Decreased T Cell Stimulatory Capacity of Monocyte‐Derived Human Macrophages following Herpes simplex Virus Type 1 Infection

Hoves, Sabine; Niller, Hans Helmut; Krause, Stefan W.; Straub, Rainer H.; Glück, Thomas; Mountz, John D.; Schölmerich, Jürgen

doi:10.1046/j.1365-3083.2001.00956.x

Cited by 10 publications

(5 citation statements)

References 41 publications

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“…The addition of anti-FasL antibodies reduced virus-induced cell death in our study. Similar effects of the virus were reported earlier on human monocytederived macrophages (27,28). The infected macrophages were reported to induce death of interacting CD8 þ T cells.…”

Section: Hsv-1 Infection Induces Apoptosis In Human Monocytic Cellssupporting

confidence: 81%

Herpes Simplex Virus Type 1-induced FasL Expression in Human Monocytic Cells and Its Implications for Cell Death, Viral Replication, and Immune Evasion

et al. 2011

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Herpes simplex virus type 1 (HSV-1) is a ubiquitously occurring pathogen that infects humans early in childhood. The virus persists as a latent infection in dorsal root ganglia, especially of the trigeminal nerve, and frequently becomes reactivated in humans under conditions of stress. Monocytic cells constitute an important component of the innate and adaptive immune responses. We show here for the first time that HSV-1 stimulates human FasL promoter and induces de novo expression of FasL on the surface of human monocytic cells, including monocytes and macrophages. This virus-induced FasL expression causes death of monocytic cells growing in suspension, but not in monolayers (e.g., macrophages). The addition of a broad-spectrum caspase inhibitor, as well as anti-FasL antibodies, reduced cell death but increased viral replication in the virus-infected cell cultures. We also show here for the first time that the virus-induced de novo expression of FasL on the cell surface acts as an immune evasion mechanism by causing the death of interacting human CD4+ T cells, CD8+ T cells, and natural killer (NK) cells. Our study provides novel insights on FasL expression and cell death in HSV-infected human monocytic cells and their impact on interacting immune cells.

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Section: Hsv-1 Infection Induces Apoptosis In Human Monocytic Cellssupporting

confidence: 81%

Herpes Simplex Virus Type 1-induced FasL Expression in Human Monocytic Cells and Its Implications for Cell Death, Viral Replication, and Immune Evasion

et al. 2011

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“…Earlier studies have shown that immunostimulatory capacity is diminished in dendritic cells, B-lymphoblastoid lines, and macrophages infected with wild-type HSV-1 (3,20,25,46). However, the significance of infections in these cell types is not clear, as they do not represent the primary target cells of HSV-1 in human infections.…”

Section: Discussionmentioning

confidence: 99%

“…Recent studies have shown that HSV-1 can diminish the T-cell stimulatory capacity of dendritic cells, B lymphoblastoid lines, and macrophages (3,20,25,46). However, these studies indicated that HSV-1 does not directly target MHC class II cell surface expression.…”

mentioning

confidence: 99%

Cell Surface Major Histocompatibility Complex Class II Proteins Are Regulated by the Products of the γ₁34.5 and U_L41 Genes of Herpes Simplex Virus 1

Trgovcich

Johnson

Roizman

2002

J Virol

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Modulation of host immune responses has emerged as a common strategy employed by herpesviruses both to establish life-long infections and to affect recovery from infection. Herpes simplex virus 1 (HSV-1) blocks the major histocompatibility complex (MHC) class I antigen presentation pathway by inhibiting peptide transport into the endoplasmic reticulum. The interaction of viral gene products with the MHC class II pathway, however, has not been thoroughly investigated, although CD4 ؉ T cells play an important role in human recovery from infection. We have investigated the stability, distribution, and state of MHC class II proteins in glioblastoma cells infected with wild-type HSV-1 or mutants lacking specific genes. We report the following findings. Herpes simplex virus 1 (HSV-1) has evolved numerous mechanisms to evade or counteract innate and specific host immune responses (reviewed in references 23, 28, and 51). These strategies promote escape from phagocytes, complement, NK cells, and cytotoxic T cells (CTL). In particular, CTL have been shown to be crucial for control of both productive and latent virus infections, and this is mirrored in the plethora of mechanisms which members of the Herpesviridae family have adopted to evade major histocompatibility complex (MHC) class I-mediated immune responses (39). HSV-1 and HSV-2 encode at least one protein, the infected cell protein (ICP) 47, which is dedicated to the evasion of CTL-mediated responses to infection (53). ICP47 disrupts normal peptide loading of MHC class I molecules by disabling peptide transport mediated by TAP1/TAP2 (13, 19). However, the extent to which HSV-1 can interfere directly with the MHC class II antigen presentation pathway is not known, despite the role of CD4 ϩ T cells in coordinating immune responses and in limiting HSV-1 replication and spread.The protective capacity of the CD4 ϩ T-lymphocyte subset has been described for several model systems. Mice deficient in CD4 ϩ T cells exhibit increased susceptibility to cutaneous HSV-induced lesions, implicating these cells in the control of zosteriform disease (29). Furthermore, MHC class II-mediated immune responses are critical in the protection of mice from ocular or intraperitoneal challenge after vaccination (15,35). Importantly, CD4ϩ T cells also act to control HSV infection in the central nervous system and trigeminal ganglia. In the murine model of infection, either CD4 ϩ T or CD8 ϩ T cells alone can clear virus from the trigeminal ganglia, suggesting that both subsets operate to promote the establishment of latency (16), and mice depleted of CD4 ϩ T cells experience more severe infections of the nervous system (37). Furthermore, CD4 ϩ cells are also implicated in limiting latent infection following challenge in a replication-defective vaccination model (35).A pathogenetic function also ascribed to CD4 ϩ T cells during HSV-1 keratitis is the induction of a bystander inflammatory response and the induction of cytokines in both human and murine infections (14,38). In humans, virus-reactiv...

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“…HSV-1 readily infects macrophages [89][90][91] and DC [92][93][94], leading to a series of functional changes in which antigen presenting capabilities are impaired. Despite this, as outlined above, the host is usually able to overcome the acute phase of infection by mounting a strong immune response.…”

Section: Interaction With Apcmentioning

confidence: 99%

Understanding HSV‐1 entry glycoproteins

Reske

Pollara

Krummenacher

et al. 2007

Reviews in Medical Virology

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Herpes Simplex Virus-1 is a common infectious agent, but the precise detail of entry and infection of cells has only now begun to be clarified. Four viral surface glycoproteins (gB, gD, gH and gL) are required. This review summarises the known structure and function of each of these essential viral envelope glycoproteins, and explores what is known about their close cooperation with each other in mediating cellular membrane fusion. It is suggested that, following gD binding to one of its entry receptors, membrane fusion is mediated by gB and the heterodimer gH/gL. Significantly, these four entry glycoproteins also play a key role in the interaction between HSV and the host immune system. The glycoproteins serve an important role as targets of adaptive immunity. However, recent studies have demonstrated that the same proteins also play a key role in initiating the early innate immune response to HSV. Understanding the complex functions of these HSV proteins may be essential for successful development of vaccines for HSV.

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Decreased T Cell Stimulatory Capacity of Monocyte‐Derived Human Macrophages following Herpes simplex Virus Type 1 Infection

Cited by 10 publications

References 41 publications

Herpes Simplex Virus Type 1-induced FasL Expression in Human Monocytic Cells and Its Implications for Cell Death, Viral Replication, and Immune Evasion

Herpes Simplex Virus Type 1-induced FasL Expression in Human Monocytic Cells and Its Implications for Cell Death, Viral Replication, and Immune Evasion

Cell Surface Major Histocompatibility Complex Class II Proteins Are Regulated by the Products of the γ₁34.5 and U_L41 Genes of Herpes Simplex Virus 1

Understanding HSV‐1 entry glycoproteins

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Decreased T Cell Stimulatory Capacity of Monocyte‐Derived Human Macrophages following Herpes simplex Virus Type 1 Infection

Cited by 10 publications

References 41 publications

Herpes Simplex Virus Type 1-induced FasL Expression in Human Monocytic Cells and Its Implications for Cell Death, Viral Replication, and Immune Evasion

Herpes Simplex Virus Type 1-induced FasL Expression in Human Monocytic Cells and Its Implications for Cell Death, Viral Replication, and Immune Evasion

Cell Surface Major Histocompatibility Complex Class II Proteins Are Regulated by the Products of the γ134.5 and UL41 Genes of Herpes Simplex Virus 1

Understanding HSV‐1 entry glycoproteins

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Product

Resources

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Cell Surface Major Histocompatibility Complex Class II Proteins Are Regulated by the Products of the γ₁34.5 and U_L41 Genes of Herpes Simplex Virus 1