Modulation of Monocyte Effector Functions and Gene Expression by Human Cytomegalovirus Infection
Monocytes are crucial players in innate immunity. The human cytomegalovirus (CMV) infection has significant impacts on monocyte effector functions and gene expression. CMV, a β-herpesvirus, disrupts key monocyte roles, including phagocytosis, antigen presentation, cytokine production, and migration,...
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| Format: | Article |
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MDPI AG
2024-11-01
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| Series: | Viruses |
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| Online Access: | https://www.mdpi.com/1999-4915/16/12/1809 |
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| author | Matthew S. Planchon Jay A. Fishman Joseph El Khoury |
| author_facet | Matthew S. Planchon Jay A. Fishman Joseph El Khoury |
| author_sort | Matthew S. Planchon |
| collection | DOAJ |
| description | Monocytes are crucial players in innate immunity. The human cytomegalovirus (CMV) infection has significant impacts on monocyte effector functions and gene expression. CMV, a β-herpesvirus, disrupts key monocyte roles, including phagocytosis, antigen presentation, cytokine production, and migration, impairing their ability to combat pathogens and activate adaptive immune responses. CMV modulates monocyte gene expression, decreasing their capacity for antigen presentation and phagocytosis while increasing pro-inflammatory cytokine production, which can contribute to tissue damage and chronic inflammation. CMV also alters monocyte migration to sites of infection while promoting trans-endothelial migration, thus aiding viral dissemination. Additionally, the virus affects reactive oxygen species (ROS) production, thereby contributing to end-organ disease associated with CMV infection. Overall, these changes enhance viral persistence during acute infection and facilitate immune evasion during latency. We highlight the clinical significance of these disruptions, particularly in immunocompromised patients such as transplant recipients, where the modulation of monocyte function by CMV exacerbates risks for infection, inflammation, and graft rejection. An understanding of these mechanisms will inform therapeutic strategies to mitigate CMV-related complications in vulnerable populations. |
| format | Article |
| id | doaj-art-b29d60b670e04bbdb235fd7aa1d6d665 |
| institution | Kabale University |
| issn | 1999-4915 |
| language | English |
| publishDate | 2024-11-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | Viruses |
| spelling | doaj-art-b29d60b670e04bbdb235fd7aa1d6d6652024-12-27T14:58:54ZengMDPI AGViruses1999-49152024-11-011612180910.3390/v16121809Modulation of Monocyte Effector Functions and Gene Expression by Human Cytomegalovirus InfectionMatthew S. Planchon0Jay A. Fishman1Joseph El Khoury2Center for Immunology and Inflammatory Diseases, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02129, USATransplant Infectious Disease and Compromised Host Program, Division of Infectious Diseases, Massachusetts General Hospital, and Harvard Medical School, Boston, MA 02114, USACenter for Immunology and Inflammatory Diseases, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02129, USAMonocytes are crucial players in innate immunity. The human cytomegalovirus (CMV) infection has significant impacts on monocyte effector functions and gene expression. CMV, a β-herpesvirus, disrupts key monocyte roles, including phagocytosis, antigen presentation, cytokine production, and migration, impairing their ability to combat pathogens and activate adaptive immune responses. CMV modulates monocyte gene expression, decreasing their capacity for antigen presentation and phagocytosis while increasing pro-inflammatory cytokine production, which can contribute to tissue damage and chronic inflammation. CMV also alters monocyte migration to sites of infection while promoting trans-endothelial migration, thus aiding viral dissemination. Additionally, the virus affects reactive oxygen species (ROS) production, thereby contributing to end-organ disease associated with CMV infection. Overall, these changes enhance viral persistence during acute infection and facilitate immune evasion during latency. We highlight the clinical significance of these disruptions, particularly in immunocompromised patients such as transplant recipients, where the modulation of monocyte function by CMV exacerbates risks for infection, inflammation, and graft rejection. An understanding of these mechanisms will inform therapeutic strategies to mitigate CMV-related complications in vulnerable populations.https://www.mdpi.com/1999-4915/16/12/1809cytomegalovirusmonocytephagocytosischemotaxismigrationcytokine production |
| spellingShingle | Matthew S. Planchon Jay A. Fishman Joseph El Khoury Modulation of Monocyte Effector Functions and Gene Expression by Human Cytomegalovirus Infection Viruses cytomegalovirus monocyte phagocytosis chemotaxis migration cytokine production |
| title | Modulation of Monocyte Effector Functions and Gene Expression by Human Cytomegalovirus Infection |
| title_full | Modulation of Monocyte Effector Functions and Gene Expression by Human Cytomegalovirus Infection |
| title_fullStr | Modulation of Monocyte Effector Functions and Gene Expression by Human Cytomegalovirus Infection |
| title_full_unstemmed | Modulation of Monocyte Effector Functions and Gene Expression by Human Cytomegalovirus Infection |
| title_short | Modulation of Monocyte Effector Functions and Gene Expression by Human Cytomegalovirus Infection |
| title_sort | modulation of monocyte effector functions and gene expression by human cytomegalovirus infection |
| topic | cytomegalovirus monocyte phagocytosis chemotaxis migration cytokine production |
| url | https://www.mdpi.com/1999-4915/16/12/1809 |
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