA persist in lung macrophages, type 2 innate lymphoid cells (ILC2s) and dendritic cells long after the infectious virus is cleared.

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Article Synopsis
  • Arenaviruses, which are transmitted by rodents and cause severe hemorrhagic fever in humans, currently lack effective antivirals and vaccines, prompting research into new ways to inhibit their replication.
  • The study discovers that arenaviruses produce deletions in the intergenic region of their small RNA genome that can inhibit the production of viral glycoproteins, especially in conditions that enhance viral interference.
  • These findings suggest that the natural interfering molecules generated by arenaviruses could be leveraged as a basis for developing new antiviral treatments targeting multiple strains within the arenavirus family.
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  • Paramyxoviruses like mumps virus, Newcastle disease virus, and Sendai virus are important pathogens, but not much is known about the host factors that help them infect cells.
  • A study using CRISPR technology discovered that two genes, CST and UGT, are crucial for these viruses to infect cells, as knocking them out results in reduced viral binding.
  • The UGT gene specifically aids in virus-cell fusion during Sendai virus entry and helps form larger syncytia (cell clusters) during mumps virus infection, indicating it plays a role in how these viruses spread between cells.
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Respiratory syncytial virus (RSV) is a common cause of respiratory infection that often leads to hospitalization of infected younger children and older adults. RSV is classified into two strains, A and B, each with several subgroups or genotypes. One issue with the definition of these subgroups is the lack of a unified method of identification or genotyping.

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Article Synopsis
  • * The study proposes that nonstandard viral genomes (nsVGs), often seen as accidental byproducts, are actually important for the virus's life cycle and play multiple roles during infection.
  • * The review suggests that understanding the generation of nsVGs changes our perspective on virus success, indicating it is a key evolutionary mechanism for maintaining RNA viruses in nature.
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The henipaviruses, including Nipah virus (NiV) and Hendra virus (HeV), are biosafety level 4 (BSL-4) zoonotic pathogens that cause severe neurological and respiratory disease in humans. To study the replication machinery of these viruses, we developed robust minigenome systems that can be safely used in BSL-2 conditions. The nucleocapsid (N), phosphoprotein (P), and large protein (L) of henipaviruses are critical elements of their replication machinery and thus essential support components of the minigenome systems.

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Respiratory syncytial virus is a common cause of respiratory infection that often leads to hospitalization of infected younger children and older adults. RSV is classified into two strains, A and B, each with several subgroups or genotypes. One issue with the definition of these subgroups is the lack of a unified method of identification or genotyping.

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Respiratory viruses including the human parainfluenza viruses (hPIVs) are a constant burden to human health, with morbidity and mortality frequently increased after the acute phase of the infection. Although is proven that respiratory viruses can persist , the mechanisms of virus or viral products persistence, their sources, and their impact on chronic respiratory diseases are unknown. Here, we used Sendai virus (SeV) to model hPIV infection in mice and test whether virus persistence associates with the development of chronic lung disease.

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Antiviral responses are often accompanied by translation inhibition and formation of stress granules (SGs) in infected cells. However, the triggers for these processes and their role during infection remain subjects of active investigation. Copy-back viral genomes (cbVGs) are the primary inducers of the mitochondrial antiviral signaling (MAVS) pathway and antiviral immunity during Sendai virus (SeV) and respiratory syncytial virus (RSV) infections.

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Arenaviruses, a family of negative-sense RNA viruses spread by rodents, are a leading cause of severe hemorrhagic fever in humans. Due to a paucity of antivirals and vaccines for arenaviruses, there is a need to identify new mechanisms for interfering with arenavirus replication. In several negative-sense RNA viruses, natural viral interference results from the production of non-standard viral genomes (nsVGs) that activate the innate immune system and/or compete for essential viral products.

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During viral replication, viruses carrying an RNA genome produce non-standard viral genomes (nsVGs), including copy-back viral genomes (cbVGs) and deletion viral genomes (delVGs), that play a crucial role in regulating viral replication and pathogenesis. Because of their critical roles in determining the outcome of RNA virus infections, the study of nsVGs has flourished in recent years, exposing a need for bioinformatic tools that can accurately identify them within next-generation sequencing data obtained from infected samples. Here, we present our data analysis pipeline, Viral Opensource DVG Key Algorithm 2 (VODKA2), that is optimized to run on a parallel computing environment for fast and accurate detection of nsVGs from large data sets.

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Antiviral responses are often accompanied by translation inhibition and formation of stress granules (SG) in infected cells. However, the triggers for these processes and their role during infection remain subjects of active investigation. Copy-back viral genomes (cbVGs) are the primary inducers of the Mitochondrial Antiviral Signaling (MAVS) pathway and antiviral immunity during Sendai Virus (SeV) and Respiratory Syncytial virus (RSV) infections.

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During viral replication, viruses carrying an RNA genome produce non-standard viral genomes (nsVGs), including copy-back viral genomes (cbVGs) and deletion viral genomes (delVGs), that play a crucial role in regulating viral replication and pathogenesis. Because of their critical roles in determining the outcome of RNA virus infections, the study of nsVGs has flourished in recent years exposing a need for bioinformatic tools that can accurately identify them within Next-Generation Sequencing data obtained from infected samples. Here, we present our data analysis pipeline, Viral Opensource DVG Key Algorithm2 (VODKA2), that is optimized to run on a High Performance Computing (HPC) environment for fast and accurate detection of nsVGs from large data sets.

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Article Synopsis
  • Respiratory viruses like influenza, RSV, and SARS-CoV-2 pose significant health risks globally, leading to both acute and long-term illness, especially in vulnerable groups.
  • Researchers gathered at the Keystone symposium from June 29 to July 2, 2022, to discuss new findings on how these viruses operate and interact with their hosts.
  • The goal of the symposium was to explore innovative treatment and prevention strategies that can effectively combat these rapidly evolving viruses and their possible resistance to current therapies.*
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There is a critical need to develop vaccine adjuvants that induce robust immune responses able to protect against intracellular pathogens, including viruses. Previously, we described defective viral genome-derived oligonucleotides (DDOs) as novel adjuvants that strongly induce type 1 immune responses, including protective Th1 CD4+ T-cells and effector CD8+ T-cells in mice. Here, we unravel the early innate response required for this type 1 immunity induction.

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RNA viruses generate nonstandard viral genomes during their replication, including viral genomes of the copy-back (cbVGs) type that cannot replicate in the absence of a standard virus. cbVGs play a crucial role in shaping virus infection outcomes due to their ability to interfere with virus replication and induce strong immune responses. However, despite their critical role during infection, the principles that drive the selection and evolution of cbVGs within a virus population are poorly understood.

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Influenza A virus (IAV) preferentially infects conducting airway and alveolar epithelial cells in the lung. The outcome of these infections is impacted by the host response, including the production of various cytokines, chemokines, and growth factors. Fibroblast growth factor-9 (FGF9) is required for lung development, can display antiviral activity in vitro, and is upregulated in asymptomatic patients during early IAV infection.

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Negative-sense RNA virus populations are composed of diverse viral components that interact to form a community and shape the outcome of virus infections. At the genomic level, RNA virus populations consist not only of a homogeneous population of standard viral genomes but also of an extremely large number of genome variants, termed viral quasispecies, and nonstandard viral genomes, which include copy-back viral genomes, deletion viral genomes, mini viral RNAs, and hypermutated RNAs. At the particle level, RNA virus populations are composed of pleomorphic particles, particles missing or having additional genomes, and single particles or particle aggregates.

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One of the most pressing challenges in medicine is to develop fast and effective strategies to combat infections. Xiao et al. report proof-of-concept experiments for the use of defective viral genomes as broad-spectrum antivirals by harnessing their ability to stimulate the innate immune response.

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