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Natural Resistance to Herpes Simplex Virus Infections: The Macrophage-Interferon Axis

  • Chapter
Herpesviruses, the Immune System, and AIDS

Part of the book series: Developments in Medical Virology ((DIMV,volume 6))

Abstract

The interactions between Herpes Simplex Virus type 1 and 2 (HSV-1, HSV-2) and the components of the host’s natural defense system and immune system have been the subject of numerous clinical studies. In addition, experimental models of HSV infection have been established in a variety of animals. In susceptible hosts, primary systemic infection results in lethal encephalitis, whereas under appropriate conditions local infection causes HSV latency. Evidence has accumulated for a central role of macrophages in controlling resistance to primary HSV infection. In inbred mice, genetically determined natural resistance to HSV correlates with low permissiveness of macrophages leading to abortive infection. Moreover, macrophages can eliminate free extracellular virus and due to their high secretory potential also inhibit HSV replication in neighbouring cells. Agents known to stimulate the secretion of macrophage mediators have been shown to increase their antiviral activity. Interferons type alpha and beta (IFN α/β) are among the most widely studied macrophage products. Macrophages are able to secrete low amounts of IFN constitutively in response to the macrophage-specific growth factor M-CSF. In addition, there is evidence that in resistant inbred mice, macrophages mainly contribute to the high level of “early” IFN α/β measurable in vivo after systemic HSV infections. IFN induced by HSV in vivo may either act directly by inhibiting virus replication in infected cells, or indirectly by stimulating natural killer cells. Under certain conditions, mouse macrophages can be persistently infected with HSV and may then serve as a vehicle for dissemination of the virus throughout the body. Freshly isolated human monocytes have been shown to restrict HSV replication but become permissive to lytic infection following prolonged in vitro culture. Human monocytes have been identified as cells producing IFN α/β in response to free infectious virions. HSV infected cells, however, induce IFN in a small population of medium-large sized lymphocytes. Clinical observations suggest that during recurrent HSV infection IFN γ is secreted locally by activated T lymphocytes and may synergize with IFN α/β in the antiviral activity against HSV. Recently, HSV infection has been shown to transactivate Human Immunodeficiency Virus (HIV) gene expression in persistently infected cells. This observation may be of clinical importance since monocytes can serve as target cells for both viruses.

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Authors and Affiliations

  1. Institute of Virus Research, German Cancer Research Center, INF 280, D 6900, Heidelberg, Germany

    Ingrid Domke-Opitz & Rainer Zawatzky

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  1. Ingrid Domke-Opitz
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  1. The University of Maryland, Baltimore, USA

    Laure Aurelian M.D.

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Domke-Opitz, I., Zawatzky, R. (1990). Natural Resistance to Herpes Simplex Virus Infections: The Macrophage-Interferon Axis. In: Aurelian, L. (eds) Herpesviruses, the Immune System, and AIDS. Developments in Medical Virology, vol 6. Springer, Boston, MA. https://doi.org/10.1007/978-1-4613-1507-0_8

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