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Mucosal Herpes Immunity and Immunopathology to Ocular and Genital Herpes Simplex Virus Infections  [PDF]
Aziz Alami Chentoufi,Lbachir BenMohamed
Journal of Immunology Research , 2012, DOI: 10.1155/2012/149135
Abstract: Herpes simplex viruses type 1 and type 2 (HSV-1 and HSV-2) are amongst the most common human infectious viral pathogens capable of causing serious clinical diseases at every stage of life, from fatal disseminated disease in newborns to cold sores genital ulcerations and blinding eye disease. Primary mucocutaneous infection with HSV-1 & HSV-2 is followed by a lifelong viral latency in the sensory ganglia. In the majority of cases, herpes infections are clinically asymptomatic. However, in symptomatic individuals, the latent HSV can spontaneously and frequently reactivate, reinfecting the muco-cutaneous surfaces and causing painful recurrent diseases. The innate and adaptive mucosal immunities to herpes infections and disease remain to be fully characterized. The understanding of innate and adaptive immune mechanisms operating at muco-cutaneous surfaces is fundamental to the design of next-generation herpes vaccines. In this paper, the phenotypic and functional properties of innate and adaptive mucosal immune cells, their role in antiherpes immunity, and immunopathology are reviewed. The progress and limitations in developing a safe and efficient mucosal herpes vaccine are discussed. 1. Introduction Herpes simplex viruses types 1 and 2 (HSV-1 and HSV-2) are among the most common human infectious viral pathogens [1–3]. So many people have HSV-1 and/or HSV-2 but do not know that they have it [4, 5]. These two viruses can cause lifelong diseases with clinical manifestations including cold sores, genital ulcerations, corneal blindness, and encephalitis [6–8]. In cases of vertical transmission to the newborn, HSV-1 and HSV-2 can cause fatal neonatal encephalitis [9–11]. In the past two decades, there have been increasing reports of a worldwide pandemic of herpes infections despite the widespread use of antiviral drug therapies (reviewed in [12]). At the site of primary infection, HSV undergoes a productive replication within the epithelial cells lining the mucosa. Thereafter, the virus enters nearby sensory neurons, and the viral genome is transported to the neuronal nuclei in the sensory ganglia (trigeminal (TG) or dorsal root (DRG)) that innervate the infected site. During the first week after infection, HSV replication takes place in ganglionic sensory neurons, but within a few days no virus can be detected. While epithelial cells are destroyed during lytic HSV replication, most neuronal cells appear largely intact and serve as a reservoir for the latent virus. During reactivation, the virus travels from the TG and DRG back to the site of primary infection
Acyclovir Suppression to Prevent Recurrent Genital Herpes at Delivery  [PDF]
L. L. Scott,L. M. Hollier,D. McIntire,P. J. Sanchez,G. L. Jackson,G. D. Wendel Jr.
Infectious Diseases in Obstetrics and Gynecology , 2002, DOI: 10.1155/s1064744902000054
Abstract: Objective: To determine if suppressive acyclovir near term decreased the frequency of clinical recurrences at delivery in women with recurrent genital herpes simplex virus (HSV) infection.
Herpes Simplex Virus 2 ICP0? Mutant Viruses Are Avirulent and Immunogenic: Implications for a Genital Herpes Vaccine  [PDF]
William P. Halford,Ringo Püschel,Brandon Rakowski
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0012251
Abstract: Herpes simplex virus 1 (HSV-1) ICP0? mutants are interferon-sensitive, avirulent, and elicit protective immunity against HSV-1 (Virol J, 2006, 3:44). If an ICP0? mutant of herpes simplex virus 2 (HSV-2) exhibited similar properties, such a virus might be used to vaccinate against genital herpes. The current study was initiated to explore this possibility. Several HSV-2 ICP0? mutant viruses were constructed and evaluated in terms of three parameters: i. interferon-sensitivity; ii. virulence in mice; and iii. capacity to elicit protective immunity against HSV-2. One ICP0? mutant virus in particular, HSV-2 0ΔNLS, achieved an optimal balance between avirulence and immunogenicity. HSV-2 0ΔNLS was interferon-sensitive in cultured cells. HSV-2 0ΔNLS replicated to low levels in the eyes of inoculated mice, but was rapidly repressed by an innate, Stat 1-dependent host immune response. HSV-2 0ΔNLS failed to spread from sites of inoculation, and hence produced only inapparent infections. Mice inoculated with HSV-2 0ΔNLS consistently mounted an HSV-specific IgG antibody response, and were consistently protected against lethal challenge with wild-type HSV-2. Based on their avirulence and immunogenicity, we propose that HSV-2 ICP0? mutant viruses merit consideration for their potential to prevent the spread of HSV-2 and genital herpes.
Acyclovir Suppression to Prevent Clinical Recurrences at Delivery After First Episode Genital Herpes in Pregnancy: An Open-Label Trial  [PDF]
L. Laurie Scott,Lisa M. Hollier,Donald McIntire,Pablo J. Sanchez,Gregory L. Jackson,George D. Wendel Jr.
Infectious Diseases in Obstetrics and Gynecology , 2001, DOI: 10.1155/s106474490100014x
Abstract: Objective: To continue evaluation of the use of acyclovir suppression in late pregnancy after first episode genital herpes simplex virus (HSV) infection, using an open-label study design.
Immunization with a highly attenuated replication-competent herpes simplex virus type 1 mutant, HF10, protects mice from genital disease caused by herpes simplex virus type 2  [PDF]
Chenhong Luo,Hiroshi Kimura
Frontiers in Microbiology , 2012, DOI: 10.3389/fmicb.2012.00158
Abstract: Genital herpes is an intractable disease caused mainly by herpes simplex virus (HSV) type 2 (HSV-2), and is a major concern in public health. A previous infection with HSV type 1 (HSV-1) enhances protection against primary HSV-2 infection to some extent. In this study, we evaluated the ability of HF10, a naturally occurring replication-competent HSV-1 mutant, to protect against genital infection in mice caused by HSV-2. Subcutaneous inoculation of HF10-immunized mice against lethal infection by HSV-2, and attenuated the development of genital ulcer diseases. Immunization with HF10 inhibited HSV-2 replication in the mouse vagina, reduced local inflammation, controlled emergence of neurological dysfunctions of HSV-2 infection, and increased survival. In HF10-immunized mice, we observed rapid and increased production of interferon-γ in the vagina in response to HSV-2 infection, and numerous CD4+ and a few CD8+ T cells localized to the infective focus. CD4+ T cells invaded the mucosal subepithelial lamina propria. Thus, the protective effect of HF10 was related to induction of cellular immunity, mediated primarily by Th1 CD4+ cells. These data indicate that the live attenuated HSV-1 mutant strain HF10 is a promising candidate antigen for a vaccine against genital herpes caused by HSV-2.
Immunization with a dominant-negative recombinant Herpes Simplex Virus (HSV) type 1 protects against HSV-2 genital disease in guinea pigs
Richard Brans, Feng Yao
BMC Microbiology , 2010, DOI: 10.1186/1471-2180-10-163
Abstract: Animals immunized with CJ9-gD developed at least 700-fold higher titers of HSV-2-specific neutralization antibodies than mock-immunized controls. After challenge with wild-type HSV-2, all 10 control guinea pigs developed multiple genital lesions with an average of 21 lesions per animal. In contrast, only 2 minor lesions were found in 2 of 8 CJ9-gD-immunized animals, representing a 40-fold reduction on the incidence of primary genital lesions in immunized animals (p < 0.0001). Immunization significantly reduced the amount and duration of viral shedding and provided complete protection against neurological symptoms, while 90% of mock-immunized animals succumbed due to the severity of disease. Importantly, immunized animals showed no signs of recurrent disease or viral shedding during a 60-days observation period after recovery from primary infection, and carried 50-fold less latent viral DNA load in their dorsal root ganglia than the surviving mock-vaccinated controls (p < 0.0001).Collectively, we demonstrate that vaccination with the HSV-1 recombinant CJ9-gD elicits strong and protective immune responses against primary and recurrent HSV-2 genital disease and significantly reduces the extent of latent infection.Genital herpes is the main cause of genital ulcer disease worldwide and is due to infections with herpes simplex virus (HSV) [1,2]. HSV-2 accounts for most cases of genital herpes [3]. Recent studies indicate that in developed countries HSV-1 has become the main causative agent for primary genital herpes, especially among adolescents, women, and homosexual men [4-7]. The prevalence of HSV-2 in the general population ranges from 10%-60%, indicating that genital herpes is one of the most common sexually transmitted diseases [2,8].After primary genital infection, HSV establishes latent infection in dorsal root ganglia with lifelong persistence, subsequently giving rise to intermittent reactivation and recurrent disease [9]. As the clinical appearance of genital H
Herpes simplex type 2 pneumonia
Calore, Edenilson Eduardo;
Brazilian Journal of Infectious Diseases , 2002, DOI: 10.1590/S1413-86702002000600006
Abstract: extensive reviews of pulmonary infections in aids have reported few herpetic infections. generally these infections are due to herpes simplex type 1. pneumonia due to herpes type 2 is extremely rare. we describe a 40 year-old hiv positive woman who complained of fever, cough and dyspnea for seven years. she had signs of heart failure and the appearance of her genital vesicles was highly suggestive of genital herpes. echocardiography showed marked pulmonary hypertension, right ventricular hypertrophy and tricuspid insufficiency. after a few days of hospitalization she was treated with aciclovir and later with ganciclovir. an open pulmonary biopsy revealed an interstitial inflammation, localized in the alveolar walls. some pulmonary arteries had widened walls and focal hyaline degeneration. immunohistochemistry indicated that the nuclei had herpes simplex virus type 2 in many endothelial cells (including vessels with widened walls), macrophages in the alveolar septa and pneumocytes. there was clinical improvement after treatment for herpes. we concluded that as a consequence of herpes infection, endothelial involvement and interstitial inflammation supervene, with thickening of vascular walls and partial obliteration of the vessel lumen. a direct consequence of these changes in pulmonary vasculature was pulmonary hypertension followed by heart failure.
Herpes simplex type 2 pneumonia  [cached]
Calore Edenilson Eduardo
Brazilian Journal of Infectious Diseases , 2002,
Abstract: Extensive reviews of pulmonary infections in AIDS have reported few herpetic infections. Generally these infections are due to Herpes simplex type 1. Pneumonia due to herpes type 2 is extremely rare. We describe a 40 year-old HIV positive woman who complained of fever, cough and dyspnea for seven years. She had signs of heart failure and the appearance of her genital vesicles was highly suggestive of genital herpes. Echocardiography showed marked pulmonary hypertension, right ventricular hypertrophy and tricuspid insufficiency. After a few days of hospitalization she was treated with Aciclovir and later with Ganciclovir. An open pulmonary biopsy revealed an interstitial inflammation, localized in the alveolar walls. Some pulmonary arteries had widened walls and focal hyaline degeneration. Immunohistochemistry indicated that the nuclei had herpes simplex virus type 2 in many endothelial cells (including vessels with widened walls), macrophages in the alveolar septa and pneumocytes. There was clinical improvement after treatment for herpes. We concluded that as a consequence of herpes infection, endothelial involvement and interstitial inflammation supervene, with thickening of vascular walls and partial obliteration of the vessel lumen. A direct consequence of these changes in pulmonary vasculature was pulmonary hypertension followed by heart failure.
Herpes simplex virus infection in pregnancy and in neonate: status of art of epidemiology, diagnosis, therapy and prevention
Elena Anzivino, Daniela Fioriti, Monica Mischitelli, Anna Bellizzi, Valentina Barucca, Fernanda Chiarini, Valeria Pietropaolo
Virology Journal , 2009, DOI: 10.1186/1743-422x-6-40
Abstract: Since the incidence of this sexually transmitted infection continues to rise and because the greatest incidence of herpes simplex virus infections occur in women of reproductive age, the risk of maternal transmission of the virus to the foetus or neonate has become a major health concern.On these purposes the Authors of this review looked for the medical literature and pertinent publications to define the status of art regarding the epidemiology, the diagnosis, the therapy and the prevention of HSV in pregnant women and neonate. Special emphasis is placed upon the importance of genital herpes simplex virus infection in pregnancy and on the its prevention to avoid neonatal HSV infections.Herpes simplex virus (HSV) infection is one of the most common viral sexually transmitted diseases (STD) worldwide [1,2]. Herpes simplex virus type 2 (HSV-2) is the cause of most genital herpes and is almost always sexually transmitted. Herpes simplex virus type 1 (HSV-1) is usually transmitted during childhood via non-sexual contacts. However, HSV-1 has emerged as a principle causative agent of genital herpes in some developed countries [1,3,4]. In the United States (US), HSV-1 is an important cause of genital herpes and its importance is increasing in college students [1,5,6].The greatest incidence of HSV infections occurs in women of reproductive age, the risk of maternal transmission of the virus to the foetus or neonate has become a major health concern [2,7-11].Recent findings reveal that first-time infection of the mother is the most important factor for the transmission of genital herpes from mother to foetus/newborn. In fact, the pregnant woman who acquires genital herpes as a primary infection in the latter half of pregnancy, rather than prior to pregnancy, is at greatest risk of transmitting these viruses to her newborn. Additional risk factors for neonatal HSV infection include the use of a foetal-scalp electrode and the age of the mother less than 21 years. Interventions
Herpes Simplex Virus-2 Genital Tract Shedding Is Not Predictable over Months or Years in Infected Persons  [PDF]
Varsha Dhankani,J. Nathan Kutz,Joshua T. Schiffer
PLOS Computational Biology , 2014, DOI: doi/10.1371/journal.pcbi.1003922
Abstract: Herpes simplex virus-2 (HSV-2) is a chronic reactivating infection that leads to recurrent shedding episodes in the genital tract. A minority of episodes are prolonged, and associated with development of painful ulcers. However, currently, available tools poorly predict viral trajectories and timing of reactivations in infected individuals. We employed principal components analysis (PCA) and singular value decomposition (SVD) to interpret HSV-2 genital tract shedding time series data, as well as simulation output from a stochastic spatial mathematical model. Empirical and model-derived, time-series data gathered over >30 days consists of multiple complex episodes that could not be reduced to a manageable number of descriptive features with PCA and SVD. However, single HSV-2 shedding episodes, even those with prolonged duration and complex morphologies consisting of multiple erratic peaks, were consistently described using a maximum of four dominant features. Modeled and clinical episodes had equivalent distributions of dominant features, implying similar dynamics in real and simulated episodes. We applied linear discriminant analysis (LDA) to simulation output and identified that local immune cell density at the viral reactivation site had a predictive effect on episode duration, though longer term shedding suggested chaotic dynamics and could not be predicted based on spatial patterns of immune cell density. These findings suggest that HSV-2 shedding patterns within an individual are impossible to predict over weeks or months, and that even highly complex single HSV-2 episodes can only be partially predicted based on spatial distribution of immune cell density.
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