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Books on the topic 'Dengue virus genome replication'

Author: Grafiati

Published: 6 September 2023

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1

Viral genome replication. New York, NY: Springer, 2009.

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2

Norwich), John Innes Symposium (7th 1986. Virus replication and genome interaction: Proceedings of the seventh John Innes Symposium. Cambridge: Company of Biologists, 1987.

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3

John, Innes Symposium (7th 1986 Norwich England). Virus replication and genome interactions: Proceedings of the seventh John Innes Symposium, Norwich, 1986. Cambridge: Company of Biologists, 1987.

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4

K, Wagner Edward, and Wagner Edward K, eds. Basic virology. 3rd ed. Malden, MA: Blackwell Pub., 2008.

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5

1963-, Feng Zhi, and Long Ming, eds. Viral genomes: Diversity, properties, and parameters. Hauppauge, NY: Nova Science Publishers, 2009.

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6

Principles of molecular virology. London: Academic Press, 1993.

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7

Principles of molecular virology. 4th ed. Amsterdam: Elsevier Academic Press, 2005.

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8

Principles of molecular virology. 2nd ed. San Diego: Academic Press, 1997.

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9

Principles of molecular virology. 4th ed. Amsterdam: Elsevier Academic Press, 2005.

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10

Virus Replication and Genome Interaction. The Company of Biologists Limited, 1987.

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11

Bloom, David, Martinez Hewlett, EDWARD K. WAGNER, and David Camerini. Basic Virology. 3rd ed. Blackwell Publishing Limited, 2007.

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12

Chang, Jung-San, and Hung-Chun Chen. Dengue and other viral haemorrhagic fevers. Edited by Vivekanand Jha. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0189_update_001.

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Human infections of dengue viruses are mediated by mosquito bites. The disease spectrum ranges from asymptomatic infection to severe dengue haemorrhagic fever, and dengue shock syndrome. Dengue virus infects a wide range of immune cells that lead to plasma leakage and dengue haemorrhagic fever. Dengue haemorrhagic fever can be complicated with renal involvement, including haematuria, proteinuria, glomerulonephritis, acute kidney injury, and haemolytic uraemic syndrome. Diagnosis can be made by serology, detection of viral proteins by Western blot assay, or detection of the dengue viral genome by reverse transcription-polymerase chain reaction. Treatment is mainly supportive. Renal involvement associated with other viral haemorrhagic fevers has mostly been described as case reports and causality has not been established.

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13

Meng, X. J. Hepatitis E virus. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198570028.003.0048.

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Hepatitis E virus (HEV) is a small, non-enveloped, single-strand, positive-sense RNA virus of approximately 7.2 kb in size. HEV is classified in the family Hepeviridae consisting of four recognized major genotypes that infect humans and other animals. Genotypes 1 and 2 HEV are restricted to humans and often associated with large outbreaks and epidemics in developing countries with poor sanitation conditions, whereas genotypes 3 and 4 HEV infect humans, pigs and other animal species and are responsible for sporadic cases of hepatitis E in both developing and industrialized countries. The avian HEV associated with Hepatitis-Splenomegaly syndrome in chickens is genetically and antigenically related to mammalian HEV, and likely represents a new genus in the family. There exist three open reading frames in HEV genome: ORF1 encodes non-structural proteins, ORF2 encodes the capsid protein, and the ORF3 encodes a small phosphoprotein. ORF2 and ORF3 are translated from a single bicistronic mRNA, and overlap each other but neither overlaps ORF1. Due to the lack of an efficient cell culture system and a practical animal model for HEV, the mechanisms of HEV replication and pathogenesis are poorly understood. The recent identification and characterization of animal strains of HEV from pigs and chickens and the demonstrated ability of cross-species infection by these animal strains raise potential public health concerns for zoonotic HEV transmission. It has been shown that the genotypes 3 and 4 HEV strains from pigs can infect humans, and vice versa. Accumulating evidence indicated that hepatitis E is a zoonotic disease, and swine and perhaps other animal species are reservoirs for HEV. A vaccine against HEV is not yet available.

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14

WAGNER, EDWARD K., and Martinez J. Hewlett. Basic Virology. 2nd ed. Blackwell Publishers, 2003.

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15

Hewlett, Martinez J., David Camerini, and David C. Bloom. Basic Virology. Wiley & Sons, Incorporated, John, 2021.

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16

Hewlett, Martinez J., David Camerini, and David C. Bloom. Basic Virology. Wiley & Sons, Limited, John, 2021.

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17

Hewlett, Martinez J. Basic Virology. Wiley & Sons, Incorporated, John, 2018.

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18

Hewlett, Martinez J., David Camerini, and David C. Bloom. Basic Virology. Wiley & Sons, Incorporated, John, 2021.

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19

WAGNER, EDWARD K. Basic Virology. Wiley & Sons, Incorporated, John, 2018.

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20

Казачинская, Е. И. ВИРУС ДЕНГЕ. Академическое изд-во «Гео», 2021. http://dx.doi.org/10.21782/b978-5-6043022-6-2.

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The review is devoted to the analysis of literature data on the history research of dengue fever, the discovery of the etiological infectious agent of this disease-dengue virus and its serotypes. A taxonomic overview of the }lavivirus family, genome organization, structure and function of viral proteins, mosquito species-viral vectors and virus transmission cycles, theories of its origin are presented. As well as the evolution, characteristics and epidemiology of viral serotypes, cellular receptors for dengue virus penetration, pathogenicity for human and factors for the development of severe disease, induced immunity, applied methods and markers for diagnosis, principles of disease treatment and drug development (more information about monoclonal antibodies-potential therapeutic drugs), vaccine options and their effectiveness are considered. The book is intended for students, graduate students, employees of research institutions and universities, as well as doctors involved in the study of }laviviruses and the problem of differential diagnosis of flavivirus infections.

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21

Principles of Molecular Virology, Student edition with CD -ROM. 3rd ed. Academic Press, 2001.

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22

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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