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Books on the topic 'HLV'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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1

Dirgahayu, Paramasari. Molecular epidemiology database of HIV, HBV, HCV, HDV, HTLV-1/2, and TTV in Central of Java, Indonesia: Final report international research collaboration and international publication. [Surakarta]: Sebelas Maret Univ., 2010.

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2

Thiemann, Lillian. Double jeopardy: The HIV/HCV co-infection handbook. New York: Community Prescription Service, 1999.

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3

Human retrovirology: Facts and concepts. Berlin: Springer-Verlag, 1990.

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4

Schüpbach, Jörg. Human retrovirology: Facts and concepts. Berlin: Springer-Verlag, 1989.

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5

Schüpbach, Jörg. Human retrovirology: Facts and concepts. Berlin: Springer-Verlag, 1989.

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6

Glew, Susan Sylvia. HLA Class II antigens and HPV in cervical neoplasia. Manchester: University of Manchester, 1992.

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7

Scientific Group on Human T-Lymphotropic Virus Tupe-1 (HTLV-1) Infections and Associated Diseases (1992 Kagoshima-shi, Japan). Report: Scientific Group on Human T-Lymphotropic Virus Type-1 (HTLV-1) Infections and Associated Diseases, Kagoshima, Japan, 13-14 October 1992. Manila, Philippines: The Office, 1993.

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8

Jürgens, Ralf. HIV/AIDS and HCV in prisons: A select annotated bibliography. Ottawa, Ont: International Affairs Directorate, Health Canada, 2005.

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9

E, Groopman Jerome, and University of California, Los Angeles., eds. Human retroviruses: Proceedings of a Chimertech-UCLA symposium, held at Tamarron, Colorado, February 4-11, 1989. New York: Wiley-Liss, 1990.

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10

Parks, Peggy J. HPV. San Diego, CA: Daniel A. Leone, Publisher, 2008.

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11

Westaway, R. D. HIV. Porstmouth, N.H. (Box 90, Portsmouth 03802): New England Book Co., 1991.

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12

Administration, United States Occupational Safety and Health. Enforcement procedures for occupational exposure to hepatitis B virus (HBV) and human immunodeficiency virus (HIV). Washington, D.C: U.S. Dept. of Labor, Assistant Secretary for Occupational Safety and Health, 1990.

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13

United States. Occupational Safety and Health Administration. Enforcement procedures for occupational exposure to Hepatitis B Virus (HBV) and Human Immunodeficiency Virus (HIV). [Washington, D.C.?: U.S. Dept. of Labor, Assistant Secretary for Occupational Safety and Health, 1988.

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14

United States. Occupational Safety and Health Administration. Enforcement procedures for occupational exposure to hepatitis B virus (HBV) and human immunodeficiency virus (HIV). Washington, D.C: U.S. Dept. of Labor, Assistant Secretary for Occupational Safety and Health, 1990.

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15

Hav: Comprising last letters from Hav, Hav of the Myrmidons. London: Faber and Faber, 2006.

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16

Charlton, Margaret. AIDS & HIV counselling handbook: HIV testing. 2nd ed. Macclesfield: Macclesfield Health Authority, 1989.

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17

1956-, Gluckman Jennifer C., and Vilmer E, eds. Acquired immunodeficiency syndrome. Amsterdam: Elsevier, 1986.

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18

HIV/AIDS. Cambridge: Independence, 2009.

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19

Dittmer, Lori. HIV/AIDS. Mankato, Minn: Creative Education, 2012.

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20

Marcus, Stephanie. HIV/AIDS. Washington, D.C. (101 Independence Ave., S.E., Washington 20540: Science Reference Section, Science and Technology Division, Library of Congress, 1998.

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21

Wexler, Barbara. AIDS/HIV. Detroit: Gale, 2012.

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22

Marcus, Stephanie. HIV/AIDS. Washington, D.C. (10 First St., S.E., Washington 20540): Science Reference Section, Science and Technology Division, Library of Congress, 1998.

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23

Stang, Lucas. HIV prevention. Santa Cruz, Calif: ETR Associates, 1994.

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24

HIV & AIDS. Shaftesbury, Dorset: Element, 1999.

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25

Wexler, Barbara. AIDS/HIV. Detroit: Gale, Cengage Learning, 2008.

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26

Svetina, Ivo. Sfing hlev. Novo mesto: GOGA, 2010.

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27

HIV positive. New York: Dutton Children's Books, 1997.

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28

Marcus, Stephanie. HIV/AIDS. Washington, D.C. (101 Independence Ave., S.E., Washington 20540: Science Reference Section, Science and Technology Division, Library of Congress, 1998.

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29

Stolley, Kathy S. HIV/AIDS. Santa Barbara, Calif: Greenwood Press, 2009.

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30

Johansen, Rune. Hiv mannskjiten. 2nd ed. Oslo: Forlaget Press, 2004.

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31

HIV/AIDS. New York: Rosen Publishing, 2016.

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32

Prasad, Vinayaka R. HIV protocols. 2nd ed. New York, N.Y: Humana Press, 2008.

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33

Carter, Michael. HIV & women. London: NAM, 2004.

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34

Sax, Paul E., Calvin J. Cohen, and Daniel R. Kuritzkes. HIV essentials. 5th ed. Burlington, MA: Jones & Bartlett Learning, 2012.

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35

Wilson, Deanna. Hepatitis. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199976805.003.0035.

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Hepatitis A (HAV) and E (HEV) viruses are spread via the fecal-oral route. Hepatitis B virus (HBV) exposure is via occupational or recreational activities. Hepatitis D virus (HDV; also spread parentally) can only coinfect or superinfect those with chronic HBV. Hepatitis C (HCV) transmission is predominantly parenteral; the highest risk group is injection drug users. Prodromal-period patients with acute hepatitis present with vague constitutional symptoms when serum transaminases peak, with elevated serum bilirubin and varying levels of hepatic protein synthesis impairment; during the icteric phase, patients develop abdominal pain, hepatomegaly, and jaundice. Acute hepatitis has limited therapy; treatment is predominantly supportive. However, most adults with acute phase HAV, HBV, HDV, and HEV spontaneously clear the virus. Most individuals with HCV develop chronic hepatitis. Patients with known HAV, HBV, or HEV exposures may be eligible for post-exposure prophylaxis to reduce their risk of infection.

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36

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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37

United States. National Aeronautics and Space Administration., ed. Final report for the HLV avionics requirements study and electronic filing system database development. [Washington, DC: National Aeronautics and Space Administration, 1994.

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38

Vejdirektoratet, Denmark, ed. Afmærkning på kørebanen: Forsøg med vejstriber på hlv. 141 i perioden sept. 86 til sept. 88. [Copenhagen?]: Vejdirektoratet, 1989.

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39

Bulterys, Marc, Julia Brotherton, and Ding-Shinn Chen. Prevention of Infection-Related Cancers. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780190238667.003.0066.

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This chapter discusses primary prevention measures that disrupt transmission of oncogenic infections. It begins by discussing vaccination against hepatitis B virus (HBV) and human papillomavirus (HPV), two major causes of cancer for which safe and effective vaccines are currently available. It briefly discusses the importance of treatment and prophylaxis against human immunodeficiency virus type 1 (HIV-1), which potentiates the virulence of other viral infections as well as directly increasing the incidence of non-Hodgkin lymphoma. It does not discuss the treatment of HBV or hepatitis C virus (HCV) infection, since these are considered in Chapters 25 and 33. Also beyond the scope of this chapter are the randomized clinical trials currently underway to assess the efficacy and feasibility of eradication of Helicobacter pylori (Chapters 24, 31), vaccination against Epstein-Barr virus (EBV) (Chapters 24, 26, 39), or the prevention of schistosomiasis and liver flukes (Chapters 24, 33, and 52).

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40

Musharraf, Husain, and Population Council (Bangladesh), eds. Prevalence of HIV, HBV, HCV and syphilis markers in pregnant women of Bangladesh. Dhaka, Bangladesh: Population Council, 1997.

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41

Herrero, Rolando, and Raul Murillo. Cervical Cancer. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780190238667.003.0048.

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Cervical cancer is the fourth most common cancer in women worldwide, with more than 500,000 cases and 250,000 deaths per year. The disease is characterized by marked regional differences, with more than 80% of the cases and deaths occurring in developing countries. The etiology and natural history of the disease are very well studied, with persistent infection with one of thirteen human papillomavirus (HPV) types now considered to be a necessary cause. The molecular mechanisms have also been elucidated and are mediated mainly by the expression of viral oncogenes that interfere with cellular pathways. The two most common HPV types, namely HPV-16 and HPV-18, are associated with about 70% of all cases around the world. Immunologic (e.g., HIV infection), hormonal (e.g., high parity), environmental (e.g., smoking), and genetic (e.g., HLA type) cofactors determine the risk of persistence and cancer among women harboring HPV infection.

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42

Price, Jennifer Cohen, Priyanka Amin, and Antoine Douaihy. Hepatitis C and HIV Co-Infection. Edited by Mary Ann Cohen, Jack M. Gorman, Jeffrey M. Jacobson, Paul Volberding, and Scott Letendre. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199392742.003.0043.

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Chronic infection with hepatitis C virus (HCV) is a leading cause of end-stage liver disease and is the most common indication for liver transplantation in the United States. Because of shared risk factors, individuals living with HIV infection are disproportionately affected by HCV. Moreover, co-infection with HIV accelerates the natural history of chronic HCV infection, increasing the risk of cirrhosis, hepatocellular carcinoma, hepatic decompensation, and death. Highly effective medications such as direct-acting antivirals (DAA) to cure HCV are now available and have the potential to profoundly improve the health of HIV-HCV-co-infected individuals. However, addressing the many gaps in the HCV care cascade is necessary to fully achieve the benefits of these drugs. This chapter reviews the natural history of HIV-HCV co-infection, the psychiatric comorbidities associated with HCV infection, the evolution of HCV treatment, and the barriers to care that HIV-HCV-co-infected individuals continue to face.

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43

Barnett, Ben J., and Margaret Hoffman-Terry. HIV/Hepatitis Co-infection. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190493097.003.0039.

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Hepatitis B virus (HBV) infection is common in people living with HIV, and all patients with HIV should be screened for HBV infection. The most common route of transmission worldwide is through perinatal or early childhood exposure, but adult transmission of HBV is often by routes similar to those for HIV, including sexual contact and injection drug use. Although it varies by exposure route, approximately 10% of HIV-positive patients also have chronic HBV infection, and up to 90% have serologic evidence of past exposure to HBV. Long-term complications of HBV infection can include cirrhosis, end-stage liver disease, and hepatocellular carcinoma.

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44

Lopes, Eurides, and Jennifer Husson. Solid Organ Transplantation in HIV-Infected Individuals. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190493097.003.0025.

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End-organ disease has become a major cause of morbidity and mortality in HIV-infected patients due to increased life expectancy, increasing the demand for organ transplantation in these patients. The care of HIV-infected transplant recipients warrants a multidisciplinary team approach, including the transplant team, pharmacists, infectious disease specialists, nurses, and patients and their families. The immunosuppression of HIV-infected recipients post-transplant does not appear to further advance HIV disease. The post-transplant risk for HIV-infected recipients of opportunistic infections does not appear to be increased by immunosuppression. However, the overall rate of infections is high, and it is even higher in hepatitis C virus (HCV) co-infected transplant recipients. HIV/HCV co-infected recipients have worse outcomes compared to both liver and kidney HIV-infected recipients.

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45

Leith, Jonathan G. Allogeneic HLA immunization as an HIV-1 vaccine strategy. 2002.

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46

Protocol to estimate mortality from cirrhosis and hepatocellular carcinoma attributable to viral hepatitis B and C. Pan American Health Organization, 2021. http://dx.doi.org/10.37774/9789275123768.

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One of the goals to be achieved by 2030 of the Global Health Sector Strategy on Viral Hepatitis 2016-2021 is to reduce mortality from hepatitis viruses B (HBV) and C (HCV). To measure and monitor it, countries need to implement a systematic process to generate national estimates of mortality from viral hepatitis, which many lack. This document is aimed at the institutions and/or ministries in charge of monitoring progress in each country. The main objective of this protocol is to present simple methods to estimate the proportion of patients with cirrhosis and hepatocellular carcinoma who have HBV and HCV infection, and then calculate the national mortality due to these sequelae attributable to viral hepatitis, preferably within a surveillance system. In addition, a general framework is provided on how the surveillance system should function, how to collect the data, and ethical considerations. The surveillance system will be based on sentinel centers where information will be collected from patients with cirrhosis and hepatocellular carcinoma. These data will be used to estimate the fraction of cirrhosis and hepatocellular carcinoma attributable to HBV and HCV. On the other hand, data will be collected on the number of deaths nationwide from cirrhosis and hepatocellular carcinoma. With this information, mortality from cirrhosis and hepatocellular carcinoma attributable to HBV and HCV will be estimated.

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47

Jadoul, Michel, Laura Labriola, and Eric Goffin. Viral infections in patients on dialysis. Edited by Jonathan Himmelfarb. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0271.

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From the early days of hemodialysis, viral hepatitis has been recognized as common in dialyzed patients.The prevalence and incidence of HBV infection have decreased markedly over the last decades in HD units. Still, the infectivity of HBV is very high. Vaccinating HD patients, preferably prior to starting dialysis, together with the strict application of hygienic precautions and adequate screening of blood donors remains required, together with the segregation of infective (HBV+) patients in a separate dialysis ward. The level of aminotransferases is markedly lower in HD patients than in the general population: any level above the normal range should thus trigger the suspicion of acute hepatitis (viral or not). The treatment of HBV infection in HD patients is rarely required, unless they are scheduled for a kidney transplant.Screening for HCV infection usually relies on a modern ELISA test. The prevalence and incidence of HCV infection in HD patients has also decreased substantially but remains higher than in the general population. The risk of post-transfusional HCV is currently extremely low, at least in western countries. The actual application of basic hygienic precautions is crucial if nosocomial transmission of HCV is to be prevented. These include optimal hand hygiene practices (hydroalcoholic solution use before contact with patient and after gloves withdrawal), the systematic wearing of gloves, to be changed between patients/stations, an adequate separation of the clean and contaminated items and circuits within the HD unit, and regular cleaning/disinfection of potentially contaminated surfaces. The necessity and usefulness to isolate HCV positive patients in a separate dialysis ward has not been demonstrated and is not recommended by current KDIGO guidelines. The field of the treatment of HCV infection is changing rapidly with many orally active drugs, some of which can be used even in dialysis patients.

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48

HIV & HTLV-I Associated Malignancies (Cancer Treatment and Research). Springer, 2001.

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49

A, Sparano Joseph, ed. HIV & HTLV-1 associated malignancies. Boston: Kluwer Academic Publishers, 2001.

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50

Services, CDC U. S. department of Health and Human. Updated U. S. Public Health Service Guidelines for the Managment of Occupational Eposures to HBV, HCV and HIV and Recommendations for Postexposure Prophylaxis. International Medical Publishing, Inc, 2003.

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