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HSV-1 Replication in different RAW 264.7 and J774.1 macrophage Phenotypes and Macrophage viability following HSV-1 infection

Alanazi, Yousef Nifaj
http://rave.ohiolink.edu/etdc/view?acc_num=wright1525211483024617

Abstract Details

2018, Master of Science (MS), Wright State University, Microbiology and Immunology.
HSV-1 is a ubiquitous virus capable of causing lifelong latent infection. The virus contains a large double strand DNA genome covered by an icosahedral capsid. HSV-1 is a cytolytic virus which can cause a lethal infection. The virus possesses critical protein ICP0 which is capable of interfering with host cell signaling and eventually prevent cell apoptosis. Innate immunity plays a crucial role in defense against HSV-1 infection and macrophage plays a significant role in the innate immune system. Macrophage cells can alter their behavior depending upon certain stimuli and tissue environments. Naive macrophage (M0) cells can be polarized to a pro-inflammatory (M1) macrophage or to an anti-inflammatory (M2) macrophage. There are subclasses of M2 macrophage which are M2a, M2b and M2c and they are stimulated with different stimuli. Macrophages phenotypes respond to HSV-1 infection differently and this study evaluates the viability of RAW 264.7 and J774.1 murine macrophage phenotypes (M0, M1 and M2) responding to HSV-1 infection 24, 48 and 72 hours following HSV-1infection. We also evaluate replication of HSV-1 in the murine macrophage cell lines and macrophage phenotypes. The M1 polarized macrophage exhibits the lowest viability among macrophage phenotypes in RAW 264.7 or J774.1 cell line. Among the M2 subclasses, IL-10 polarized M2 cells demonstrates markedly lower viability than IL-13 or IL-4 polarized M2 cells 24h and 72h following HSV-1 infection in RAW 264.7 cells and at 48h and 72h in J774.1 cells. Furthermore, HSV-1 titer was decreased in M1 macrophage at 24h, 48h and 72h. In M0 and M2 subtypes, HSV-1 titer was increased markedly during infection. In all macrophage cell lines, IL-10 polarized M2 cells yielded less HSV-1 Plaque Forming Unite (pfu/ml) than IL-4 polarized M2 cells after 72h of infection in Raw 264.7 or J774.1 cell lines at 72h of infection.
Nancy Bigley, Ph.D. (Advisor)
Barbara Hull, Ph.D. (Committee Member)
Dawn Wooley, Ph.D. (Committee Member)
66 p.
Immunology; Microbiology
HSV-1; phenotype; macrophage

Recommended Citations

Citations

  • Alanazi, Y. N. (2018). HSV-1 Replication in different RAW 264.7 and J774.1 macrophage Phenotypes and Macrophage viability following HSV-1 infection [Master's thesis, Wright State University]. OhioLINK Electronic Theses and Dissertations Center. http://rave.ohiolink.edu/etdc/view?acc_num=wright1525211483024617

    APA Style (7th edition)

  • Alanazi, Yousef. HSV-1 Replication in different RAW 264.7 and J774.1 macrophage Phenotypes and Macrophage viability following HSV-1 infection. 2018. Wright State University, Master's thesis. OhioLINK Electronic Theses and Dissertations Center, http://rave.ohiolink.edu/etdc/view?acc_num=wright1525211483024617.

    MLA Style (8th edition)

  • Alanazi, Yousef. "HSV-1 Replication in different RAW 264.7 and J774.1 macrophage Phenotypes and Macrophage viability following HSV-1 infection." Master's thesis, Wright State University, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=wright1525211483024617

    Chicago Manual of Style (17th edition)

wright1525211483024617
346
© 2018, some rights reserved.Creative Commons License HSV-1 Replication in different RAW 264.7 and J774.1 macrophage Phenotypes and Macrophage viability following HSV-1 infection by Yousef Nifaj Alanazi is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 3.0 Unported License. Based on a work at etd.ohiolink.edu.
This open access ETD is published by Wright State University and OhioLINK.