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Journal articles on the topic 'Herpes virus, infection'

Author: Grafiati

Published: 4 June 2021

Last updated: 16 February 2022

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1

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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2

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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3

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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4

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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5

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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6

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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7

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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8

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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9

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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10

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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11

McMinn, Peter C., and Irene S. Lim. "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.tb125134.x.

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12

Kabani, Nazia, and David W. Kimberlin. "Neonatal Herpes Simplex Virus Infection." NeoReviews 19, no. 2 (February 2018): e89-e96. http://dx.doi.org/10.1542/neo.19-2-e89.

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13

Kohl, Steve. "Neonatal Herpes Simplex Virus Infection." Clinics in Perinatology 24, no. 1 (March 1997): 129–50. http://dx.doi.org/10.1016/s0095-5108(18)30188-x.

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14

Schomogyi, Mark, Anna Wald, and Lawrence Corey. "HERPES SIMPLEX VIRUS–2 INFECTION." Infectious Disease Clinics of North America 12, no. 1 (March 1998): 47–61. http://dx.doi.org/10.1016/s0891-5520(05)70408-6.

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15

KOSKINIEMI, MARJALEENA, JUHA-MATTI HAPPONEN, ANNA-LIISA JÄRVENPÄÄ, OSSI PETTAY, and ANTTI VAHERI. "Neonatal herpes simplex virus infection." Pediatric Infectious Disease Journal 8, no. 1 (January 1989): 30–35. http://dx.doi.org/10.1097/00006454-198901000-00009.

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16

BROWN, ZANE A., RHODA ASHLEY, JOHN DOUGLAS, MICHAEL KEILLY, and LAWRENCE COREY. "Neonatal herpes simplex virus infection." Pediatric Infectious Disease Journal 6, no. 11 (November 1987): 1057–61. http://dx.doi.org/10.1097/00006454-198706110-00013.

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17

BROWN, ZANE A., RHODA ASHLEY, JOHN DOUGLAS, MICHAEL KEILLY, and LAWRENCE COREY. "Neonatal herpes simplex virus infection." Pediatric Infectious Disease Journal 6, no. 11 (November 1987): 1057–61. http://dx.doi.org/10.1097/00006454-198711000-00013.

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18

Whitley, Richard. "Neonatal herpes simplex virus infection." Current Opinion in Infectious Diseases 17, no. 3 (June 2004): 243–46. http://dx.doi.org/10.1097/00001432-200406000-00012.

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19

Malm, Gunilla. "Neonatal herpes simplex virus infection." Seminars in Fetal and Neonatal Medicine 14, no. 4 (August 2009): 204–8. http://dx.doi.org/10.1016/j.siny.2009.01.005.

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20

CHERPES, THOMAS L., DEAN B. MATTHEWS, and SAMANTHA A. MARYAK. "Neonatal Herpes Simplex Virus Infection." Clinical Obstetrics and Gynecology 55, no. 4 (December 2012): 938–44. http://dx.doi.org/10.1097/grf.0b013e31827146a7.

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21

Baldwin, Steven, and Richard J. Whitley. "Intrauterine herpes simplex virus infection." Teratology 39, no. 1 (January 1989): 1–10. http://dx.doi.org/10.1002/tera.1420390102.

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22

Steben, Marc. "Genital Herpes Simplex Virus Infection." Clinical Obstetrics and Gynecology 48, no. 4 (December 2005): 838–44. http://dx.doi.org/10.1097/01.grf.0000179634.87533.da.

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23

Caviness, A. Chantal. "Neonatal Herpes Simplex Virus Infection." Clinical Pediatric Emergency Medicine 14, no. 2 (June 2013): 135–45. http://dx.doi.org/10.1016/j.cpem.2013.04.002.

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24

James, Scott H., and David W. Kimberlin. "Neonatal Herpes Simplex Virus Infection." Infectious Disease Clinics of North America 29, no. 3 (September 2015): 391–400. http://dx.doi.org/10.1016/j.idc.2015.05.001.

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25

James, Scott H., and David W. Kimberlin. "Neonatal Herpes Simplex Virus Infection." Clinics in Perinatology 42, no. 1 (March 2015): 47–59. http://dx.doi.org/10.1016/j.clp.2014.10.005.

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26

Schlech, Walter F., Nancy Meagher, Allan D. Cohen, Philip Belitsky, AS MacDonald, and John C. LeBlanc. "A Randomized Double-Blind Placebo Controlled Trial of Oral Acyclovir in Renal Allograft Recipients." Canadian Journal of Infectious Diseases 4, no. 2 (1993): 84–88. http://dx.doi.org/10.1155/1993/845236.

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Fifty renal transplant patients were randomized to receive either 800 mg acyclovir by mouth four times daily or identical placebo tablets for prophylaxis of herpes simplex infection. Patients were followed weekly to assess reactivation of herpes simplex, varicella zoster virus, Epstein-Barr virus or cytomegalovirus (CMV) infections. The patients received standard immunosuppressive regimens including cyclosporine A. Acyclovir suppressed secretion of herpes simplex virus in treated patients (P=0.001). Three episodes of mucocutaneous herpes simplex virus occurred in placebo recipients and one in a noncompliant acyclovir recipient. A clinically important difference in graft survival was demonstrated, but because of sample size failed to reach statistical significance (P=0.11). No reactivation of varicella zoster virus, Epstein-Barr virus or CMV infection was detected in either group. Toxicity was limited to central nervous irritability. The authors conclude that high dose oral acyclovir provides effective prophylaxis for prevention of herpes simplex virus infections in renal transplantation and may be associated with increased graft survival, perhaps from suppression of CMV infection.

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27

Jovanović, Marina. "Genital Herpes / Genitalni herpes." Serbian Journal of Dermatology and Venerology 3, no. 1 (January 1, 2011): 7–22. http://dx.doi.org/10.2478/v10249-011-0033-9.

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Abstract Genital herpes is a chronic, nearly always active herpes simplex virus (HSV) infection of sacral ganglia, that may appear bilaterally and in more ganglia than previously thought. It represents one of the most prevalent sexually transmitted infections, and the most frequent cause of genital ulcer disease in the general populations of developed countries. It is caused by HSV type-2 (HSV-2) in 60-80% of cases, with HSV-1 infections causing the remainder. Genital herpes caused by HSV-1 is on the rise. Since genital HSV-1 infections have higher risk for transmission from mother to infant during delivery than HSV-2, they account for 30% of all cases of neonatal herpes. Serological studies have found prevalence of HSV-2 in the general population of developed contries to be up to 25%. Thirty years ago, herpes was defined as “Today’s Scarlet Letter”in the absence of reliable serological tests and highly effective medications, for diagnosis and treatment of genital herpes. In 2000, apart from virus isolation in cell culture (70% sensitivity), that has long been regarded as the diagnostic gold standard, type specific serological tests and higly effective antiviral agents have evolved. However, the following questions were raised: should serological testing be routinely recommended in asymptomatic patients; can antiviral therapy reduce asymptomatic shedding of the virus; can antiviral therapy reduce sexual transmission of infection; can antiviral therapy reduce acquisitation of viral copathogens, such as human immunodeficiency virus (HIV)? Now, ten years later, we know the answers. Type specific HSV DNA detection by real-time PCR assays (100% sensitivity) are tests of choice for every person with recurrent genital ulcers lasting more than 4 days, and must be available in those laboratories currently performing a significant number of PCR tests for different purposes. Type specific IgG serology assays are indicated in all asymptomatic persons who are at increased risk for HSV infection. In sexually active patients experiencing ≥ 6 recurrences per year, daily supressive dose of acyclovir, valacyclovir or famciclovir should be discontinued after a maximum of a year of continuous antiviral therapy in order to reassess recurrence frequency. If necessary, the therapy should be restarted after at least two recurrences. With such expansive diagnostic possibilities and more aggressive therapeutic approaches, we can define genital herpes not as a “Scarlet Letter”, but as a “widespread untoward consequence of human sexuality”.

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28

Bayanova, T. A., D. P. Kudryavtseva, Yu K. Plotnikova, and A. D. Botvinkin. "THE CHANGE IN THE INCIDENCE OF SOME HERPES VIRUS INFECTIONS IN POPULATIONS WITH A HIGH PREVALENCE OF HIV INFECTION." HIV Infection and Immunosuppressive Disorders 11, no. 3 (September 14, 2019): 75–84. http://dx.doi.org/10.22328/2077-9828-2019-11-3-75-84.

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Objective: to characterize the structure and dynamics of the incidence of herpes virus infections (recorded in statistical forms) in a region with a high prevalence of HIV infection. Materials and methods. The state medical statistics for the Irkutsk region for the first 20 years after the start of the spread of HIV infection (2002–2017) was used as the material for the study. At the first stage, a retrospective analysis of the incidence of herpes virus infections was performed. The long-term incidence of herpes virus infections among children, adolescents and adults was compared with the prevalence of HIV infection in the population with the calculation of the Spearman correlation. At the second stage, a cohort study was conducted. The incidence rates of cytomegalovirus infection were compared in a cohort of patients with HIV infection and among the rest of the population. Relative risks of cytomegalovirus infection detection were assessed over the years 2008 and 2015. Conclusion. By 2017, the prevalence of HIV infection in the general population reached 1,7%. There was a direct strong correlation (0,7–0,8) between the prevalence of HIV infection and the incidence of chickenpox, infectious mononucleosis and cytomegalovirus infection. Starting in 2007, incidence of herpes virus infections was increased among children as well as among adults. In 2008–2015 the relative risk of cytomegalovirus infection in a cohort of HIV patients increased from 70,1 to 130,3. The incidence of herpes simplex among HIV patients was also increased.

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29

Veropotvelyan, P. M., I. C. Tsekhmistrenko, A. N. Chuvakov, M. C. Pivnev, and N. V. Pivnevа. "Diseases of the vagina and cervix, associated with viral infections: view of the practical doctor." HEALTH OF WOMAN, no. 2(118) (March 29, 2017): 111–17. http://dx.doi.org/10.15574/hw.2017.118.111.

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Kliniko-epidemiological these papillomas virus and herpes – a viral infection, in particular about genital herpes – one of the most widespread viral infections are presented in article. Key words: virus of papilloma of the person, cancer of a neck of uterus, persistention, reinfection, carriage of virus, immunomodulators, herpesviridae infection, genital herp, interferon inductors.

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30

Demina, O. I., T. A. Chebotareva, L. N. Mazankova, V. B. Tetova, and O. N. Uchaeva. "Clinical manifestations of infectious mononucleosis in primary or reactivated herpes virus infection." Rossiyskiy Vestnik Perinatologii i Pediatrii (Russian Bulletin of Perinatology and Pediatrics) 65, no. 1 (March 6, 2020): 37–44. http://dx.doi.org/10.21508/1027-4065-2020-65-1-37-44.

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Based on the analysis of foreign and domestic literature, the article presents the features of infectious mononucleosis caused by the main pathogens from the Herpesviridae family, course of the disease at various phases of the infectious process. The article identifies clinical and laboratory manifestations characteristic of each pathogen. The authors discuss the issues related to the lack of the unified terminology for describing chronic herpes virus infection. The article discusses the causes of persistent herpes virus infections, risk factors for the adverse course and outcome of herpes virus infections.

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31

Savinkov, P. A., T. N. Rybalkina, N. V. Karazhas, R. E. Boshyan, M. Yu Kalugina, M. N. Kornienko, E. V. Rusakova, E. M. Burmistrov, and I. A. Soldatova. "DETECTION OF MARKERS OF HERPES VIRUS INFECTION AND PNEUMOCYSTOSIS IN CHILDREN FROM HIV-INFECTED MOTHERS." Journal of microbiology epidemiology immunobiology, no. 4 (August 28, 2017): 67–74. http://dx.doi.org/10.36233/0372-9311-2017-4-67-74.

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Aim. Study the role of herpes viruses and pneumocystis in infectious complications in children from HIV-infected mothers. Materials and methods. Sera and blood cells from 59 children from HIV-infected mothers were studied for the presence of various markers of herpes virus infections and pneumocystosis by a complex of methods of modem laboratory diagnostics. Results. Frequency of detection of markers of herpes virus infection was from 10% for chicken pox in children with non-final HIV test to 93% for herpes simplex virus in HIV-infected children from closed organized groups. Signs of active infection in children with laboratory confirmed HIV infection were diagnosed 2.5 times more frequently for HSV infection and chicken pox and 1.8 times more frequently for HHV-6 and pneumocystis than in children with non-final HIV test. Markers of various disease stages with opportunistic infections (01) were detected in children with confirmed HIV-infection: primary acute and latent forms of the infection, reactivation, reconvalescence, whereas in children with non-final HIV test maternal antibodies against herpes virus and pneumocystis predominated. Markers of active infections excluding HSV and HHV-6 were more frequently detected in children from families than in children from closed organized groups. Conclusion. The feature detected - a lower percentage of detection of markers of active forms of 01 in HI V-infected children from social institutions - is determined by the fact that observation of these children is carried out by medical personnel that have the knowledge and experience of prophylaxis of infectious complications in HIV-infected children, whereas quality anti-epidemic regimen is frequently not maintained regarding home children with HIV infection. Another factor facilitating spread of opportunistic infections is the asocial lifestyle of most of the examined families. These data dictate the necessity of enhancement of anti-epidemic regimen and prophylaxis of opportunistic infections in family loci. Not only HIV-infected children, but also all the family members should be examined for markers of herpes virus infection and pneumocystosis in order to detect sources of the infection and timely execution of the prophylaxis measures.

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32

Nandi, S., Manoj Kumar, M. Manohar, and R. S. Chauhan. "Bovine herpes virus infections in cattle." Animal Health Research Reviews 10, no. 1 (June 2009): 85–98. http://dx.doi.org/10.1017/s1466252309990028.

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AbstractBovine herpes virus 1 (BHV-1) is primarily associated with clinical syndromes such as rhinotracheitis, pustular vulvovaginitis and balanoposthitis, abortion, infertility, conjunctivitis and encephalitis in bovine species. The main sources of infection are the nasal exudates and the respiratory droplets, genital secretions, semen, fetal fluids and tissues. The BHV-1 virus can become latent following a primary infection with a field isolate or vaccination with an attenuated strain. The viral genomic DNA has been demonstrated in the sensory ganglia of the trigeminal nerve in infectious bovine rhinotracheitis (IBR) and in sacral spinal ganglia in pustular vulvovaginitis and balanoposthitis cases. BHV-1 infections can be diagnosed by detection of virus or virus components and antibody by serological tests or by detection of genomic DNA by polymerase chain reaction (PCR), nucleic acid hybridization and sequencing. Inactivated vaccines and modified live virus vaccines are used for prevention of BHV-1 infections in cattle; subunit vaccines and marker vaccines are under investigation.

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33

Marshall, Catherine S., Felicity Murphy, Shannon E. McCarthy, and Allen C. Cheng. "Herpes compunctorum: cutaneous herpes simplex virus infection complicating tattooing." Medical Journal of Australia 187, no. 10 (November 2007): 598. http://dx.doi.org/10.5694/j.1326-5377.2007.tb01435.x.

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34

Johnson, R. M., and P. G. Spear. "Herpes simplex virus glycoprotein D mediates interference with herpes simplex virus infection." Journal of Virology 63, no. 2 (1989): 819–27. http://dx.doi.org/10.1128/jvi.63.2.819-827.1989.

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35

Egorova, N. Yu, O. V. Molochkova, L. N. Guseva, N. L. Waltz, and K. P. Chusov. "Active Herpes Virus Infection in Young Children." CHILDREN INFECTIONS 17, no. 4 (December 1, 2018): 22–28. http://dx.doi.org/10.22627/2072-8107-2018-17-4-22-28.

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Under observation were 122 young children (up to 3 years of age), who were identified markers of active forms of herpes virus infections. Markers were studied by PCR in blood, smear from tonsils, saliva, cerebrospinal fluid, urine with determination DNA of HSV 1—2 type, EBV, CMV, HHV-6 type, antigens were determined by indirect immunofluorescence in blood lymphocytes, by ELISA in serum — antibodies of the classes IgM and IgG. Herpesvirus infection occurs at an early age and contributes to the formation of various infectious and somatic pathology. In children from birth to 1 year of life, CMV infection in the form of a mono-infection with symptoms of CNS damage, generalized forms, neutropenia is more common (79% of cases). In children aged 1 to 2 years, in 76% of cases, HHV-6 infection is detected, more often in mixed variants. Patients of this group are observed with a long subfebrile condition, neutropenia, infectious mononucleosis. In the third year of life, there is an increase in infection of children with EBV, with approximately the same frequency of EBV and HHV-6, most often in mixed forms, the clinical manifestations of which is a typical symptom complex of infectious mononucleosis. At this age, the active persistence of herpes viruses contributes to the formation of a group of frequently ill children. Thus, when examining young children with various pathologies, it is necessary to diagnose herpes virus infection using modern methods to detect its active forms for the timely administration of etiotropic therapy.

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36

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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37

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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38

Lee, Bongjin, Jinsol Hwang, Yu Hyeon Choi, Young Joo Han, Young Hun Choi, and June Dong Park. "Disseminated Neonatal Herpes Simplex Virus Infection." Korean Journal of Critical Care Medicine 28, no. 4 (2013): 331. http://dx.doi.org/10.4266/kjccm.2013.28.4.331.

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39

Robb, James A., Kurt Benirschke, and Robert Barmeyer. "Intrauterine latent herpes simplex virus infection." Human Pathology 17, no. 12 (December 1986): 1196–209. http://dx.doi.org/10.1016/s0046-8177(86)80561-5.

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40

Robb, James A., Kurt Benirschke, Frank Mannino, and Joseph Voland. "Intrauterine latent herpes simplex virus infection." Human Pathology 17, no. 12 (December 1986): 1210–17. http://dx.doi.org/10.1016/s0046-8177(86)80562-7.

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41

Yura, Yoshiaki, Hiroki Iga, Kazuyoshi Terashima, Hideo Yoshida, Tetsuo Yanagawa, Masayuki Azuma, Yoshio Hayashi, and Mitsunobu Sato. "Recurrent intraoral herpes simplex virus infection." International Journal of Oral and Maxillofacial Surgery 15, no. 4 (August 1986): 457–63. http://dx.doi.org/10.1016/s0300-9785(86)80038-2.

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42

Stephenson-Famy, Alyssa, and Carolyn Gardella. "Herpes Simplex Virus Infection During Pregnancy." Obstetrics and Gynecology Clinics of North America 41, no. 4 (December 2014): 601–14. http://dx.doi.org/10.1016/j.ogc.2014.08.006.

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43

Doble, A., J. R. W. Harris, and D. Taylor-Robinson. "Prostatodynia and herpes simplex virus infection." Urology 38, no. 3 (September 1991): 247–48. http://dx.doi.org/10.1016/s0090-4295(91)80355-b.

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44

Marzano, A. V., A. Tourlaki, V. Merlo, D. Spinelli, L. Venegoni, and C. Crosti. "Herpes Simplex Virus Infection and Pemphigus." International Journal of Immunopathology and Pharmacology 22, no. 3 (July 2009): 781–86. http://dx.doi.org/10.1177/039463200902200324.

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45

Oh, Seong Hee. "Herpes Simplex Virus Infection in Children." Korean Journal of Pediatric Infectious Diseases 4, no. 1 (1997): 37. http://dx.doi.org/10.14776/kjpid.1997.4.1.37.

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Woo, Sook-Bin, and Samson Fu-Keung Lee. "Oral recrudescent herpes simplex virus infection." Oral Surgery, Oral Medicine, Oral Pathology, Oral Radiology, and Endodontology 83, no. 2 (February 1997): 239–43. http://dx.doi.org/10.1016/s1079-2104(97)90011-1.

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Colmone, Angela. "Epigenetic control during herpes virus infection." Science 346, no. 6214 (December 4, 2014): 1195.5–1195. http://dx.doi.org/10.1126/science.346.6214.1195-e.

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Vassantachart, Janna M., and Alan Menter. "Recurrent Lumbosacral Herpes Simplex Virus Infection." Baylor University Medical Center Proceedings 29, no. 1 (January 2016): 48–49. http://dx.doi.org/10.1080/08998280.2016.11929356.

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GOODKIN, MARGOT L., ELISE R. MORTON, and JOHN A. BLAHO. "HERPES SIMPLEX VIRUS INFECTION AND APOPTOSIS." International Reviews of Immunology 23, no. 1-2 (January 2004): 141–72. http://dx.doi.org/10.1080/08830180490265574.

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Yasmeen, Asma, and Samuel E. Ibhanesebhor. "Severe congenital herpes simplex virus infection." Archives of Disease in Childhood - Fetal and Neonatal Edition 99, no. 2 (August 7, 2013): F157. http://dx.doi.org/10.1136/archdischild-2013-304394.

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