Platelet-endothelial associations may promote cytomegalovirus replication in the salivary gland in mice
| Autor: | Karl T. Johnson, Selena M. Guerrero-Martin, Catherine G. Cryer, Yu Pin Su, Kirstin McGee, Jacqueline K. Brockhurst, Brenna Daly, S. Andrew Aston, Griffin Cyphers, Shefali Vijay, Kelly A. Metcalf Pate, Claire E. Lyons, Kevin Najarro, Alicia M. Braxton, Ravit Arav-Boger, Alyssa L. Chalmin |
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| Rok vydání: | 2019 |
| Předmět: |
Blood Platelets
Male 0301 basic medicine Endothelium Congenital cytomegalovirus infection Cytomegalovirus 030204 cardiovascular system & hematology Article Salivary Glands Pathogenesis 03 medical and health sciences 0302 clinical medicine Immune system medicine Animals Humans Platelet Virus quantification Mice Inbred BALB C Salivary gland business.industry Endothelial Cells Hematology General Medicine medicine.disease Disease Models Animal 030104 developmental biology medicine.anatomical_structure Immunology business Viral load |
| Zdroj: | Platelets |
| DOI: | 10.6084/m9.figshare.10310468 |
| Popis: | Platelet decline is a feature of many acute viral infections, including cytomegalovirus (CMV) infection in humans and mice. Platelet sequestration in association with other cells, including endothelium and circulating leukocytes, can contribute to this decline and influence the immune response to and pathogenesis of viral infection. We sought to determine if platelet-endothelial associations (PEAs) contribute to platelet decline during acute murine CMV (mCMV) infection, and if these associations affect viral load and production. Male BALB/c mice were infected with mCMV (Smith strain), euthanized at timepoints throughout acute infection and compared to uninfected controls. An increase in PEA formation was confirmed in the salivary gland at all post-inoculation timepoints using immunohistochemistry for CD41+ platelets co-localizing with CD34+ vessels. Platelet depletion did not change amount of viral DNA or timecourse of infection, as measured by qPCR. However, platelet depletion reduced viral titer of mCMV in the salivary glands while undepleted controls demonstrated robust replication in the tissue by plaque assay. Thus, platelet associations with endothelium may enhance the ability of mCMV to replicate within the salivary gland. Further work is needed to determine the mechanisms behind this effect and if pharmacologic inhibition of PEAs may reduce CMV production in acutely infected patients. |
| Databáze: | OpenAIRE |
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