Relevant bibliographies by topics / Herpes virus, infection

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Herpes virus, infection'

Author: Grafiati
Published: 4 June 2021
Last updated: 16 February 2022

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Journal articles on the topic "Herpes virus, infection"

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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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Straface, Gianluca, Alessia Selmin, Vincenzo Zanardo, Marco De Santis, Alfredo Ercoli, and Giovanni Scambia. "Herpes Simplex Virus Infection in Pregnancy." Infectious Diseases in Obstetrics and Gynecology 2012 (2012): 1–6. http://dx.doi.org/10.1155/2012/385697.

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Infection with herpes simplex is one of the most common sexually transmitted infections. Because the infection is common in women of reproductive age it can be contracted and transmitted to the fetus during pregnancy and the newborn. Herpes simplex virus is an important cause of neonatal infection, which can lead to death or long-term disabilities. Rarely in the uterus, it occurs frequently during the transmission delivery. The greatest risk of transmission to the fetus and the newborn occurs in case of an initial maternal infection contracted in the second half of pregnancy. The risk of transmission of maternal-fetal-neonatal herpes simplex can be decreased by performing a treatment with antiviral drugs or resorting to a caesarean section in some specific cases. The purpose of this paper is to provide recommendations on management of herpes simplex infections in pregnancy and strategies to prevent transmission from mother to fetus.
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Straus, E. S. "HERPES SIMPLEX VIRUS INFECTION." Pediatric Infectious Disease Journal 5, no. 2 (March 1986): 284. http://dx.doi.org/10.1097/00006454-198603000-00043.

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Liesegang, Thomas J. "Herpes zoster virus infection." Current Opinion in Ophthalmology 15, no. 6 (December 2004): 531–36. http://dx.doi.org/10.1097/01.icu.0000143686.68103.46.

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Jainkittivong, Aree, and Robert P. Langlais. "Herpes B virus infection." Oral Surgery, Oral Medicine, Oral Pathology, Oral Radiology, and Endodontology 85, no. 4 (April 1998): 399–403. http://dx.doi.org/10.1016/s1079-2104(98)90064-6.

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Whitley, Richard J. "Herpes simplex virus infection." Seminars in Pediatric Infectious Diseases 13, no. 1 (January 2002): 6–11. http://dx.doi.org/10.1053/spid.2002.29752.

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Marlina, Erni, Ali Yusran, and Zohra Nazaruddin. "Diagnosis dan tatalaksana nyeri pada rongga mulut yang disebabkan oleh infeksi virus herpes Diagnosis and management of pain in oral cavity caused by herpes virus infection." Journal of Dentomaxillofacial Science 11, no. 1 (February 28, 2012): 33. http://dx.doi.org/10.15562/jdmfs.v11i1.291.

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There are 80 types of known herpes virus, 8 of them can cause infection on humans. They are herpes simplex virus(HSV) 1 and 2, varicella zoster virus (VZV), cytomegalovirus, Epstein-Barr virus, human herpes virus (HHV6) Aand B, and paramyxovirus. HSV1, HSV2, and VZV are the virus known to cause oral mucosal diseases. This paperaims to review and discuss orofacial pain caused by herpes virus infection. Detail anamnesis about prodromal signand symptom with clinical features that vesicles, labial and intraoral lesions, and unilateral distribution of lesionsare characterized oral herpes virus infections. It can be concluded that detailed anamnesis and an understandingabout oral clinical sign and symptom may confirm diagnosis of herpes virus infections.
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Hidayat, Lukman Hakim. "HERPES ASSOCIATED-ERYTHEMA MULTIFORME (HAEM) IN YOUNG ADULT." ODONTO : Dental Journal 5, no. 2 (December 28, 2018): 152. http://dx.doi.org/10.30659/odj.5.2.152-156.

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Background: Erythema multiforme is an acute and a self-limiting mucocutaneoushypersensitivity reaction triggered by infections and medications. The mostcommon predisposing factors for erythema multiforme is infection with herpessimplex virus. Herpes associated erythema multiforme (HAEM) is an acuteexudative dermatic and mucosal disease caused by the infecting herpes simplexvirus. Most common ages is in childhood.Case and management: We report a case of recurrent herpes-associatederythema multiforme in a 23-year-old female patient, with crustae lesion in thelips and in pain. The patient had history of HSV infection. The patient had afever and prodromal before the lesion emerge. And the cutaneous lesion wasmistaken with the pimpleacne.Conclusions: Although the etiology of EM is still often unknown, infections withherpes simplex virus have been implicated as common predisposing a possibleprecipitating factor. This case illustrates the association of the occurrence of EMwith a herpes simplex virus (HSV) infection and how to managed the lesion
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Guerriere-Kovach, Pamela M., and Robert T. Brodell. "Recurrent herpes simplex virus infection." Postgraduate Medicine 107, no. 6 (May 2000): 139–47. http://dx.doi.org/10.3810/pgm.2000.5.15.1104.

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Bradford, David. "Disseminated herpes simplex virus infection." Medical Journal of Australia 152, no. 3 (February 1990): 167. http://dx.doi.org/10.5694/j.1326-5377.1990.tb125133.x.

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Dissertations / Theses on the topic "Herpes virus, infection"

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Ewing, Stephen Michael George. "Herpes simplex virus type 1 infection of dendritic leucocytes." Thesis, University of Oxford, 1992. http://ora.ox.ac.uk/objects/uuid:e83750b1-3aa7-452e-a876-be51690252be.

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McBride, Brian William. "Mucosal immune responses induced by herpes simplex virus infection." Thesis, University of Southampton, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.254770.

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Brown, Elizabeth L. "Consequences of genital herpes simplex virus infection among vulnerable populations /." Thesis, Connect to this title online; UW restricted, 2006. http://hdl.handle.net/1773/10885.

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Sayers, Charlotte. "Herpes simplex virus type 1 infection of human keratinocyte cells." Thesis, Imperial College London, 2013. http://hdl.handle.net/10044/1/11112.

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Infection of herpes simplex virus type 1 (HSV-1) begins at the epidermis, a stratified layer composed primarily of keratinocytes. The physiologically relevant cell type for the study of HSV-1 assembly is therefore the human keratinocyte. Nonetheless, relatively little is known about the replication of HSV-1 in this natural host cell. Comparison of virus growth in monolayers of keratinocyte cells and Vero cells, a routinely used cell line for HSV-1 studies, revealed that these keratinocytes support a more productive virus replication than Vero cells. Furthermore, newly assembled virus is produced more rapidly in keratinocytes and this enhancement occurs prior to, or upon the initiation of immediate early gene transcription. This augmented replication in keratinocytes can be at least partially attributed to the method of entry of the virus. We have found by penetration assays and electron microscopy that the virus is able to penetrate keratinocyte cells much more rapidly than Vero cells. We have also shown that the virus entry mechanism is more efficient at lower temperatures in nTERT cells, with virus entering cells at temperatures as low as 7°C. Additionally preliminary work implies that depletion of one of the herpes virus entry receptors, Nectin-1, does not affect entry into nTERT cells, whereas entry is reduced up to 65% in HeLa cells. Taken together, these results imply a role for other entry receptors, possibly as yet unidentified, in the entry of human keratinocyte cells. This work also identifies a role for cellular Rab proteins, GTPases essential for the regulation of vesicle trafficking, in HSV-1 infection of keratinocytes. In particular Rab6, which was also found to play a role in infected HeLa cells (Elliott Group), appears to have a similar function in both these cells and together support a model for HSV-1 morphogenesis involving Rab-regulated vesicle trafficking of viral glycoproteins to the cell surface. Several other Rabs identified by this screen now provide interesting opportunities to elucidate further roles of Rab proteins in HSV-1 infection of keratinocyte cells. This project has broadly characterised the replication of HSV-1 in keratinocyte cells and explored the role of Rab GTPases in virus trafficking within keratinocytes - a cell type that is physiologically relevant to infection.
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Williams, N. A. "The role of Langerhans cells in infection with herpes simplex virus." Thesis, University of Bristol, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.235240.

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LABAUNE, JEAN-MARC. "Infection herpetique neonatale : etude lyonnaise sur 5 ans." Lyon 1, 1994. http://www.theses.fr/1994LYO1M208.

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Simmonds, Peter. "Detection of antibody responses to infection with herpes simplex virus and human immunodeficiency virus." Thesis, University of Edinburgh, 1988. http://hdl.handle.net/1842/26933.

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Lee, Jennifer Sohn. "Epigenetic Regulation of Lytic and Latent Herpes Simplex Virus 1 Infection." Thesis, Harvard University, 2015. http://nrs.harvard.edu/urn-3:HUL.InstRepos:17467322.

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Epigenetic regulation plays a major role in whether the herpes simplex virus 1 (HSV-1) will initiate viral gene expression and lytic infection or instead suppress its gene expression and establish a latent infection. Prior to this study, it was known that cells respond to naked DNA by assembling chromatin to silence foreign genetic material. However, during lytic infection of epithelial cells, viral proteins VP16 and ICP0 have been implicated in limiting chromatin association and promoting euchromatic histone modifications on the HSV-1 genome. We hypothesized that the viral genome would also be subject to silencing by heterochromatin modification during lytic infection. To test this we examined the association of chromatin and heterochromatic modifications during lytic infection with WT viruses and ICP0-null mutant viruses. We found that heterochromatin modifications H3K9me3 and H3K27me3 associate initially with all viruses, but were removed rapidly during infection with WT HSV-1. ICP0-null viruses were not able to remove histones or heterochromatin, indicating a role for ICP0 in reversing epigenetic silencing. In latent infection, HSV-1 undergoes epigenetic silencing as a means to suppress gene expression and persist in neurons. Surprisingly, in this study, we find that ICP0-null viruses accumulate less heterochromatin on lytic gene promoters relative to WT viruses. This suggests that ICP0 may function to promote infection of neurons, or assist in the establishment or maintenance of latent infection. Additionally, during latency the viral genome maintains active expression from the latency-associated transcript (LAT) region, and this region retains markers of euchromatin that are excluded from the lytic viral genes. The insulator protein, CTCF, binds to a site downstream of this region between the LAT and ICP0 promoters. We find that during latent infection, deletion of this site promoted accumulation of H3K27me3 at the LAT promoter and reduced reactivation competence of the virus, but surprisingly enhanced LAT expression. This suggests that CTCF balances epigenetic repression to promote latency and maintain reactivation competence. In summary, this dissertation suggests that during lytic infection HSV reverses cell-mediated epigenetic repression and promotes viral gene expression, while during latency, the virus co-opts epigenetic mechanisms to maintain a silenced but poised genome.
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Littlejohn, Emma Sophie Vout. "The Sensitivity of Adenovirus and Herpes simplex virus to Honey." The University of Waikato, 2009. http://hdl.handle.net/10289/2804.

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Honey has been used for centuries as a medicine to treat various ailments and infections. A large amount of research has established that honey has potent antibacterial activity. However, the sensitivity to honey of viral species that cause infections has been studied in only a small number of cases. The aim of this study was to obtain data to clarify and extend knowledge obtained from these previous studies of honey's antiviral activity, and especially study those viruses that cause localised infections which have limited or no therapy available, which are suitable to treatment with topically applied honey. The susceptible A549 cell line and viral isolates of Adenovirus serotypes 1, 3, and 8, and Herpes simplex virus serotypes 1 and 2, were provided by the Waikato Hospital Virology Laboratory. A number of types of honey were investigated from a range of sources: Manuka honey with high concentrations of methylglyoxal, unique manuka factor activity, and phenolics, Honeydew and Rewarewa honeys which have high antioxidant activity, and Ling Heather honey which is high in phenolic compounds. These honeys were selected due to their range of characteristic activities in order to make comparisons with antiviral activity. A variety of tests using cell culture were developed to evaluate the sensitivity of the viruses to whole honey. Each test scored and monitored the development of morphological changes to the cells, to observe whether the honey treatment can prevent the development of these changes known as viral cytopathic effect. These included tests for: protection, in which the cells were pre-treated with, and iii incubated either with or without honey; prevention, where honey was used to treat infected cells, and in plaque reduction assays, to examine whether it can reduce the resultant number of plaques; and neutralisation, in which the virus was directly exposed to the honey for a defined period. It was found with each type of test using cell culture that many of the honeys studied can lower the severity of viral cytopathic effect or delay its onset compared with the development observed with virus that was not treated with honey. This can suggest that the antiviral activity may be a feature of more than one type of honey. In general the antiviral effect increased with the concentration of honey and time the virus was exposed to it. Manuka honey M116 at a concentration of 10% was effective in preventing the development of viral cytopathic effect of each of virus, after the viruses at concentrations in excess of the tissue culture infectious dose had been exposed to the honey for 8 hours. Enzyme-linked immunosorbant assays were used to measure the effect the successful treatments found in the extended neutralisation experiments had on viral surface proteins necessary for viral entry into the cells. The results using this technique suggested that there was very little virus present in the samples that had been treated with honey and with the untreated virus. Therefore it could not be shown whether the honey was acting via this mechanism. It is concluded from the findings in this study that honey is likely to be an effective antiviral treatment for the therapy of localised viral infections, this needs to be verified by clinical trials.
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Laycock, K. A. "Herpes simplex virus gene expression in establishment and maintenance of latent infection." Thesis, University of Bristol, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.234807.

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Books on the topic "Herpes virus, infection"

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Stanberry, Lawrence R. Understanding herpes. Jackson, Miss: University Press of Mississippi, 2006.

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Understanding herpes. Jackson: University Press of Mississippi, 1998.

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Scandinavian Symposium on Herpes Virus Infections and Acyclovir (Zovirax) (1985 Copenhagen, Denmark). Scandinavian Symposium on Herpes Virus Infections and Acyclovir (Zovirax), Copenhagen, Denmark, March 13-15, 1985. Stockholm, Sweden: Distributed by Almqvist & Wiksell Periodical Co., 1985.

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Tabery, Helena M. Varicella-Zoster Virus Epithelial Keratitis in Herpes Zoster Ophthalmicus: In Vivo Morphology in the Human Cornea. Berlin, Heidelberg: Springer-Verlag Berlin Heidelberg, 2011.

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Reisaku, Kōno, and Nakajima Akira 1927-, eds. Herpes viruses and virus chemotherapy: Pharmocological and clinical approaches : proceedings of the International Symposium on Pharmacological and Clinical Approaches to Herpes Viruses and Virus Chemotherapy, Oiso, Japan, 10-13 September 1984. Amsterdam: Excerpta Medica, 1985.

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Sexually transmitted diseases sourcebook: Basic consumer health information about sexual health and the screening, diagnosis, treatment, and prevention of common sexually transmitted diseases (STDs), including chancroid, chlamydia, gonorrhea, herpes, hepatitis, human immunodeficiency virus/acquired immunodeficiency syndrome (HIV/AIDS), human papillomavirus (HPV), syphilis, and trichomoniasis ; along with facts about risk factors and complications, trends and disparities in infection rates, tips for discussing STDs with sexual partners, a glossary of related terms, and resources for additional help and information. 5th ed. Detroit, MI: Omnigraphics, Inc., 2013.

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Current issues in clinical neurovirology: Pathogenesis, diagnosis and treatment. Philadelphia, Pa: Saunders, 2008.

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Alyazidi, Raidan, and Soren Gantt. Herpes simplex Virus. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190604813.003.0007.

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Herpes simplex virus (HSV) types 1 and 2 cause several important syndromes, including congenital and perinatal infections that can cause devastating consequences in newborns (i.e., neonatal HSV). Most neonatal HSV infections are acquired intrapartum in the infected maternal birth canal. Since genital HSV infections are common, neonatal HSV is an important complication in infected women, even if maternal symptoms are absent. As a result of the developmental status of the fetal and newborn immune system, neonatal HSV infection is associated with life-threatening disease. This chapter reviews the clinical presentations of neonatal HSV infection, as well as advances in diagnosis and therapy. Skin vesicles and fever are often absent, which contributes to a delay in initiating effective therapy. Early recognition is key. Despite significant advances in diagnostic testing and antiviral treatment for neonatal HSV, morbidity and mortality remain high and no vaccine is currently available for clinical use.
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Brown, David W. G. Herpes B virus (Cercopithecine Herpes 1). Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198570028.003.0036.

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Herpes B virus or Cercopithecine herpes 1 as it is formally classified causes a persistent infection of monkeys of the Macaca genus. In monkey colonies and social groups, it is transmitted by close contact and sexually. Human infection is rare with less than 50 human cases described it has been seen in monkey handlers exposed to infected monkeys following bites, scratches and abraded skin. Infection has also been recognized in two cases following exposure through laboratory work. Following an incubation period of 9-59 days typically an ascending encephalomyelitis develops which is fatal in 80% of cases. Prevention and control of the risk of B virus is based on avoiding direct contact with infected animals by screening, following handling guidelines for monkeys used in biomedical research and rigorous laboratory safety precautions. Treatment with acyclovir has been successful and halved mortality in recent cases. It is also recommended for prophylaxis in potential exposures.
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Struyf, Frank. Genetic Analysis Of Herpesvirus Entry Receptors And Host Susceptibility To Herpes Simplex Virus Infection. Leuven Univ Pr, 2004.

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Book chapters on the topic "Herpes virus, infection"

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Mindel, Adrian. "Clinical Features: Disseminated Infection." In Herpes Simplex Virus, 75–95. London: Springer London, 1989. http://dx.doi.org/10.1007/978-1-4471-1683-7_5.

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Kabani, Nazia, and David Kimberlin. "Neonatal Herpes Simplex Virus Infection." In Neonatal Infections, 119–26. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-90038-4_13.

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Vergou, Theognosia. "Herpes Simplex Virus Infection (Orofacial)." In European Handbook of Dermatological Treatments, 373–77. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-662-45139-7_38.

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Orbell, Sheina, Havah Schneider, Sabrina Esbitt, Jeffrey S. Gonzalez, Jeffrey S. Gonzalez, Erica Shreck, Abigail Batchelder, et al. "Herpes Simplex Virus (HSV) Infection." In Encyclopedia of Behavioral Medicine, 961. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4419-1005-9_100794.

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Kroon, S. "Herpes simplex virus infection (orofacial)." In European Handbook of Dermatological Treatments, 193–96. Berlin, Heidelberg: Springer Berlin Heidelberg, 2003. http://dx.doi.org/10.1007/978-3-662-07131-1_38.

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Kroon, S. "Herpes Simplex Virus Infection (Oro-Facial)." In European Handbook of Dermatological Treatments, 229–33. Berlin, Heidelberg: Springer Berlin Heidelberg, 2000. http://dx.doi.org/10.1007/978-3-662-03835-2_42.

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Burdett, L., W. Clark, and J. J. Docherty. "Genital herpes simplex virus infection in young adults." In Common Infections, 101–8. Dordrecht: Springer Netherlands, 1985. http://dx.doi.org/10.1007/978-94-009-4878-5_5.

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Tabery, Helena M. "Healing of Herpes Simplex Virus Epithelial Keratitis Treated with Acyclovir Ointment and Short-Term Sequelae of the Infection." In Herpes Simplex Virus Epithelial Keratitis, 25–34. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-642-01012-5_2.

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Stroop, William G., and J. Richard Baringer. "Herpes Simplex Virus Infections of the Nervous System." In Clinical and Molecular Aspects of Neurotropic Virus Infection, 343–67. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4613-1675-6_13.

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Kurt-Jones, Evelyn A., Megan H. Orzalli, and David M. Knipe. "Innate Immune Mechanisms and Herpes Simplex Virus Infection and Disease." In Cell Biology of Herpes Viruses, 49–75. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-53168-7_3.

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Conference papers on the topic "Herpes virus, infection"

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Bilasco, Ancuta, Szidonia Florea, Ramona Cirt, Anca Draganescu, Magda Vasile, Camelia Kouris, Cristina Negulescu, and Monica Luminos. "GP45 Autoimmune encephalitis triggered by herpes simplex virus 1 infection." In Faculty of Paediatrics of the Royal College of Physicians of Ireland, 9th Europaediatrics Congress, 13–15 June, Dublin, Ireland 2019. BMJ Publishing Group Ltd and Royal College of Paediatrics and Child Health, 2019. http://dx.doi.org/10.1136/archdischild-2019-epa.111.

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Mailloux, Breion, Chris Flannery, and Gregory Ahearn. "An Acute Presentation Of Idiopathic Pulmonary Fibrosis Associated With Herpes Virus Infection." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a4517.

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WAJIMA, T. "THROMBOCYTOPENIA IN ACQUIRED IMMUNE DEFICIENCY SYNDRGME(AIDS)-RELATED COMPLEXES:RESOLUTION DURING HERPES VIRAL INFECTION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644145.

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Immune thrombocytopenia has been recognized as a major hematologic manifestation associated with the acquired immune deficiency syndrome(AIDS) and AIDS-related complexes. The mechanism of thrombocytopenia in human immune deficiency virus infection is probably multifactorial.. The role of platelet-associated immuno-globulin(PAIgG)and circulating immune complexes(CIC) in mediating thrombocytopenia is controversial.. We experienced a case in which immune thrombocytopenia in AIDS-related complexes resolved during herpes zoster infection. A 37 y.o. white homosexual male with AIDS-related complexes and thrombocytopenia presented a 4-day history of painful, violaceous, non-pruritic vesicles which started on the right arm and hand, which then progressed to the chest wall, abdomen, back, and left arm. Peripheral lymphadenop-athy and splenomegaly was not noted. On admission WBG 13.5 Hct 40.8, platelet 46,000, Tzanck smear of vesicles revealed herpetic type giant cells. HTLV-III pos., Helper/suppressor T-cell ratio 0.3, Total protein 7.9 gm%, . Alb 3.95gm% IgG 1740 mg%, IgA 157 mg IgM 91.2 mg, Monospot neg., HBsAg Neg., HBsAb pos., HBcAb pos., VDRL neg. Before this admission, immune thrombocytopenia was documented by increased levels of PAIgG, CIC, bone marrow magakaryocytic hyperplasia, peripheral thrombocytopenia with giant platelets, absence of splenomegaly, and response to prednisone. He was treated with Acyclovir 250 mg/m2 1-hr infusion Q8h for 9 days ;to control the spread of his herpes infection. Recovery of thrombocytopenia wasobserved during herpes zo.ster infection. The platelet count rose to 158,000 and sustained over 4- weeks. Duringnormalization of platelet count thelevel of GIC (assayed by Raji cells, reference ranges, less than 12) droppedfrom 300 to less than 12 and PAIgG(fluorescence-activated flow cytometric assay, reference ranges, less than 1.5 RF) was markedly decreased from 90 to 2.9 When herpes infection had subsided the platelet count again decreased. These findings suggestthat PAIgG and GIG were contributing factors to immune thrombocytopenia and that herpes viral infection and Acyclovir altered this immunologically mediated thrombocytopenia in AIDS-related complexes.
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Adonchiyalage, BAS, L. Fernando, and K. Patrick. "G543(P) Severe multisystem haemophagocytic lymphohistiocytosis secondary to herpes simplex virus infection; a case report." In Royal College of Paediatrics and Child Health, Abstracts of the RCPCH Conference and exhibition, 13–15 May 2019, ICC, Birmingham, Paediatrics: pathways to a brighter future. BMJ Publishing Group Ltd and Royal College of Paediatrics and Child Health, 2019. http://dx.doi.org/10.1136/archdischild-2019-rcpch.526.

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Yin, Quiyan, Michael Strong, Erik Flemington, and Joseph Lasky. "RNA-seq analysis does not substantiate a causative link between herpes virus infection and IPF." In Annual Congress 2015. European Respiratory Society, 2015. http://dx.doi.org/10.1183/13993003.congress-2015.oa3511.

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Kostina, J., and E. Tarasova. "DIAGNOSTIC SIGNIFICANCE OF THE ELISA METHOD TO DETERMINE THE SHAPE, STAGES AND HERPES SIMPLEX VIRUS INFECTION." In SAKHAROV READINGS 2020: ENVIRONMENTAL PROBLEMS OF THE XXI CENTURY. Minsk, ICC of Minfin, 2020. http://dx.doi.org/10.46646/sakh-2020-2-222-224.

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Vashchenko, Oksana, Olena Babiy, Nadiya Zholobak, and Kateryna Vashchenko. "Investigation of Acute Toxicity of Tilorone Ointment for Topical Treatment of Herpes Virus Infection." In 2nd International Electronic Conference on Medicinal Chemistry. Basel, Switzerland: MDPI, 2016. http://dx.doi.org/10.3390/ecmc-2-a028.

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Ekblad, Maria, Edward Trybala, Craig Freeman, Christopher R. Parish, Vito Ferro, and Tomas Bergstrom. "INHIBITION OF HERPES SIMPLEX VIRUS INFECTION BY PI-88, AN ANTAGONIST OF HEPARAN SULFATE-PROTEIN INTERACTIONS." In XXIst International Carbohydrate Symposium 2002. TheScientificWorld Ltd, 2002. http://dx.doi.org/10.1100/tsw.2002.442.

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Tahboub, M., A. Al-Shyoukh, L. Numan, O. Abughanimeh, M. Younis, and A. Gohar. "A Lethal Combination of Disseminated Herpes Simplex Virus-1 (HSV-1) and Varicella Zoster Virus (VZV) Co-Infection in an Immunosuppressed Adult." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a6587.

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Ruggiero, M., D. Schrump, M. Lionakis, A. Rajan, and K. P. Fennelly. "Hemidiaphragmatic Paralysis Due to Herpes Zoster Virus Infection in a Patient with Autoimmune Pneumonitis Associated with Thymoma." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a5738.

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