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Cunningham, Anthony L., Cheryl A. Jones, and Min Kim. "Herpes simplex virus vaccines." Microbiology Australia 32, no. 3 (2011): 123. http://dx.doi.org/10.1071/ma11123.
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Herpes simplex virus (HSV) types 1 and 2 cause herpes labialis and genital herpes respectively, although genital herpes caused by HSV-1 is increasing in adolescence. Adult HSV-1 seroprevalence in western countries is 55% to 80% (80% in Australia) and acquired in two peaks, in infancy and adolescence. HSV-2 seroprevalence is highly variable geographically, reaching 12% in Australian adults but up to 90% in African countries. After initial HSV-1 or 2 infection, asymptomatic shedding occurs in the mouth and genital tract respectively in nearly all infected subjects. Complications of HSV-1 include keratitis and blindness and life-threatening encephalitis. Severe complications of HSV-2 include acute urinary retention, meningitis and neonatal herpes (25% fatality). In addition, prior infection with HSV-2 consistently enhances HIV acquisition three- to fourfold. In immunosuppressed persons, HSV-1 and 2 may cause indolent ulcers, oesophagitis and pneumonia. Ultimately, a childhood vaccine effective against both HSV-1 and 2 disease is needed.
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KAWAGUCHI, Yasushi. "Herpes simplex virus (HSV)." Uirusu 60, no. 2 (2010): 187–96. http://dx.doi.org/10.2222/jsv.60.187.
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Lachmann, Robin. "Herpes simplex virus latency." Expert Reviews in Molecular Medicine 5, no. 29 (December 5, 2003): 1–14. http://dx.doi.org/10.1017/s1462399403006975.
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Herpes simplex virus type 1 (HSV-1) and type 2 (HSV-2) are ubiquitous human pathogens. They share with other herpesviruses the ability to establish lifelong latent infection of the host. Periodic reactivation from latency is responsible for most of the clinical disease burden of HSV infection. This review focuses on what we have learned from molecular studies in model systems of HSV latency, and the implications these findings have for treating recurrent HSV disease.
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Whitley, Richard J., and Cecelia Hutto. "Neonatal Herpes Simplex Virus Infections." Pediatrics In Review 7, no. 4 (October 1, 1985): 119–26. http://dx.doi.org/10.1542/pir.7.4.119.
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Infections caused by herpes simplex viruses have been recognized since ancient Roman times, when Herodotus associated mouth ulcers and lip vesicles with fever. However, neonatal herpes simplex infection was not identified as a distinct disease until centuries later. Only 50 years ago, the first written descriptions of neonatal herpes were attributed nearly simultaneously to Hass, who described the histopathologic findings in a fatal case, and to Batingani who described a newborn child with herpes simplex virus (HSV) keratitis. For several decades our understanding of neonatal infections with herpes simplex virus was predicated upon histopathologic descriptions of the disease. These indicated a broad spectrum of involvement in infants. In the mid-1960s, Nahmias and Dowdle demonstrated two antigenic types of herpes simplex virus, HSV-1 and HSV-2. Recognition of these types prompted a rapid series of developments leading to a better characterization of the biochemical and molecular characteristics of the virus. One consequence of these advances has been the development of methods of typing of viruses which have been utilized to define the epidemiology of HSV infections. Herpes simplex viral infections "above-the-belt," primarily of the lip and oropharynx, have been found in most cases to be associated with HSV-1, whereas infections "below-the-belt" are usually caused by HSV-2.
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Singh, Shweta, Nikesh Sinha, and Manoj Kumar Shashank Nand Tiwari. "Disease Burden of Herpes Simplex Virus among Patients Attending Rajendra Institute of Medical Sciences, Ranchi, Jharkhand." International Journal of Current Microbiology and Applied Sciences 11, no. 1 (January 10, 2022): 219–23. http://dx.doi.org/10.20546/ijcmas.2022.1101.026.
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HSV-1 has been associated with oro-labial disease, with most infections occurring during childhood, and HSV-2 with genital disease. Additionally, HSV-2 likely contributes substantially to the spread of HIV infection. To estimate the disease burden of Herpes Simplex Virus among the patients attending Rajendra Institute of Medical Sciences. Samples of clinically suspected cases of herpes simplex virus received in the Department of Microbiology, RIMS, Ranchi, from January 2020 to December 2021 were included in the study. Results: During the study period, a total of 1737 samples from clinically suspected cases of herpes simplex virus were received for testing. Of these 1737 samples, 150 samples tested positive for herpes simplex virus. Of total suspected cases, 935 were males and 802 were females. The global burden of HSV-2 infection is large, causing increased risk of genital ulcer disease, HIV acquisition, and transmission of HSV-2 to partners or neonates. These estimates highlight the critical need for development of vaccines, and other new HSV prevention strategies.
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Kobty, Magidah. "Herpes Simplex Virus: Beyond the Basics." Neonatal Network 34, no. 5 (2015): 279–83. http://dx.doi.org/10.1891/0730-0832.34.5.279.
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AbstractOne of the most common sexually transmitted infections is the herpes simplex virus (HSV) Type 2. Although the incidence of newborn infection is not as common as in adults, approximately 1,500 neonates are diagnosed annually with HSV infection. HSV can be detrimental to the life of a newborn, with morbidity and mortality rates of up to 65 percent. This article addresses the maternal and fetal complications of HSV and the impact of HSV on the newborn along with diagnostic evaluation methods. In addition, treatment options and evidence-based practices regarding HSV are defined. Despite growing technology and medical treatment for early identification of HSV, this virus remains challenging and can deeply impact the life of an infant and his or her family. Early diagnosis, treatment, and intervention of an infant with HSV are crucial to ensure the livelihood of the newborn.
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Simmons, Bryan P., and Michael S. Gelfand. "Herpes Simplex Virus." Infection Control 7, no. 7 (July 1986): 380–83. http://dx.doi.org/10.1017/s0195941700064511.
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Herpes simplex virus (HSV) causes a variety of illnesses in th e community and hospital settings (Table). Nosocomial infections with this virus may result from: 1) reactivation of latent infection, especially in patients whose immune systems are compromised; 2) spread from mother to infant; 3) spread from patients to hospital personnel; 4) spread from hospital personnel to patients; and 5) cross-infection among patients. The latter two possibilities seem to occur infrequently but merit some discussion because of the serious implications of such infections.
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Jackson, Julia O., and Richard Longnecker. "Reevaluating Herpes Simplex Virus Hemifusion." Journal of Virology 84, no. 22 (September 15, 2010): 11814–21. http://dx.doi.org/10.1128/jvi.01615-10.
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ABSTRACT Membrane fusion induced by enveloped viruses proceeds through the actions of viral fusion proteins. Once activated, viral fusion proteins undergo large protein conformational changes to execute membrane fusion. Fusion is thought to proceed through a “hemifusion” intermediate in which the outer membrane leaflets of target and viral membranes mix (lipid mixing) prior to fusion pore formation, enlargement, and completion of fusion. Herpes simplex virus type 1 (HSV-1) requires four glycoproteins—glycoprotein D (gD), glycoprotein B (gB), and a heterodimer of glycoprotein H and L (gH/gL)—to accomplish fusion. gD is primarily thought of as a receptor-binding protein and gB as a fusion protein. The role of gH/gL in fusion has remained enigmatic. Despite experimental evidence that gH/gL may be a fusion protein capable of inducing hemifusion in the absence of gB, the recently solved crystal structure of HSV-2 gH/gL has no structural homology to any known viral fusion protein. We found that in our hands, all HSV entry proteins—gD, gB, and gH/gL—were required to observe lipid mixing in both cell-cell- and virus-cell-based hemifusion assays. To verify that our hemifusion assay was capable of detecting hemifusion, we used glycosylphosphatidylinositol (GPI)-linked hemagglutinin (HA), a variant of the influenza virus fusion protein, HA, known to stall the fusion process before productive fusion pores are formed. Additionally, we found that a mutant carrying an insertion within the short gH cytoplasmic tail, 824L gH, is incapable of executing hemifusion despite normal cell surface expression. Collectively, our findings suggest that HSV gH/gL may not function as a fusion protein and that all HSV entry glycoproteins are required for both hemifusion and fusion. The previously described gH 824L mutation blocks gH/gL function prior to HSV-induced lipid mixing.
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Weston, William L., Sylvia L. Brice, Joy D. Jester, Scott Stockert, J. Clark Huff, and Alfred T. Lane. "Herpes Simplex Virus in Childhood Erythema Multiforme." Pediatrics 89, no. 1 (January 1, 1992): 32–34. http://dx.doi.org/10.1542/peds.89.1.32.
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Although an association between herpes simplex virus (HSV) infection and erythema multiforme (EM) minor has been documented in adults, this has not been reported in the pediatric population. This study assessed the potential role of HSV infection in the pathogenesis of EM minor in children. Erythema multiforme skin lesions from 20 children, aged 1 to 16 years, were examined for the presence of HSV by using the polymerase chain reaction. The children included all fit strict clinical criteria for EM minor. Ten had a clinical history of an antecedent herpes infection ("herpes-associated EM"), and 10 did not ("idiopathic EM"). Herpes simplex virus DNA was detected in skin lesions of 8 of 10 children with herpes-associated EM and in 8 of 10 with idiopathic EM. Control skin biopsies from children with other bullous inflammatory diseases were negative. In addition, no HSV could be detected in a biopsy of normal uninvolved skin of a child in whom HSV was present in lesional skin. In situ hybridization on selected biopsies by means of an HSV-specific riboprobe confirmed the presence of HSV and localized it to the epidermis. It is concluded that HSV is a significant precipitating factor for EM minor in children, as it is in adults, and that clinicians should maintain a high index of suspicion of HSV even in the absence of a known history of herpes infection.
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Shintaku, Masayuki, Yasushi Umehara, Keiko Iwaisako, Masao Tahara, and Yasushi Adachi. "Herpes Simplex Pancreatitis." Archives of Pathology & Laboratory Medicine 127, no. 2 (February 1, 2003): 231–34. http://dx.doi.org/10.5858/2003-127-231-hs.
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Abstract Lesions of the pancreas induced by viral infection have drawn relatively little attention because of their low incidence, and the histopathologic features of viral pancreatitis have not been fully elucidated. We report the autopsy findings of 2 patients, a 59-year-old woman with allergic granulomatous angiitis and a 73-year-old man with invasive pulmonary aspergillosis who had a disseminated visceral herpes simplex virus (HSV) infection. In both cases, the liver was the organ most severely affected by the viral infection. The pancreas showed multiple small foci of hemorrhagic necrosis, which were not accompanied by fat necrosis of the surrounding adipose tissue. Histopathologically, Cowdry type A intranuclear inclusions and a ground-glass appearance of the nuclei were found in many degenerated acinar cells around the necrotic foci. The gross appearance and histopathologic features of HSV pancreatitis were characteristic and, in particular, distinct from those of the more common acute hemorrhagic pancreatitis. Immunohistochemistry using an anti-HSV antibody revealed immunoreactivity in the intranuclear inclusions and ground-glass nuclei, and polymerase chain reaction analysis disclosed that the causative virus in these 2 cases was HSV-1. Herpes simplex virus pancreatitis constitutes a rare, but distinct pathologic entity among a group of acute pancreatitis diseases with diverse etiopathogenesis.
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Silke Heilingloh, Christiane, Christopher Lull, Elissa Kleiser, Mira Alt, Leonie Schipper, Oliver Witzke, Mirko Trilling, Anna-Maria Eis-Hübinger, Ulf Dittmer, and Adalbert Krawczyk. "Herpes Simplex Virus Type 2 Is More Difficult to Neutralize by Antibodies Than Herpes Simplex Virus Type 1." Vaccines 8, no. 3 (August 27, 2020): 478. http://dx.doi.org/10.3390/vaccines8030478.
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Infections with herpes simplex virus type 1 (HSV-1) and type 2 (HSV-2) are a global health burden. Besides painful oral or genital lesions in otherwise healthy subjects, both viruses can cause devastating morbidity and mortality in immune-compromised and immune-immature individuals. The latter are particularly susceptible to a disseminated, life-threatening disease. Neutralizing antibodies (NAb) constitute a correlate of protection from disease, and are promising candidates for the prophylactic or therapeutic treatment of severe HSV infections. However, a clinical vaccine trial suggested that HSV-2 might be more resistant to NAbs than HSV-1. In the present study, we investigated the antiviral efficacy of the well-characterized humanized monoclonal antibody (mAb) hu2c against HSV-2, in a NOD/SCID immunodeficiency mouse model. Despite the fact that hu2c recognizes a fully conserved epitope and binds HSV-1 and HSV-2 glycoprotein B with equal affinity, it was much less effective against HSV-2 in vitro and in NOD/SCID mice. Although intravenous antibody treatment prolonged the survival of HSV-2-infected mice, complete protection from death was not achieved. Our data demonstrate that HSV-2 is more resistant to NAbs than HSV-1, even if the same antibody and antigen are concerned, making the development of a vaccine or therapeutic antibodies more challenging.
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Yudovin-Farber, Ira, Irina Gurt, Ronen Hope, Abraham J. Domb, and Ehud Katz. "Inhibition of Herpes Simplex Virus by Polyamines." Antiviral Chemistry and Chemotherapy 20, no. 2 (October 2009): 87–98. http://dx.doi.org/10.3851/imp1401.
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Background: Herpes simplex virus (HSV) establishes latent infection in humans with periodic reactivation. Acyclovir, valacyclovir and foscarnet are in medical use today against HSV type-1 (HSV-1) and type-2 (HSV-2), inhibiting the DNA synthesis of the viruses. Additional drugs that will affect the growth of these viruses by other mechanisms and also decrease the frequency of appearance of drug-resistant mutants are required. Methods: Cationic polysaccharides were synthesized by conjugation of various oligoamines to oxidized polysaccharides by reductive amination. Polycations of dextran, pullulan and arabinogalactan were grafted with oligoamines of 2–4 amino groups forming Schiff-base imine-based conjugates followed by reduction with borohydride to obtain the stable amine-based conjugate. Evaluation of toxicity to BS-C-1 cells and antiviral activity against HSV-1 and HSV-2 of the different compounds was performed in vitro by a semiquantitative assay. A quantitative study with a selected compound followed. Results: Structure–activity relationship studies showed that the nature of the grafted oligoamine of the polycation plays an essential role in the antiviral activity against HSV-1 and HSV-2. Dextran-propan-1,3-diamine (DPD) was found to be the most potent of all the compounds examined. DPD did not decrease the infectivity of HSV upon direct exposure to the virions. The growth of HSV was significantly inhibited when DPD was added to the host cells 1 h prior to infection, thus preventing the adsorption and penetration of the virus into the cells. Conclusions: Our in vitro data warrant clinical investigation. DPD could have an advantage as a topical application in combination therapy of HSV lesions.
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Bloom, David C., Joyce Feller, Peterjon McAnany, Nuria Vilaboa, and Richard Voellmy. "Replication-Competent Controlled Herpes Simplex Virus." Journal of Virology 89, no. 20 (August 12, 2015): 10668–79. http://dx.doi.org/10.1128/jvi.01667-15.
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ABSTRACTWe present the development and characterization of a replication-competent controlled herpes simplex virus 1 (HSV-1). Replication-essential ICP4 and ICP8 genes of HSV-1 wild-type strain 17syn+ were brought under the control of a dually responsive gene switch. The gene switch comprises (i) a transactivator that is activated by a narrow class of antiprogestins, including mifepristone and ulipristal, and whose expression is mediated by a promoter cassette that comprises an HSP70B promoter and a transactivator-responsive promoter and (ii) transactivator-responsive promoters that drive the ICP4 and ICP8 genes. Single-step growth experiments in different cell lines demonstrated that replication of the recombinant virus, HSV-GS3, is strictly dependent on an activating treatment consisting of administration of a supraphysiological heat dose in the presence of an antiprogestin. The replication-competent controlled virus replicates with an efficiency approaching that of the wild-type virus from which it was derived. Essentially no replication occurs in the absence of activating treatment or if HSV-GS3-infected cells are exposed only to heat or antiprogestin. These findings were corroborated by measurements of amounts of viral DNA and transcripts of the regulated ICP4 gene and the glycoprotein C (gC) late gene, which was not regulated. Similar findings were made in experiments with a mouse footpad infection model.IMPORTANCEThe alphaherpesviruses have long been considered vectors for recombinant vaccines and oncolytic therapies. The traditional approach uses vector backbones containing attenuating mutations that restrict replication to ensure safety. The shortcoming of this approach is that the attenuating mutations tend to limit both the immune presentation and oncolytic properties of these vectors. HSV-GS3 represents a novel type of vector that, when activated, replicates with the efficiency of a nonattenuated virus and whose safety is derived from deliberate, stringent regulation of multiple replication-essential genes. By directing activating heat to the region of virus administration, replication is strictly confined to infected cells within this region. The requirement for antiprogestin provides an additional level of safety, ensuring that virus replication cannot be triggered inadvertently. Replication-competent controlled vectors such as HSV-GS3 may have the potential to be superior to conventional attenuated HSV vaccine and oncolytic vectors without sacrificing safety.
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Arvin, Ann M., and Charles G. Prober. "Herpes Simplex Virus Infections: The Genital Tract and the Newborn." Pediatrics In Review 13, no. 3 (March 1, 1992): 107–11. http://dx.doi.org/10.1542/pir.13.3.107.
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There are six recognized members of the human herpes group of viruses. These include type 1 and type 2 herpes simplex viruses (HSV-1 and HSV-2), cytomegalovirus (CMV), Epstein-Barr virus (EBV), varicellazoster virus (VZV), and human herpes virus type 6 (HHV-6). These ubiquitous double-stranded DNA viruses are relatively large and lipid-enveloped. The capacity to induce a state of latency in the infected host has been proved for all of the herpes viruses. That is, after primary infection, the viruses remain forever with the host with the possibility for subsequent reactivations. The mechanisms of these reactivations are not understood completely. Both primary infections and recurrences may be associated with clinical illness or may be asymptomatic. To a large extent, the status of the host immune system determines the severity of the infection and the likelihood of recurrences. In general, infections are more severe and recurrences are more frequent in the most compromised hosts. This review focuses on HSV-1 and HSV-2, with emphasis on neonatal infections and maternal genital infections as a source of infection in the newborn. The clinical illnesses caused by HSV-1 and HSV-2 are usually quite distinct. HSV-1 is the predominant cause of oral, ocular, and central nervous system infections occurring after the neonatal period, and HSV-2 is the predominant cause of genital and neonatal infections.
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Ngo, T. D., O. Laeyendecker, C. Li, H. Tai, M. Cui, S. Lai, and T. C. Quinn. "Herpes simplex virus type 2 infection among commercial sex workers in Kunming, Yunnan Province, China." International Journal of STD & AIDS 19, no. 10 (October 2008): 694–97. http://dx.doi.org/10.1258/ijsa.2008.008072.
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A cross-sectional survey was conducted to determine the sociodemographic correlates of herpes simplex virus type 2 (HSV-2) infection among male and female commercial sex workers in Kunming, Yunnan Province of China. HSV-2 prevalence was 33.0%, human immunodeficiency virus (HIV) infection was 2.4% and hepatitis C virus (HCV) infection was 6.8%. Subjects who were positive for HSV-2 had a significantly higher prevalence of HIV infection (5.5% versus 0.9%, P = 0.002; odds ratio [OR]: 6.4, P = 0.006) and HCV infection (18.7% versus 2.4%, P < 0.001; OR: 7.6, P < 0.001) compared with HSV-2-negative individuals. Risk factors that increased the odds of HSV-2 infection were HIV infection, HCV infection, being female, and having a steady sex partner within the last six months ( P ≤ 0.01). In a multivariate analysis, being female (OR: 6.6, P < 0.001), having HCV infection (OR: 5.9, P < 0.001) and having a sex partner within the last six months (OR: 2.2, P < 0.05) showed greater odds of being infected with HSV-2. A strong relationship was found between HSV-2, HIV and HCV infections.
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Csernus, Adriána Evelin, Annamária Rózsa, and Rolland Gyulai. "Age-specific incidence of herpes simplex infection in the light of clinical appearance." Bőrgyógyászati és Venerológiai Szemle 97, no. 2 (May 6, 2021): 83–92. http://dx.doi.org/10.7188/bvsz.2021.97.2.3.
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Herpes simplex virus (HSV) infection is extremely common in both children and adults. HSV has two serotypes, HSV-1 primarily causes orolabial while HSV-2 anogenital symptoms. In recent decades there has been a change in the predilection to affected anatomical regions in both serotypes, participation of HSV-1 serotype in genital infections is increasing. The primary acquisition of HSV-1 has increasingly shifted from early childhood to young adulthood over the past years. Asymptomatic infection and virulence factors are crucial in the spread of the virus. Cutaneous symptoms, erosions and crusted lesions after vesicular stage present various differential diagnostic problems in the involved regions. Early diagnosis and timely adequate therapy in serious cases are essential as well as suppressive treatment of recurrent symptoms. Several clinical trials are underway to develop more effective antivirals. Vaccination against HSV would be a key to prevent latent infections, transmission and reactivation. The authors present characteristics of HSV, age-specific clinical manifestations, differential diagnostic problems and adequate treatment strategies.
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Koelle, David M., and Lawrence Corey. "Recent Progress in Herpes Simplex Virus Immunobiology and Vaccine Research." Clinical Microbiology Reviews 16, no. 1 (January 2003): 96–113. http://dx.doi.org/10.1128/cmr.16.1.96-113.2003.
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SUMMARY Herpes simplex virus types 1 and 2 (HSV-1 and HSV-2) cause prevalent, chronic infections that have serious outcomes in some individuals. Neonatal herpes may occur when the infant traverses the cervix during maternal genital herpes. Genital herpes is a major risk factor for human immunodeficiency virus type 1 transmission. Considerable efforts have been made to design and test vaccines for HSV, focusing on genital infection with HSV-2. Several protein subunit vaccines based on HSV-2 envelope glycoproteins have reached advanced-phase clinical trials. These antigens were chosen because they are the targets of neutralizing-antibody responses and because they elicit cellular immunity. Encouraging results have been reported in studies of treatment of HSV-seronegative women with a vaccine consisting of truncated glycoprotein D of HSV-2 and a novel adjuvant. Because most sexual HSV transmission occurs during asymptomatic shedding, it is important to evaluate the impact of vaccination on HSV-2 infection, clinically apparent genital herpes, and HSV shedding among vaccine recipients who acquire infection. There are several other attractive formats, including subunit vaccines that target cellular immune responses, live attenuated virus strains, and mutant strains that undergo incomplete lytic replication. HSV vaccines have also been evaluated for the immunotherapy of established HSV infection.
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Duffus, W. A., J. Mermin, R. Bunnell, R. H. Byers, G. Odongo, P. Ekwaru, and R. Downing. "Chronic herpes simplex virus type-2 infection and HIV viral load." International Journal of STD & AIDS 16, no. 11 (November 1, 2005): 733–35. http://dx.doi.org/10.1258/095646205774763298.
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By December 2003, the estimated adult HIV/AIDS prevalence rate in sub-Saharan Africa was 7.5–8.5%, and rates of herpes simplex virus type-2 (HSV-2) infection among adults aged >30 years ranged from 60% to 82%. However, little is known about the natural history of HIV/HSV-2 co-infection in this population. We evaluated HIV viral load and CD4+ cell counts among persons with and without chronic HSV-2 co-infection in a cross-sectional study of HIV-infected persons not receiving antiretroviral therapy. HSV-2 and HIV co-infection was associated with a 0.3 log copies/mL higher HIV viral load compared with persons without HSV-2 infection ( P=0.014). Chronic HSV-2 infection may have a negative effect on the clinical course of persons with HIV.
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Ayoade, Folusakin, Jose Armando Gonzales Zamora, and Youley Tjendra. "Herpes Simplex Virus Proctitis Masquerading as Rectal Cancer." Diseases 7, no. 2 (April 21, 2019): 36. http://dx.doi.org/10.3390/diseases7020036.
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Herpes simplex virus (HSV) is the leading cause of proctitis in HIV-infected individuals. However, no cases of rectal masses secondary to HSV infection have been reported to date. Herein, we present the case of a 45-year-old man with HIV infection who developed rectal pain and bleeding, along with dysuria and voiding difficulty. Colonoscopy revealed proctitis and a rectal mass with features concerning for rectal cancer. Histologic sections of the rectal mass biopsy demonstrated colorectal mucosa with viral cytopathic changes, ulceration, granulation tissue, marked inflammatory infiltrate, and fibrinopurulent exudate. Immunohistochemistry for herpes simplex virus-1 was positive in epithelial cells demonstrating a viral cytopathic effect. The patient was treated with valacyclovir for 3 weeks, which led to complete resolution of his symptoms. Follow-up sigmoidoscopy at 6 months did not show any masses. Our case illustrates the importance of considering HSV in the differential diagnosis of rectal masses. We advocate the routine use of viral immunohistochemistry for the evaluation of rectal tumors, especially in patients with clinical manifestations and endoscopic findings consistent with proctitis.
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Monjo, Andrea, Eric Pringle, Mackenzie Thornbury, Brett Duguay, Susan Monro, Marc Hetu, Danika Knight, Colin Cameron, Sherri McFarland, and Craig McCormick. "Photodynamic Inactivation of Herpes Simplex Viruses." Viruses 10, no. 10 (September 29, 2018): 532. http://dx.doi.org/10.3390/v10100532.
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Herpes simplex virus (HSV) infections can be treated with direct acting antivirals like acyclovir and foscarnet, but long-term use can lead to drug resistance, which motivates research into broadly-acting antivirals that can provide a greater genetic barrier to resistance. Photodynamic inactivation (PDI) employs a photosensitizer, light, and oxygen to create a local burst of reactive oxygen species that inactivate microorganisms. The botanical plant extract OrthoquinTM is a powerful photosensitizer with antimicrobial properties. Here we report that Orthoquin also has antiviral properties. Photoactivated Orthoquin inhibited herpes simplex virus type 1 (HSV-1) and herpes simplex virus type 2 (HSV-2) infection of target cells in a dose-dependent manner across a broad range of sub-cytotoxic concentrations. HSV inactivation required direct contact between Orthoquin and the inoculum, whereas pre-treatment of target cells had no effect. Orthoquin did not cause appreciable damage to viral capsids or premature release of viral genomes, as measured by qPCR for the HSV-1 genome. By contrast, immunoblotting for HSV-1 antigens in purified virion preparations suggested that higher doses of Orthoquin had a physical impact on certain HSV-1 proteins that altered protein mobility or antigen detection. Orthoquin PDI also inhibited the non-enveloped adenovirus (AdV) in a dose-dependent manner, whereas Orthoquin-mediated inhibition of the enveloped vesicular stomatitis virus (VSV) was light-independent. Together, these findings suggest that the broad antiviral effects of Orthoquin-mediated PDI may stem from damage to viral attachment proteins.
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Annunziato, Paula W. "Herpes Simplex Virus Infections." Pediatrics In Review 17, no. 12 (December 1, 1996): 415–23. http://dx.doi.org/10.1542/pir.17.12.415.
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Case Report A term female developed fever and tachypnea and had a transient episode of poor color and tone on the third day of life. She was delivered by cesarean section 5 hours after rupture of membranes to a 19-year-old, gravida 4, para 0 mother whose serology was negative for syphilis, human immunodeficiency virus (HIV), and hepatitis B surface antigen. The mother had no history of sexually transmitted diseases. Apgar scores were 8 at 1 minute and 9 at 10 minutes. When the infant was admitted to the nursery, scalp abrasions were noticed by the nurse. On the third day of life, a sepsis evaluation was initiated, and the infant received ampicillin and gentamicin intravenously: no bacterial infection was found. On the fifth day of life, vesicular lesions were noticed on her scalp. Bilateral interstitial infiltrates were present On chest radiograph and laboratory studies revealed mild elevations in liver function tests. There were no cerebrospinal fluid (CSF) abnormalities. She was started on intravenous acyclovir, and herpes simplex virus (HSV)-2 subsequently was isolated from both her pharynx and scalp lesions. After receiving intravenous acyclovir for 3 weeks, she was discharged with no evidence of residual sequelae. Four days after acyclovir was discontinued, new scalp vesicles appeared and the infant developed a temperature of 38.8°C (102°F).
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Ensor, Deirdre. "The Significance of Herpes Simplex for School Nurses." Journal of School Nursing 21, no. 1 (February 2005): 10–16. http://dx.doi.org/10.1177/10598405050210010401.
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Herpes simplex is a common recurrent viral infection caused by the herpes simplex virus. The two closely related but distinct viruses that cause herpes simplex infections are herpes simplex 1 (HSV-1) and herpes simplex 2 (HSV-2). HSV-1 is commonly associated with infections around the oral mucosa and is the cause of herpes labialis, often referred to as a fever blister or cold sore. HSV-2 infections are usually acquired sexually. Genital herpes is a sexually transmitted disease with the highest prevalence among adolescents and young adults. Knowledge of viral activity, disease management, and community resources will assist the school nurse in developing and implementing strategies to prevent and manage this chronic disease.
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Kim, Hyeon Cheol, and Heung Kyu Lee. "Vaccines against Genital Herpes: Where Are We?" Vaccines 8, no. 3 (July 27, 2020): 420. http://dx.doi.org/10.3390/vaccines8030420.
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Genital herpes is a venereal disease caused by herpes simplex virus (HSV). Although HSV symptoms can be reduced with antiviral drugs, there is no cure. Moreover, because HSV infected individuals are often unaware of their infection, it is highly likely that they will transmit HSV to their sexual partner. Once infected, an individual has to live with HSV for their entire life, and HSV infection can lead to meningitis, encephalitis, and neonatal herpes as a result of vertical transmission. In addition, HSV infection increases the rates of human immunodeficiency virus (HIV) infection and transmission. Because of the high burden of genital herpes, HSV vaccines have been developed, but none have been very successful. In this review, we discuss the current status of genital herpes vaccine development.
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Le Goaster, Jacqueline, Patrice Bouree, Franck N. El Sissy, Florence Phuong Bui, Johanna Pokossy Epee, Paul Rollin, Frédéric Tangy, and Anne-Lise Haenni. "HSV-1/HSV-2 Infection-Related Cancers in Bantu Populations Driving HIV-1 Prevalence in Africa: Tracking the Origin of AIDS at the Onset of the 20th Century." Case Reports in Oncology 9, no. 3 (November 29, 2016): 815–25. http://dx.doi.org/10.1159/000450939.
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Introduction: At the onset of the 20th century, ancient clinical observations of cancer epidemics in Bantu populations of Sub-Saharan Africa were discovered. They were reported from 1914 to 1960, but remained unexplained. In 1983, in San Francisco, Calif., USA, cancer epidemics were related to infections by the human immunodeficiency virus type 1 (HIV-1) known as AIDS disease. Yet since 1996, it is known that HIV-1 strains are not the only ones involved. In Sub-Saharan Africa, recurrent orobuccal herpes simplex virus type 1 (HSV-1) and genital recurrent herpes simplex virus type 2 (HSV-2) appeared many times prior to infection by HIV-1. Case Reports: Data on these ancient medical observations regarding African cancer epidemics can today be referred to as the relationship between the unfortunate immune deficiency of herpes in Bantu populations and HIV-1 viral strains. For centuries, the Bantu populations dispersed in forests were living in close proximity to chimpanzees infected by simian immunodeficiency virus (SIV) and were exposed to SIV contamination which became HIV-1 in human beings. Presently, these unexplained Bantu cancer epidemics can be linked to the viral partnership of HSV-1/HSV-2 to HIV-1 strains. Conclusion: The key issue is now to prevent HSV-1/HSV-2 diseases related to HIV-1. An anti-herpes treatment administered early during childhood to Bantu populations will offer a mean of preventing herpes diseases related to HIV-1 infection and hence avoid cancer epidemics.
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Välimaa, H., M. Waris, V. Hukkanen, M. F. J. Blankenvoorde, A. V. Nieuw Amerongen, and J. Tenovuo. "Salivary Defense Factors in Herpes Simplex Virus Infection." Journal of Dental Research 81, no. 6 (June 2002): 416–21. http://dx.doi.org/10.1177/154405910208100612.
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Saliva may contribute to a lowering of the infectious herpes simplex virus (HSV) dose during transmission and consequently abrogate infection or lead to decreased reactivation. To test this hypothesis, we assayed saliva for innate defense factors, immunoglobulin content, and the capacity to interfere with HSV infection. Serum or salivary anti-HSV IgG levels did not correlate with control of recurrent labial herpes (RLH) and were significantly higher in subjects with RLH compared with asymptomatic seropositive subjects. Although no differences in levels or output rate of innate defense factors between the groups were observed, the salivary neutralizing activity correlated with lactoferrin and hypothiocyanite concentrations in the asymptomatic seropositive group. Our results suggest that saliva contains factors, in addition to anti-HSV immunoglobulins, that neutralize HSV and may indirectly contribute to the control of RLH.
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Ikeda, Marina, Akihiro Ito, Yuichi Sekine, and Masahiro Fujimuro. "UBE1a Suppresses Herpes Simplex Virus-1 Replication." Viruses 12, no. 12 (December 4, 2020): 1391. http://dx.doi.org/10.3390/v12121391.
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Herpes simplex virus-1 (HSV-1) is the causative agent of cold sores, keratitis, meningitis, and encephalitis. HSV-1-encoded ICP5, the major capsid protein, is essential for capsid assembly during viral replication. Ubiquitination is a post-translational modification that plays a critical role in the regulation of cellular events such as proteasomal degradation, protein trafficking, and the antiviral response and viral events such as the establishment of infection and viral replication. Ub-activating enzyme (E1, also named UBE1) is involved in the first step in the ubiquitination. However, it is still unknown whether UBE1 contributes to viral infection or the cellular antiviral response. Here, we found that UBE1a suppressed HSV-1 replication and contributed to the antiviral response. The UBE1a inhibitor PYR-41 increased HSV-1 production. Immunofluorescence analysis revealed that UBE1a highly expressing cells presented low ICP5 expression, and vice versa. UBE1a inhibition by PYR-41 and shRNA increased ICP5 expression in HSV-1-infected cells. UBE1a reduced and retarded ICP5 protein expression, without affecting transcription of ICP5 mRNA or degradation of ICP5 protein. Additionally, UBE1a interacted with ICP27, and both partially co-localized at the Hsc70 foci/virus-induced chaperone-enriched (VICE) domains. PYR-41 reduced the co-localization of UBE1a and ICP27. Thus, our findings provide insights into the mechanism of UBE1a in the cellular response to viral infection.
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Chang, Weizhong, Xiaoli Jiao, Hongyan Sui, Suranjana Goswami, Brad T. Sherman, Caroline Fromont, Juan Manuel Caravaca, Bao Tran, and Tomozumi Imamichi. "Complete Genome Sequence of Herpes Simplex Virus 2 Strain G." Viruses 14, no. 3 (March 5, 2022): 536. http://dx.doi.org/10.3390/v14030536.
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Herpes simplex virus type 2 (HSV-2) is a common causative agent of genital tract infections. Moreover, HSV-2 and HIV infection can mutually increase the risk of acquiring another virus infection. Due to the high GC content and highly repetitive regions in HSV-2 genomes, only the genomes of four strains have been completely sequenced (HG52, 333, SD90e, and MS). Strain G is commonly used for HSV-2 research, but only a partial genome sequence has been assembled with Illumina sequencing reads. In the current study, we de novo assembled and annotated the complete genome of strain G using PacBio long sequencing reads, which can span the repetitive regions, analyzed the ‘α’ sequence, which plays key roles in HSV-2 genome circulation, replication, cleavage, and packaging of progeny viral DNA, identified the packaging signals homologous to HSV-1 within the ‘α’ sequence, and determined both termini of the linear genome and cleavage site for the process of concatemeric HSV-2 DNA produced via rolling-circle replication. In addition, using Oxford Nanopore Technology sequencing reads, we visualized four HSV-2 genome isomers at the nucleotide level for the first time. Furthermore, the coding sequences of HSV-2 strain G have been compared with those of HG52, 333, and MS. Moreover, phylogenetic analysis of strain G and other diverse HSV-2 strains has been conducted to determine their evolutionary relationship. The results will aid clinical research and treatment development of HSV-2.
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Carey, Barbara. "Neonatal Herpes Simplex: Pulmonary and Intracranial Findings." Neonatal Network 21, no. 6 (January 2002): 63–67. http://dx.doi.org/10.1891/0730-0832.21.6.63.
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AS THE RATE OF HERPES infection has risen in the general population and specifically in women of childbearing age, the rate of fetal and newborn acquisition has also increased. Neonatal herpes virus infection has been estimated to range from 1 in 3,000 to 1 in 20,000 live births.1 Approximately two-thirds of these cases are caused by herpes simplex virus (HSV) Type II, and the remaining third is caused by HSV Type I.2
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Isaacs, Charles E., Jun Hua Jia, and Weimin Xu. "A Lipid-Peptide Microbicide Inactivates Herpes Simplex Virus." Antimicrobial Agents and Chemotherapy 48, no. 8 (August 2004): 3182–84. http://dx.doi.org/10.1128/aac.48.8.3182-3184.2004.
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ABSTRACT A microbicide combining the lipid-ether 1-0-octyl-sn-glycerol (OG; 3 mM) and peptide D2A21 (9 μM) reduced herpes simplex virus type 1 (HSV-1) and HSV-2 titers by at least 1,000-fold, more than the sum of the inactivations produced by OG and D2A21 alone. OG plus D2A21 reduced HSV-1 and HSV-2 titers by ≥1,000-fold in ≤10 and ≤20 min, respectively, whereas OG and D2A21 used alone produced almost no virus inactivation during these times.
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Rimawi, Bassam H., Joseph Meserve, Ramzy H. Rimawi, Zaw Min, and John W. Gnann. "Disseminated Herpes Simplex Virus with Fulminant Hepatitis." Case Reports in Hepatology 2015 (2015): 1–4. http://dx.doi.org/10.1155/2015/463825.
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Disseminated herpes simplex virus (HSV) is a rare cause of acute fulminant liver failure. We hereby present a case series of three patients with acute disseminated HSV with necrotizing hepatitis successfully treated with a week course of acyclovir. Early empiric administration of acyclovir therapy while awaiting confirmatory tests is critical in this potentially lethal disease.
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Singh, Ameeta, Jutta Preiksaitis, and Barbara Romanowski. "The Laboratory Diagnosis of Herpes Simplex Virus Infections." Canadian Journal of Infectious Diseases and Medical Microbiology 16, no. 2 (2005): 92–98. http://dx.doi.org/10.1155/2005/318294.
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Herpes simplex virus (HSV) types 1 and 2 cause genital herpes infections and are the most common cause of genital ulcer disease in industrialized nations. Although these infections are very common, the majority of them remain underdiagnosed because they are asymptomatic or unrecognized. A clinical diagnosis of genital herpes should always be confirmed by laboratory testing; this can be accomplished through the use of direct tests for viral isolation, the detection of antigen or, more recently, the detection of HSV DNA using molecular diagnostic techniques. Testing for serotypes is recommended because of the different prognostic and counselling implications. Type-specific HSV serology is becoming more readily available and will enhance the ability to make the diagnosis and guide clinical management in select patients.
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Gantt, Soren, Eliora Gachelet, Jacquelyn Carlsson, Serge Barcy, Corey Casper, and Michael Lagunoff. "Nelfinavir Impairs Glycosylation of Herpes Simplex Virus 1 Envelope Proteins and Blocks Virus Maturation." Advances in Virology 2015 (2015): 1–9. http://dx.doi.org/10.1155/2015/687162.
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Nelfinavir (NFV) is an HIV-1 aspartyl protease inhibitor that has numerous effects on human cells, which impart attractive antitumor properties. NFV has also been shown to havein vitroinhibitory activity against human herpesviruses (HHVs). Given the apparent absence of an aspartyl protease encoded by HHVs, we investigated the mechanism of action of NFV herpes simplex virus type 1 (HSV-1) in cultured cells. Selection of HSV-1 resistance to NFV was not achieved despite multiple passages under drug pressure. NFV did not significantly affect the level of expression of late HSV-1 gene products. Normal numbers of viral particles appeared to be produced in NFV-treated cells by electron microscopy but remain within the cytoplasm more often than controls. NFV did not inhibit the activity of the HSV-1 serine protease nor could its antiviral activity be attributed to inhibition of Akt phosphorylation. NFV was found to decrease glycosylation of viral glycoproteins B and C and resulted in aberrant subcellular localization, consistent with induction of endoplasmic reticulum stress and the unfolded protein response by NFV. These results demonstrate that NFV causes alterations in HSV-1 glycoprotein maturation and egress and likely acts on one or more host cell functions that are important for HHV replication.
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Tenser, Richard B., Andrew Gaydos, and Kathleen A. Hay. "Inhibition of Herpes Simplex Virus Reactivation by Dipyridamole." Antimicrobial Agents and Chemotherapy 45, no. 12 (December 1, 2001): 3657–59. http://dx.doi.org/10.1128/aac.45.12.3657-3659.2001.
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ABSTRACT Herpes simplex virus (HSV) reactivation from latency was investigated. Reactivation of thymidine kinase-negative HSV, which is defective for reactivation, was greatly enhanced by thymidine (TdR). The reactivation-enhancing effect of TdR was blocked by dipyridamole (DPM), a known nucleoside transport inhibitor. DPM also inhibited wild-type HSV reactivation, suggesting potential antiviral use.
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Isaacs, Charles E., Guang Y. Wen, Weimin Xu, Jun Hua Jia, Lisa Rohan, Christopher Corbo, Vincenzo Di Maggio, Edmund C. Jenkins, and Sharon Hillier. "Epigallocatechin Gallate Inactivates Clinical Isolates of Herpes Simplex Virus." Antimicrobial Agents and Chemotherapy 52, no. 3 (January 14, 2008): 962–70. http://dx.doi.org/10.1128/aac.00825-07.
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ABSTRACT In the absence of a fully effective herpes simplex virus (HSV) vaccine, topical microbicides represent an important strategy for preventing HSV transmission. (−)-Epigallocatechin gallate (EGCG) (molecular weight, 458.4) is the primary catechin in green tea. The present study shows that EGCG has greater anti-HSV activity than other green tea catechins and inactivates multiple clinical isolates of HSV type 1 (HSV-1) and HSV-2. EGCG reduced HSV-2 titers by ≥1,000-fold in 10 to 20 min and reduced HSV-1 titers by the same amount in 30 to 40 min. The anti-HSV activity of EGCG is due to a direct effect on the virion, and incubating Vero and CV1 cells with EGCG for 48 h prior to infection with HSV-1 and HSV-2, respectively, does not reduce HSV production. Electron microscopic (EM) studies showed that purified virions exposed to EGCG were damaged, and EM immunogold labeling of the envelope glycoproteins gB and gD was significantly reduced following EGCG treatment while capsid protein labeling was unchanged. When purified HSV-1 envelope glycoproteins gB and gD were incubated with EGCG and then examined by sodium dodecyl sulfate-polyacrylamide gel electrophoresis, lower-molecular-weight gB and gD bands decreased and new higher-molecular-weight bands appeared, indicating the EGCG-dependent production of macromolecular complexes. gB and gD are essential for HSV infectivity, and these results suggest that EGCG could inactivate HSV virions by binding to gB, gD, or another envelope glycoprotein. EGCG is stable in the pH range found in the vagina and appears to be a promising candidate for use in a microbicide to reduce HSV transmission.
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Danovich, R. M., and N. Frenkel. "Herpes simplex virus induces the replication of foreign DNA." Molecular and Cellular Biology 8, no. 8 (August 1988): 3272–81. http://dx.doi.org/10.1128/mcb.8.8.3272.
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Plasmids containing the simian virus 40 (SV40) DNA replication origin and the large T gene are replicated efficiently in Vero monkey cells but not in rabbit skin cells. Efficient replication of the plasmids was observed in rabbit skin cells infected with herpes simplex virus type 1 (HSV-1) and HSV-2. The HSV-induced replication required the large T antigen and the SV40 replication origin. However, it produced concatemeric molecules resembling replicative intermediates of HSV DNA and was sensitive to phosphonoacetate at concentrations known to inhibit the HSV DNA polymerase. Therefore, it involved the HSV DNA polymerase itself or a viral gene product(s) which was expressed following the replication of HSV DNA. Analyses of test plasmids lacking SV40 or HSV DNA sequences showed that, under some conditions, HSV also induced low-level replication of test plasmids containing no known eucaryotic replication origins. Together, these results show that HSV induces a DNA replicative activity which amplifies foreign DNA. The relevance of these findings to the putative transforming potential of HSV is discussed.
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Danovich, R. M., and N. Frenkel. "Herpes simplex virus induces the replication of foreign DNA." Molecular and Cellular Biology 8, no. 8 (August 1988): 3272–81. http://dx.doi.org/10.1128/mcb.8.8.3272-3281.1988.
Full textAbstract:
Plasmids containing the simian virus 40 (SV40) DNA replication origin and the large T gene are replicated efficiently in Vero monkey cells but not in rabbit skin cells. Efficient replication of the plasmids was observed in rabbit skin cells infected with herpes simplex virus type 1 (HSV-1) and HSV-2. The HSV-induced replication required the large T antigen and the SV40 replication origin. However, it produced concatemeric molecules resembling replicative intermediates of HSV DNA and was sensitive to phosphonoacetate at concentrations known to inhibit the HSV DNA polymerase. Therefore, it involved the HSV DNA polymerase itself or a viral gene product(s) which was expressed following the replication of HSV DNA. Analyses of test plasmids lacking SV40 or HSV DNA sequences showed that, under some conditions, HSV also induced low-level replication of test plasmids containing no known eucaryotic replication origins. Together, these results show that HSV induces a DNA replicative activity which amplifies foreign DNA. The relevance of these findings to the putative transforming potential of HSV is discussed.
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Jones, C. "Cervical cancer: is herpes simplex virus type II a cofactor?" Clinical Microbiology Reviews 8, no. 4 (October 1995): 549–56. http://dx.doi.org/10.1128/cmr.8.4.549.
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In many ways, cervical cancer behaves as a sexually transmitted disease. The major risk factors are multiple sexual partners and early onset of sexual activity. Although high-risk types of human papillomaviruses (HPV) play an important role in the development of nearly all cases of cervical cancer, other sexually transmitted infectious agents may be cofactors. Herpes simplex virus type 2 (HSV-2) is transmitted primarily by sexual contact and therefore has been implicated as a risk factor. Several independent studies suggest that HSV-2 infections correlate with a higher than normal incidence of cervical cancer. In contrast, other epidemiological studies have concluded that infection with HSV-2 is not a major risk factor. Two separate transforming domains have been identified within the HSV-2 genome, but continued viral gene expression apparently is not necessary for neoplastic transformation. HSV infections lead to unscheduled cellular DNA synthesis, chromosomal amplifications, and mutations. These observations suggest that HSV-2 is not a typical DNA tumor virus. It is hypothesized that persistent or abortive infections induce permanent genetic alterations that interfere with differentiation of cervical epithelium and subsequently induce abnormal proliferation. Thus, HSV-2 may be a cofactor in some but not all cases of cervical cancer.
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Odani, Kentaro, Mitsuhiro Tachibana, Rintaro Tamashima, and Yutaka Tsutsumi. "Herpes Simplex Virus Pneumonia: Importance of Aspiration Etiology." Case Reports in Pathology 2019 (December 10, 2019): 1–3. http://dx.doi.org/10.1155/2019/7623576.
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Herpes simplex virus (HSV) pneumonia caused by aspiration from the oropharyngeal exudates is described. An 89-year-old Japanese male in a poor performance state complained of appetite loss followed by difficulty in swallowing, and bilateral pulmonary infiltrates with interstitial reactions were radiologically pointed out. Antibiotics administration was ineffective, and he died on the 6th day of hospitalization. At autopsy, HSV-induced multiple mucosal erosions were observed on the tongue, pharynx, epiglottis, and trachea. In bilateral lower lobes of the lung, HSV infected bronchiolar and type-II alveolar cells in association with acute interstitial reactions. The infected cells with intranuclear inclusion bodies were immunoreactive with HSV antiserum. HSV-1 infection was confirmed by immunostaining with monospecific monoclonal antibodies and by type-specific real-time polymerase chain reaction. It is very likely that HSV pneumonia was provoked by aspiration of infected exudates from the upper airway (namely, sequential infection from the tongue, epiglottis, and trachea to lung). Oropharyngeal herpes might cause anorexia and difficulty in swallowing, probably accelerating aspiration. The medical staff did not recognize the oropharyngeal lesions of this aged patient. We must realize again the importance of oral care for hospitalized patients to avoid aspiration pneumonia, including herpetic pneumonia.
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Mues, Mascha B., Natalia Cheshenko, Duncan W. Wilson, Leslie Gunther-Cummins, and Betsy C. Herold. "Dynasore Disrupts Trafficking of Herpes Simplex Virus Proteins." Journal of Virology 89, no. 13 (April 15, 2015): 6673–84. http://dx.doi.org/10.1128/jvi.00636-15.
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ABSTRACTDynasore, a small-molecule inhibitor of the GTPase activity of dynamin, inhibits the entry of several viruses, including herpes simplex virus (HSV), but its impact on other steps in the viral life cycle has not been delineated. The current study was designed to test the hypothesis that dynamin is required for viral protein trafficking and thus has pleiotropic inhibitory effects on HSV infection. Dynasore inhibited HSV-1 and HSV-2 infection of human epithelial and neuronal cells, including primary genital tract cells and human fetal neurons and astrocytes. Similar results were obtained when cells were transfected with a plasmid expressing dominant negative dynamin. Kinetic studies demonstrated that dynasore reduced the number of viral capsids reaching the nuclear pore if added at the time of viral entry and that, when added as late as 8 h postentry, dynasore blocked the transport of newly synthesized viral proteins from the nucleus to the cytosol. Proximity ligation assays demonstrated that treatment with dynasore prevented the colocalization of VP5 and dynamin. This resulted in a reduction in the number of viral capsids isolated from sucrose gradients. Fewer capsids were observed by electron microscopy in dynasore-treated cells than in control-treated cells. There were also reductions in infectious progeny released into culture supernatants and in cell-to-cell spread. Together, these findings suggest that targeting dynamin-HSV interactions may provide a new strategy for HSV treatment and prevention.IMPORTANCEHSV infections remain a global health problem associated with significant morbidity, particularly in neonates and immunocompromised hosts, highlighting the need for novel approaches to treatment and prevention. The current studies indicate that dynamin plays a role in multiple steps in the viral life cycle and provides a new target for antiviral therapy. Dynasore, a small-molecule inhibitor of dynamin, has pleiotropic effects on HSV-1 and HSV-2 infection and impedes viral entry, trafficking of viral proteins, and capsid formation.
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Cannon, Luke, Eleni Tholouli, Chris Ward, Hamzah Farooq, and Margaret Kingston. "Use of pritelivir in refractory aciclovir-resistant herpes simplex virus type 2." International Journal of STD & AIDS 32, no. 10 (May 4, 2021): 978–80. http://dx.doi.org/10.1177/09564624211006568.
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Recurrence of mucocutaneous herpes simplex virus (HSV) infections is common in immunosuppressed patients. Thymidine kinase mutations conferring resistance to the antiviral agent aciclovir have been observed in such patients. Recommended second-line therapeutic agents against HSV are associated with significant side effects contributing to disease burden. We present a case of aciclovir-resistant herpes simplex virus 2 (HSV-2) in an immunosuppressed (HIV negative) allogenic peripheral blood stem cell transplant (SCT) recipient which was refractory to second-line therapy. Compassionate acquisition of the novel oral helicase-primase inhibitor pritelivir provided both symptomatic and virological control for the duration of its use. We believe this to be the first clinical use of this therapeutic agent in the United Kingdom
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Cokarić Brdovčak, Maja, Andreja Zubković, and Igor Jurak. "Herpes Simplex Virus 1 Deregulation of Host MicroRNAs." Non-Coding RNA 4, no. 4 (November 23, 2018): 36. http://dx.doi.org/10.3390/ncrna4040036.
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Viruses utilize microRNAs (miRNAs) in a vast variety of possible interactions and mechanisms, apparently far beyond the classical understanding of gene repression in humans. Likewise, herpes simplex virus 1 (HSV-1) expresses numerous miRNAs and deregulates the expression of host miRNAs. Several HSV-1 miRNAs are abundantly expressed in latency, some of which are encoded antisense to transcripts of important productive infection genes, indicating their roles in repressing the productive cycle and/or in maintenance/reactivation from latency. In addition, HSV-1 also exploits host miRNAs to advance its replication or repress its genes to facilitate latency. Here, we discuss what is known about the functional interplay between HSV-1 and the host miRNA machinery, potential targets, and the molecular mechanisms leading to an efficient virus replication and spread.
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Kimberlin, David W. "Neonatal Herpes Simplex Infection." Clinical Microbiology Reviews 17, no. 1 (January 2004): 1–13. http://dx.doi.org/10.1128/cmr.17.1.1-13.2004.
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SUMMARY Tremendous advances have occurred over the past 30 years in the diagnosis and management of neonatal herpes simplex virus (HSV) disease. Mortality in patients with disseminated disease has decreased from 85 to 29%, and that in patients with central nervous system (CNS) disease has decreased from 50 to 4%. Morbidity has been improved more modestly: the proportion of patients with disseminated disease who are developing normally at 1 year has increased from 50 to 83%. While the proportion of patients with neurologic morbidity following CNS disease has remained essentially unchanged over the past three decades, the total number of patients who are developing normally following HSV CNS disease has increased due to the improved survival. Although additional therapeutic advances in the future are possible, more immediate methods for further improvements in outcome for patients with this potentially devastating disease lie in an enhanced awareness of neonatal HSV infection and disease. A thorough understanding of the biology and natural history of HSV in the gravid woman and the neonate provides the basis for such an index of suspicion and is provided in this article.
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Nakama, Shinji, Kazumi Tamaki, Chie Ishikawa, Masayuki Tadano, and Naoki Mori. "Efficacy ofBidens pilosaExtract against Herpes Simplex Virus InfectionIn VitroandIn Vivo." Evidence-Based Complementary and Alternative Medicine 2012 (2012): 1–10. http://dx.doi.org/10.1155/2012/413453.
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The development of strains of herpes simplex virus (HSV) resistant to drugs has been reported among the immunocompromised patients. Thus, there is a need to develop new therapeutic agents for HSV infections. We evaluated the anti-HSV activity ofBidens pilosa(B. pilosa), a tropical weed, in tissue culture cells and a mouse model.B. pilosaextract showed potent virucidal activity. It inhibited plaque formation and suppressed virus yield in Vero and RAW 264.7 cells infected with HSV-1 and HSV-2. Both the binding of virus to host cells and penetration of virus into cells were also blocked byB. pilosa. Furthermore,B. pilosawas effective against thymidine kinase-deficient and phosphonoacetate-resistant HSV-1 strains.B. pilosatreatment increased the survival rate of HSV-infected mice and limited the development of skin lesions. Our results indicate thatB. pilosahas anti-HSV activity and is thus a potentially useful medical plant for treatment of HSV infection.
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Belova, Anastasiya V., O. R. Astsaturova, N. S. Naumenko, and A. P. Nikonov. "GENITAL HERPES AND PREGNANCY." V.F.Snegirev Archives of Obstetrics and Gynecology 4, no. 3 (September 15, 2017): 124–30. http://dx.doi.org/10.18821/2313-8726-2017-4-3-124-130.
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Herpes simplex virus of two types - HSV-1 and HSV-2, which can manifest as a primary and recurrent infection is the etiological factor of genital herpes. Herpes simplex virus is one of the most common sexually transmitted infections, in connection with which there is an increase in physical and psychological morbidity, which often remains an underestimated medical problem. With the vertical transmission of HSV during labor, diseases that are dangerous to the life and health in newborns can occur. Pregnant women with a primary infection of genital herpes belong to the high-risk group for the transmission of HSV to the newborn. Prophylaxis and prevention of vertical transmission of HSV are implemented in three directions: prevention of the recurrence of maternal genital HSV infection; prevention of transmission of the virus during pregnancy and childbirth; puerperal prophylaxis of the disease in a neonate infant born of a mother belonging to a high-risk group. This review focuses on such important aspects as laboratory diagnosis of HSV, antiviral therapy and prevention of viral infection during pregnancy, delivery and in the early neonatal period.
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Aynaud, Olivier, Jean-Dominique Poveda, Bernard Huynh, Aline Guillemotonia, and Renzo Barrasso. "Frequency of herpes simplex virus, cytomegalovirus and human papillomavirus DNA in semen." International Journal of STD & AIDS 13, no. 8 (August 1, 2002): 547–50. http://dx.doi.org/10.1258/095646202760159666.
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Herpes simplex virus (HSV-2) and cytomegalovirus (CMV) infections produce brain damage in the newborn, and human papillomavirus (HPV) plays a role in cervical carcinogenesis. To assess the frequency of herpes virus and HPV in semen and its role in transmission, semen from 111 male partners of women with histologically-detected genital HPV infection was analysed for HSV, CMV and HPV infection. We used cell culture to detect HSV and CMV, and polymerase chain reaction (PCR) for HPV. Virological findings in the sperm were correlated to the presence or absence of HPV-associated genital lesions and to the viral type. Viral cultures yielded HSV-2 DNA in 9% and CMV DNA in 6.3% of cases. No correlation was established with a history of clinically apparent infection for HSV. HPV-DNA was detected in 23.4% of semen by PCR techniques: in 48% of subjects with urethral lesions, in 22% of patients with penile lesions, in 2% of patients without HPV-associated lesions. HPV-DNA type 16 was detected in 3.6% of cases. Patients with a positive HPV semen sample and penile or urethral lesions had the same HPV type detected in the two specimens. The study shows a high detection of clinically inapparent HSV and CMV, but does not confirm high HPV prevalence in semen from men without detectable lesions. Our study also suggests that the mechanism for semen contamination by HPV is the exfoliation of infected cells from urethral lesions during semen ejaculation, and probably, by abrasion from penile lesions. This could result in the contamination of semen used in assisted reproductive technology.
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Sun, Le, and Qihan Li. "The miRNAs of Herpes Simplex Virus (HSV)." Virologica Sinica 27, no. 6 (November 9, 2012): 332–37. http://dx.doi.org/10.1007/s12250-012-3266-5.
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Goins, William F., Bonnie Hall, Justus B. Cohen, and Joseph C. Glorioso. "Retargeting of herpes simplex virus (HSV) vectors." Current Opinion in Virology 21 (December 2016): 93–101. http://dx.doi.org/10.1016/j.coviro.2016.08.007.
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Dolan, Aidan, Fiona E. Jamieson, Charles Cunningham, Barbara C. Barnett, and Duncan J. McGeoch. "The Genome Sequence of Herpes Simplex Virus Type 2." Journal of Virology 72, no. 3 (March 1, 1998): 2010–21. http://dx.doi.org/10.1128/jvi.72.3.2010-2021.1998.
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ABSTRACT The genomic DNA sequence of herpes simplex virus type 2 (HSV-2) strain HG52 was determined as 154,746 bp with a G+C content of 70.4%. A total of 74 genes encoding distinct proteins was identified; three of these were each present in two copies, within major repeat elements of the genome. The HSV-2 gene set corresponds closely with that of HSV-1, and the HSV-2 sequence prompted several local revisions to the published HSV-1 sequence (D. J. McGeoch, M. A. Dalrymple, A. J. Davison, A. Dolan, M. C. Frame, D. McNab, L. J. Perry, J. E. Scott, and P. Taylor, J. Gen. Virol. 69:1531–1574, 1988). No compelling evidence for the existence of any additional protein-coding genes in HSV-2 was identified.
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Isaacs, Charles E., Weimin Xu, George Merz, Sharon Hillier, Lisa Rohan, and Guang Y. Wen. "Digallate Dimers of (−)-Epigallocatechin Gallate Inactivate Herpes Simplex Virus." Antimicrobial Agents and Chemotherapy 55, no. 12 (September 26, 2011): 5646–53. http://dx.doi.org/10.1128/aac.05531-11.
Full textAbstract:
ABSTRACTTopical microbicides are potentially an alternative method to vaccines for reducing the spread of herpes simplex virus (HSV). We have previously shown (S. Liu et al., Biochim. Biophys. Acta 1723:270–281, 2005) that the catechin (−)-epigallocatechin gallate (EGCG) inactivates HSV at neutral pH; however, to function in the female genital tract EGCG must also be effective at acidic pH. EGCG inactivated HSV-1 and HSV-2 at pH 8.0 by 3 log10to 4 log10but was ineffective at pH 5.7. The EGCG digallate dimers theasinensin A, P2, and theaflavin-3,3′-digallate (TF-3) inactivated both viruses by 3 log10to 4 log10at pH 5.7 and as much as 5 log10at pH 8.0. TF-3 inactivated HSV-1 and HSV-2 by 4 to 5 log10in the pH range of 4.0 to 5.7. Dimers with one gallate moiety had antiviral activity intermediate between the activities of EGCG and digallate dimers. Confocal and electron microscopy showed that theasinensin A did not damage Vero cells. All EGCG dimers inactivated enveloped viruses with class I, class II, and class III (HSV-1, HSV-2) fusion proteins more effectively than did monomeric EGCG. EGCG had no activity against the nonenveloped viruses tested, but TF-3 reduced the titer of 4 of 5 nonenveloped viruses by ≅2 to 3.5 log10. Results also showed that HSV-1 glycoprotein B (gB) was aggregated more rapidly by theasinensin A than EGCG, which, when taken together with the nonenveloped virus data, suggests that dimers may inhibit the function of viral proteins required for infectivity. Digallate dimers of EGCG appear to have excellent potential as microbicidal agents against HSV at acidic and neutral pHs.
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Kadayakkara, Deepak K., Angela Candelaria, Ye Eun Kwak, and Caroline Loeser. "Herpes Simplex Virus-2 Esophagitis in a Young Immunocompetent Adult." Case Reports in Gastrointestinal Medicine 2016 (2016): 1–3. http://dx.doi.org/10.1155/2016/7603484.
Full textAbstract:
Herpes simplex esophagitis (HSE) is commonly identified in immunosuppressed patients. It is rare among immunocompetent patients and almost all of the reported cases are due to HSV-1 infection. HSV-2 esophagitis is extremely rare. We report the case of a young immunocompetent male who presented with dysphagia, odynophagia, and epigastric pain. Endoscopy showed multitudes of white nummular lesions in the distal esophagus initially suspected to be candida esophagitis. However, classic histopathological findings of multinucleated giant cells with eosinophilic intranuclear inclusions and positive HSV-2 IgM confirmed the diagnosis of HSV-2 esophagitis. The patient rapidly responded to acyclovir treatment. Although HSV-2 is predominantly associated with genital herpes, it can cause infections in other parts of the body previously attributed to only HSV-1 infection.