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25 results on '"Pesola, Jean M."'

3. A small molecule exerts selective antiviral activity by targeting the human cytomegalovirus nuclear egress complex

Author

Chen, Han, primary, Lye, Ming F., additional, Gorgulla, Christoph, additional, Ficarro, Scott B., additional, Cuny, Gregory D., additional, Scott, David A., additional, Wu, Fan, additional, Rothlauf, Paul W., additional, Wang, Xiaoou, additional, Fernandez, Rosio, additional, Pesola, Jean M., additional, Draga, Sorin, additional, Marto, Jarrod A., additional, Hogle, James M., additional, Arthanari, Haribabu, additional, and Coen, Donald M., additional

Published
2023
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5. Human Cytomegalovirus Nuclear Egress Complex Subunit, UL53, Associates with Capsids and Myosin Va, but Is Not Important for Capsid Localization towards the Nuclear Periphery.

Author

Wilkie, Adrian R., Sharma, Mayuri, Coughlin, Margaret, Pesola, Jean M., Ericsson, Maria, Lawler, Jessica L., Fernandez, Rosio, and Coen, Donald M.

Subjects
CAPSIDS, HUMAN cytomegalovirus, HERPESVIRUSES, MYOSIN, NUCLEAR membranes, VIRAL genetics, MASS spectrometry, ELECTRON microscopy
Abstract

After herpesviruses encapsidate their genomes in replication compartments (RCs) within the nuclear interior, capsids migrate to the inner nuclear membrane (INM) for nuclear egress. For human cytomegalovirus (HCMV), capsid migration depends at least in part on nuclear myosin Va. It has been reported for certain herpesviruses that the nucleoplasmic subunit of the viral nuclear egress complex (NEC) is important for this migration. To address whether this is true for HCMV, we used mass spectrometry and multiple other methods to investigate associations among the HCMV NEC nucleoplasmic subunit, UL53, myosin Va, major capsid protein, and/or capsids. We also generated complementing cells to derive and test HCMV mutants null for UL53 or the INM NEC subunit, UL50, for their importance for these associations and, using electron microscopy, for intranuclear distribution of capsids. We found modest associations among the proteins tested, which were enhanced in the absence of UL50. However, we found no role for UL53 in the interactions of myosin Va with capsids or the percentage of capsids outside RC-like inclusions in the nucleus. Thus, UL53 associates somewhat with myosin Va and capsids, but, contrary to reports regarding its homologs in other herpesviruses, is not important for migration of capsids towards the INM. [ABSTRACT FROM AUTHOR]

Published
2022
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6. Linking indirect effects of cytomegalovirus in transplantation to modulation of monocyte innate immune function

Author

Sen, Pritha, primary, Wilkie, Adrian R., additional, Ji, Fei, additional, Yang, Yiming, additional, Taylor, Ian J., additional, Velazquez-Palafox, Miguel, additional, Vanni, Emilia A. H., additional, Pesola, Jean M., additional, Fernandez, Rosio, additional, Chen, Han, additional, Morsett, Liza M., additional, Abels, Erik R., additional, Piper, Mary, additional, Lane, Rebekah J., additional, Hickman, Suzanne E., additional, Means, Terry K., additional, Rosenberg, Eric S., additional, Sadreyev, Ruslan I., additional, Li, Bo, additional, Coen, Donald M., additional, Fishman, Jay A., additional, and El Khoury, Joseph, additional

Published
2020
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14. Mutations Inactivating Herpes Simplex Virus 1 MicroRNA miR-H2 Do Not Detectably Increase ICP0 Gene Expression in Infected Cultured Cells or Mouse Trigeminal Ganglia.

Author

Dongli Pan, Pesola, Jean M., Gang Li, McCarron, Seamus, and Coen, Donald M.

Subjects
*HERPES simplex virus, *GENETIC mutation, *MICRORNA, *LYTIC cycle, *CELL culture, *TRIGEMINAL nerve, *GENE expression in viruses
Abstract

Herpes simplex virus 1 (HSV-1) latency entails the repression of productive ("lytic") gene expression. An attractive hypothesis to explain some of this repression involves inhibition of the expression of ICP0, a lytic gene activator, by a viral microRNA, miR-H2, which is completely complementary to ICP0 mRNA. To test this hypothesis, we engineered mutations that disrupt miR-H2 without affecting ICP0 in HSV-1. The mutant virus exhibited drastically reduced expression of miR-H2 but showed wild-type levels of infectious virus production and no increase in ICP0 expression in lytically infected cells, which is consistent with the weak expression of miR-H2 relative to the level of ICP0 mRNA in that setting. Following corneal inoculation of mice, the mutant was not significantly different from wild-type virus in terms of infectious virus production in the trigeminal ganglia during acute infection, mouse mortality, or the rate of reactivation from explanted latently infected ganglia. Critically, the mutant was indistinguishable from wild-type virus for the expression of ICP0 and other lytic genes in acutely and latently infected mouse trigeminal ganglia. The latter result may be related to miR-H2 being less effective in inhibiting ICP0 expression in transfection assays than a host microRNA, miR-138, which has previously been shown to inhibit lytic gene expression in infected ganglia by targeting ICP0 mRNA. Additionally, transfected miR-138 reduced lytic gene expression in infected cells more effectively than miR-H2. While this study provides little support for the hypothesis that miR-H2 promotes latency by inhibiting ICP0 expression, the possibility remains that miR-H2 might target other genes during latency. [ABSTRACT FROM AUTHOR]

Published
2017
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25. Linking indirect effects of cytomegalovirus in transplantation to modulation of monocyte innate immune function.

Author

Pritha Sen, Wilkie, Adrian R., Fei Ji, Jiming Yang, Taylor, Ian J., Velazquez-Palafox, Miguel, Vanni, Emilia A. H., Pesola, Jean M., Fernandez, Rosio, Han Chen, Morsett, Liza M., Abels, Erik R., Piper, Mary, Lane, Rebekah J., Hickman, Suzanne E., Means, Terry K., Rosenberg, Eric S., Sadreyev, Ruslan I., Bo Li, and Coen, Donald M.

Subjects
*CYTOMEGALOVIRUS diseases, *MONOCYTES, *BIOCHEMISTRY, *HUMAN cytomegalovirus diseases, *BACTERIAL artificial chromosomes, *CELL receptors, *GREEN fluorescent protein
Abstract

The article focuses on the Cytomegalovirus (CMV), an important cause of morbidity and mortality in the immunocompromised host. It mentions that human monocytes infected with CMV do not effectively phagocytose fungal pathogens, a functional deficit which occurs with decreased expression of fungal recognition receptors; and also mentions that CMV modulates both immunosuppressive and immunostimulatory monocyte phenotypes.

Published
2020
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