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Books on the topic 'Herpes virus, infection'

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

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1

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

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2

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

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3

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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4

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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5

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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6

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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7

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

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8

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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9

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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10

Struyf, Frank. Genetic Analysis Of Herpesvirus Entry Receptors And Host Susceptibility To Herpes Simplex Virus Infection. Leuven Univ Pr, 2004.

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11

Bunker, Professor Christopher, and Dr Arani Chandrakumar. Dermatological diseases and emergencies. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199565979.003.00017.

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Chapter 17 covers dermatological diseases and emergencies including a general introduction to the subject, followed by information on erythroderma, drug eruptions, angio-oedema, Kawasaki disease, staphylococcal toxic shock syndrome, Streptococcal toxic shock syndrome (streptococcal TSS), staphylococcal scalded skin syndrome, necrotizing fasciitis, psoriasis, eczema and dermatitis, cutaneous vasculitis, immunobullous disorders, pyoderma gangrenosum, scarring alopecia, herpes simplex viruses 1 and 2, varicella zoster virus infection, bacterial infections affecting the skin, fungal infections affecting the skin, ectoparasitic disease, HIV infection and the skin, malignant melanoma, non-melanoma skin cancer, and cutaneous T cell lymphoma.
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12

Arvin, Ann. Herpes Virus Infections. Elsevier, 1996.

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13

Keshav, Satish, and Palak Trivedi. Viral hepatitis. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0212.

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Hepatitis means ‘inflammation of the liver’ and is manifest with symptoms that include malaise, anorexia, fever, flu-like symptoms, and pain in the right upper quadrant of the abdomen, with the pain being caused by swelling of the liver and its capsule. Elevations in circulating hepatic enzymes, particularly aspartate transaminase and alanine transaminase, are common, with jaundice occurring some time after the onset of other symptoms and signs. There are five viruses that primarily cause viral hepatitis: hepatitis A, B, C, D, and E viruses, abbreviated HAV, HBV, HCV, HDV, and HEV, respectively. These viruses are all hepatotrophic, in that the liver is the primary site of infection. HAV, HBV, and HEV are usually acute, self-limiting infections that may, nonetheless, cause morbidity and, in the case of HEV, fatality. However, HBV and, more so, HCV can cause chronic carriage of the virus over many years, as well as the development of chronic hepatitis. HDV is only pathogenic in conjunction with HBV. After recovery from acute infection with HAV, individuals have long-lasting immunity against further infection. The same holds true for the majority of individuals with acute HBV infection. There seems to be little natural immunity to HCV infection, and a significant proportion of cases result in chronic hepatitis. Immunity to HEV is not long-lasting, and repeated infections are possible. Many other viruses can cause hepatitis, of which cytomegalovirus, herpes simplex virus, Epstein–Barr virus, and flaviviruses such as dengue and yellow fever are the most important. The liver, however, is not their primary site of replication or cellular damage.
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14

Van Calsteren, Kristel. Chronic maternal infections. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198713333.003.0050.

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Pregnant women diagnosed with chronic infections are a worldwide problem. In developed countries, the most frequently encountered are hepatitis B and C, toxoplasmosis, syphilis, herpes simplex, and Cytomegalovirus infections. In developing countries, human immunodeficiency virus and malaria are also seen commonly in pregnant women. Maternal infections are associated with various complications in pregnant women, but also with congenital infections with or without structural anomalies and long-term sequelae, fetal growth restriction, preterm delivery, and perinatal mortality. Moreover, increasing evidence suggests that maternal infection during pregnancy affects the developing immune system of the fetus independently of the vertical transmission of pathogens. This chapter discusses the pathogen characteristics, ways of transmission, clinical presentation, diagnostic options, treatment, and, if relevant, prophylaxis for the most common infections in pregnant women (excluding hepatitis which is discussed elsewhere).
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15

Baker, David A. Acyclovir Therapy for Herpes Virus Infections (Infectious Disease and Therapy). Informa Healthcare, 1989.

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16

DeAugustinas, M., and A. Kiely. Infectious Keratitis. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199976805.003.0016.

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Keratitis is an inflammation of the cornea, which can lead to corneal opacification or ulceration. The most common cause of infectious keratitis is herpes simplex virus type 1 (HSV-1). Noninfectious corneal infiltrates related to trauma, collagen vascular disease, autoimmune inflammation, vasculitis, or atopy (which predisposes to HSV keratitis) must be considered. HSV-associated stromal keratitis is the most common cause of infectious corneal blindness in the United States, yet its presentation can be fairly subtle. For this reason, symptoms out of proportion to exam findings or a history concerning for viral infection is an indication for prompt referral to ophthalmology. Topical antibiotic drops achieve high tissue concentrations and are the treatment of choice. Empiric coverage should be prescribed and tailored later under the care of an ophthalmologist. Other keys to effective treatment include discontinuing contact lens use and protecting the eye with a rigid shield without a patch, as patching provides a reservoir for infection.
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17

Wittmann, G. Latent Herpes Virus Infections in Veterinary Medicine. Springer, 2011.

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18

Bale, James F. Congenital and Perinatal Viral Infections. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0160.

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Despite remarkable advancements in the treatment and prevention of infectious diseases, congenital (also known as intrauterine) and perinatal (also known as neonatal) infections remain major causes of permanent neurodevelopmental disabilities worldwide. Fortunately, relatively few viral pathogens can infect the developing fetus or the newborn postnatally and induce neurological disease. These pathogens include cytomegalovirus, rubella virus, herpes simplex virus types 1 and 2, varicella zoster virus, lymphocytic choriomeningitis virus, the nonpolio enteroviruses, parechovirus, and human immunodeficiency virus. This chapter describes the clinical manifestations, diagnosis, treatment, and outcome of these congenital and perinatal viral infections.
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19

(Editor), Marie Studahl, Paola Cinque (Editor), and Tomas Bergstrom (Editor), eds. Herpes Simplex Viruses (Infectious Disease and Therapy). Informa Healthcare, 2005.

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20

Harrison, Mark. Infections. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198765875.003.0042.

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This chapter describes the pharmacology of infections as they apply to Emergency Medicine, and in particular the Primary FRCEM examination. The chapter lists notifiable diseases and outlines the key details of antibacterial drugs, penicillins, cephalosporins tetracyclines, aminoglycosides, macrolides, the management of tuberculosis, quinolones, urinary tract infections, antifungal preparations, herpes virus infections, and antimalarials. This chapter is laid out exactly following the RCEM syllabus, to allow easy reference and consolidation of learning.
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21

Lydyard, Peter, Michael Cole, John Holton, Will Irving, Nino Porakishvili, Pradhib Venkatesan, and Kate Ward. Case Studies in Infectious Disease: Herpes simplex virus 1. Garland Science, 2009. http://dx.doi.org/10.4324/9780203853863.

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22

Lydyard, Peter, Michael Cole, John Holton, Will Irving, Nino Porakishvili, Pradhib Venkatesan, and Kate Ward. Case Studies in Infectious Disease: Herpes simplex virus 2. Garland Science, 2009. http://dx.doi.org/10.4324/9780203853870.

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23

Lopez, Carlos. Human Herpes Virus Infections: Pathogenesis, Diagnosis, and Treatment/Order No, 1694. Raven Pr, 1986.

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24

Gilden, Don, Randall J. Cohrs, Ravi Mahalingam, and Maria A. Nagel. Varicella Zoster Virus Infection of the Nervous System. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0149.

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Varicella zoster virus (VZV) is a human herpesvirus that causes varicella (chickenpox), after which virus becomes latent in ganglionic neurons along the entire neuraxis. Reactivation of VZV due to a decline in the cell-mediated immune response to VZV in elderly or immunocompromised individuals causes zoster (shingles), frequently complicated by chronic pain (postherpetic neuralgia) and serious neurological disease (meningoencephalitis, myelitis and VZV vasculopathy due to retrograde spread of virus after zoster. Here, we describe clinical, laboratory and pathological features of neurological complications of VZV reactivation, including diagnostic testing to verify VZV infection of the nervous system, since all neurological complications of zoster may occur without rash. We also discuss VZV latency, primate models to study varicella pathogenesis and immunity, and immunization of elderly individuals to prevent VZV reactivation.
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25

R, Stanberry Lawrence, ed. Genital and neonatal herpes. Chichester: John Wiley, 1996.

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26

(Contributor), WHO, ed. Epstein-Barr Virus and Kaposi's Sarcoma Herpes Virus/Human Herpesvirus 8 (IARC Monographs on Eval of Carcinogenic Risk to Humans). World Health Organisation, 1997.

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27

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

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28

Buhner, Stephen Harrod. Herbal Antivirals: Natural Remedies for Emerging and Resistant Viral Infections. Storey Publishing, LLC, 2013.

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29

Herbal antivirals: Natural remedies for emerging resistant and epidemic viral infections. 2013.

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30

Newman, Chris, and Andrew Byrne. Musteloid diseases: implications for conservation and species management. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780198759805.003.0009.

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The role of disease in population regulation is often overlooked in ecology and conservation. Due to their diversity, the musteloids host a wide range of pathogens. These include diseases of commercial importance, such Aleutian mink disease virus which impacts mink ranching, or bovine tuberculosis leading to interventions to manage European badgers. Skunks and raccoons are major rabies hosts in North America, and because these small carnivores insinuate themselves into close proximity with people, they can pose substantial zoonotic risks. Musteloids also share diseases between species, such as mustelid herpes virus, canine distemper and infectious hepatitis viruses, along with a range of nematodes and protozoans; presenting a contagion risk when vulnerable musteloids are being conserved or reintroduced. Managing host density, vaccination and host isolation are thus the best tools for managing disease, where we advocate the UN-led ‘One Health approach, aimed at reducing risks of infectious diseases at the Animal-Human-Ecosystem interface
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31

Swanepoel, R., and J. T. Paweska. Crimean-Congo haemorrhagic fever. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198570028.003.0033.

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Crimean-Congo haemorrhagic fever (CCHF) is an acute disease of humans, caused by a tick-borne virus which is widely distributed in eastern Europe, Asia and Africa. Cattle, sheep and small mammals such as hares undergo inapparent or mild infection with transient viraemia, and serve as hosts from which the tick vectors of the virus can acquire infection. Despite serological evidence that there is widespread infection of livestock in nature, infection of humans is relatively uncommon. Humans acquire infection from tick bite, or from contact with infected blood or other tissues of livestock or human patients, and the disease is characterized by febrile illness with headache, malaise, myalgia, and a petechial rash, frequently followed by a haemorrhagic state with necrotic hepatitis. The mortality rate is variable but averages about approximately 30 per cent. Inactivated vaccine prepared from infected mouse brain was used for the protection of humans in eastern Europe and the former Soviet Union in the past, but the development of a modern vaccine is inhibited by limited potential demand. The voluminous literature on the disease has been the subject of several reviews from which the information presented here is drawn, except where indicated otherwise (Chumakov 1974; Hoogstraal 1979; 1981; Watts et al. 1989; Swanepoel 1994; 1995; Swanepoel and Burt, 2004; Burt and Swanepoel, 2005; Whitehouse 2004; Ergunol and Whitehouse 2007; Ergunol 2008).
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32

Swanepoel, R., and J. T. Paweska. Rift Valley fever. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198570028.003.0043.

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Rift Valley fever (RVF) is an acute disease of domestic ruminants in mainland Africa and Madagascar, caused by a mosquito borne virus and characterized by necrotic hepatitis and a haemorrhagic state. Large outbreaks of the disease in sheep, cattle and goats occur at irregular intervals of several years when exceptionally heavy rains favour the breeding of the mosquito vectors, and are distinguished by heavy mortality among newborn animals and abortion in pregnant animals. Humans become infected from contact with tissues of infected animals or from mosquito bite, and usually develop mild to moderately severe febrile illness, but severe complications, which occur in a small proportion of patients, include ocular sequelae, encephalitis and fatal haemorrhagic disease. Despite the occurrence of low case fatality rates, substantial numbers of humans may succumb to the disease during large outbreaks. Modified live and inactivated vaccines are available for use in livestock, and an inactivated vaccine was used on a limited scale in humans with occupational exposure to infection. The literature on the disease has been the subject of several extensive reviews from which the information presented here is drawn, except where indicated otherwise (Henning 1956; Weiss 1957; Easterday 1965; Peters and Meegan 1981; Shimshony and Barzilai 1983; Meegan and Bailey 1989; Swanepoel and Coetzer 2004; Flick and Bouloy 2005). In September 2000, the disease appeared in south-west Saudi Arabia and adjacent Yemen, and the outbreak lasted until early 2001 (Al Hazmi et al. 2003; Madani et al. 2003; Abdo-Salem et al. 2006). The virus was probably introduced with infected livestock from the Horn of Africa, and it remains to be determined whether it has become endemic on the Arabian Peninsula.
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