HSV‐2 replication sites, monocyte and lymphocytic cell infection and virion phagocytosis by neutrophils, in vesicular lesions on penile skin

Boddingius, J.; Dijkman, H.; Hendriksen, E.G.J.; Schift, R.; Stolz, Erwin

doi:10.1111/j.1600-0560.1987.tb00492.x

Cited by 15 publications

(9 citation statements)

References 12 publications

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“…These results strongly suggest that the diminished protection was directly due to a loss of neutrophil effector function rather than an unintentional alteration of antigen-specific B-or T-cell function. The exact mechanism by which neutrophils clear HSV-2 is currently unknown but may include phagocytosis of free virions or virus-infected cells (2,37), release of antiviral cytokines (3) or defensins (7,8), and antibody-dependent cellmediated cytolysis of HSV-infected cells (22,28). Additionally, given the ability of human neutrophils to secrete cytokines, including interleukin-12 (4) and IFN-␥ (43), local release of these cytokines by tissue neutrophils may help bias immune responses towards the development of protective Th1 responses.…”

Section: Discussionmentioning

confidence: 99%

Neutrophils Aid in Protection of the Vaginal Mucosae of Immune Mice against Challenge with Herpes Simplex Virus Type 2

Milligan

1999

J Virol

121

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Large numbers of polymorphonuclear leukocytes (PMNs) infiltrated the murine vaginal mucosa within 24 h after intravaginal inoculation with an attenuated strain of herpes simplex virus type 2 (HSV-2). The role of these cells in resolution of a primary genital infection and in protection of HSV-immune animals against challenge with a fully virulent HSV-2 strain was investigated. Depletion of greater than 95% of the PMNs at the vaginal mucosal surface prior to intravaginal inoculation with an attenuated HSV-2 strain resulted in significantly higher virus titers on days 3 to 7 but only slightly delayed resolution of the primary genital infection. These results suggest that neutrophils helped control the infection but that other immune mechanisms ultimately cleared the virus. Interestingly, depletion of PMNs from HSV-immune mice prior to challenge with a fully virulent HSV-2 strain resulted in a rise in virus titers to levels comparable to those of nonimmune mice and a more pronounced diminution of virus clearance from the vaginal mucosa despite the presence of HSV-specific B and T cells. Levels of gamma interferon (IFN-γ) and HSV-specific antibody were comparable in neutrophil-depleted and control-treated immune mice following HSV-2 challenge, suggesting that RB6-8C5 treatment did not impair T- and B-cell function. Therefore, these results suggest that neutrophils play a role in limiting and clearing HSV-2 vaginal infections and that they are, in association with HSV-specific B and T cells, an important component in immune protection of the vaginal mucosa.

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Section: Discussionmentioning

confidence: 99%

Neutrophils Aid in Protection of the Vaginal Mucosae of Immune Mice against Challenge with Herpes Simplex Virus Type 2

Milligan

1999

J Virol

121

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“…This feature could contribute to the observed infiltration of neutrophils to the local site(s) of HSV-2 infection (33), where they phagocytose and degrade viral particles (34) and thus contribute to the antiviral defense, as implicated in both experimental animals and humans (13)(14)(15). Besides this more obvious reason for the HSV-2 release of a FPR-activating agonist, i.e., to increase the number of phagocytes at the site of infection and thereby increase the tissue damage and thus enabling viral spread and propagation, the FPR (as well as FPRL1) has been shown to be able to downregulate other chemotactic receptors in vivo.…”

Section: Discussionmentioning

confidence: 99%

A Proinflammatory Peptide from Herpes Simplex Virus Type 2 Glycoprotein G Affects Neutrophil, Monocyte, and NK Cell Functions

Bellner

Thorén²,

Nygren

et al. 2005

The Journal of Immunology

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We have identified a synthetic peptide derived from the secreted portion of HSV type 2 glycoprotein G, denoted gG-2p20, which has proinflammatory properties in vitro. The gG-2p20 peptide, corresponding to aa 190–205 of glycoprotein G-2, was a chemoattractant for both monocytes and neutrophils in a dose-dependent fashion, and also induced the release of reactive oxygen from these cells. The receptor mediating the responses was identified as the formyl peptide receptor. The gG-2p20-induced activation of phagocytes had a profound impact on NK cell functions. The reactive oxygen species produced by gG-2p20-activated phagocytes both inhibited NK cell cytotoxicity and accelerated the apoptotic cell death in NK cell-enriched lymphocyte populations. Hence, we have for the first time been able to identify a potential function of the secreted portion of HSV-2 glycoprotein G. We propose that the proinflammatory gG-2p20 peptide identified could contribute to a reduced function and viability of NK cells during HSV-2 infection due to its ability to recruit and activate phagocytic cells.

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“…The pathology of HSV infections is mainly caused by a direct cytopathic effect of the virus, resulting in cellular lysis and focal necrosis of the infected area [119,127,128]. In tissues capable of regeneration, this is not devastating, provided that the lesions do not totally destroy the organ or result in functional disability during the infection.…”

Section: Epidemiologymentioning

confidence: 99%

Macrophages and cytokines in the early defence against herpes simplex virus

Ellermann-Eriksen

2005

Virol J

113

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Herpes simplex virus (HSV) type 1 and 2 are old viruses, with a history of evolution shared with humans. Thus, it is generally well-adapted viruses, infecting many of us without doing much harm, and with the capacity to hide in our neurons for life. In rare situations, however, the primary infection becomes generalized or involves the brain.Normally, the primary HSV infection is asymptomatic, and a crucial element in the early restriction of virus replication and thus avoidance of symptoms from the infection is the concerted action of different arms of the innate immune response. An early and light struggle inhibiting some HSV replication will spare the host from the real war against huge amounts of virus later in infection. As far as such a war will jeopardize the life of the host, it will be in both interests, including the virus, to settle the conflict amicably. Some important weapons of the unspecific defence and the early strikes and beginning battle during the first days of a HSV infection are discussed in this review.Generally, macrophages are orchestrating a multitude of anti-herpetic actions during the first hours of the attack. In a first wave of responses, cytokines, primarily type I interferons (IFN) and tumour necrosis factor are produced and exert a direct antiviral effect and activate the macrophages themselves. In the next wave, interleukin (IL)-12 together with the above and other cytokines induce production of IFN-γ in mainly NK cells. Many positive feed-back mechanisms and synergistic interactions intensify these systems and give rise to heavy antiviral weapons such as reactive oxygen species and nitric oxide. This results in the generation of an alliance against the viral enemy.However, these heavy weapons have to be controlled to avoid too much harm to the host. By IL-4 and others, these reactions are hampered, but they are still allowed in foci of HSV replication, thus focusing the activity to only relevant sites. So, no hero does it alone. Rather, an alliance of cytokines, macrophages and other cells seems to play a central role. Implications of this for future treatment modalities are shortly considered.

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HSV‐2 replication sites, monocyte and lymphocytic cell infection and virion phagocytosis by neutrophils, in vesicular lesions on penile skin

Cited by 15 publications

References 12 publications

Neutrophils Aid in Protection of the Vaginal Mucosae of Immune Mice against Challenge with Herpes Simplex Virus Type 2

Neutrophils Aid in Protection of the Vaginal Mucosae of Immune Mice against Challenge with Herpes Simplex Virus Type 2

A Proinflammatory Peptide from Herpes Simplex Virus Type 2 Glycoprotein G Affects Neutrophil, Monocyte, and NK Cell Functions

Macrophages and cytokines in the early defence against herpes simplex virus

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