Abstract
Chapter 7 discussed the concept of CTL-induced pathology, where CTL-mediated lysis of infected cells can lead to tissue damage and mortality of the host, instead of virus control. A fast rate of viral replication relative to the efficacy of the CTL was found to promote the occurrence of CTL-induced pathology. Lysis of infected cells, however, is not the only mechanism by which CTL can fight viral infections (Fig 8.1). CTL can also secrete soluble factors that bind to infected cells [(1994a)]. This triggers a reaction inside the cell that inhibits virus replication (Fig 8.1). Consequently, while the cell remains infected and is not killed, it stops producing virus particles and does not contribute to virus spread anymore. This type of mechanism is called nonlytic activity of CTL. There are examples of this mode of CTL-mediated activity across several infections. In LCMV infection, IFN-γ, secreted by CTL, can reduce the rate of viral replication [(2000)]. In HIV infection, a soluble factor has been identified that can stop virus production by infected cells. It has been termed CTL secreted antiviral factor (CAF), and its exact identity if subject to debate [(1996); (2002)]. In addition, HIV specific CTL can secrete chemokines that can inhibit the entry of certain HIV strains into their target cells [(1995); (1997); (1997); (1997)]. nonlytic CTL responses are thought to play an important role in HBV infection [(1994b); (1999a); (1996); (1996a); (1999b)].
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(2007). Lytic versus Nonlytic Activity. In: Wodarz, D. (eds) Killer Cell Dynamics. Interdisciplinary Applied Mathematics, vol 32. Springer, New York, NY. https://doi.org/10.1007/978-0-387-68733-9_8
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DOI: https://doi.org/10.1007/978-0-387-68733-9_8
Publisher Name: Springer, New York, NY
Print ISBN: 978-0-387-30893-7
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