Structure and Molecular Virology

McGarvey, Michael J.; Houghton, Michael

doi:10.1002/9780470987131.ch24

Cited by 5 publications

(7 citation statements)

References 356 publications

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“…Hepatitis C (HCV) is a small RNA virus that usually causes chronic hepatitis in infected humans . In some cases, this can progress to liver cirrhosis and hepatocellular carcinoma and the virus is therefore a significant cause of global mortality .…”

Section: Introductionmentioning

confidence: 99%

“…Hepatitis C (HCV) is a small RNA virus that usually causes chronic hepatitis in infected humans. 1 In some cases, this can progress to liver cirrhosis and hepatocellular carcinoma 2 and the virus is therefore a significant cause of global mortality. 3 However, in recent years, new therapies for HCV have been developed which directly target the virus and achieve an effective cure in over 90% of treated patients.…”

Section: Introductionmentioning

confidence: 99%

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The testing of people with any risk factor for hepatitis C in community pharmacies is cost‐effective

Buchanan

Cooper

Grellier

et al. 2019

Journal of Viral Hepatitis

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New antiviral drugs with high efficacy mean the hepatitis C virus (HCV) can now be eliminated. To achieve this, it is necessary to identify undiagnosed cases of HCV. However, the costs of testing should be considered when judging the overall cost‐effectiveness of treatment. This study describes the cost‐effectiveness of a community pharmacy testing service in a population of people at risk of HCV living on the Isle of Wight (United Kingdom). Dry blood spot testing was conducted in anyone with a known risk factor for HCV in 20 community pharmacies. The outcomes and costs were entered into a Markov model. Cost and health utilities from the model were used to calculate an incremental cost‐effectiveness ratio (ICER). In 24 months, 186 tests were conducted, 13 were positive for HCV RNA and six of these (46%) received treatment during the follow‐up period. All achieved a sustained virological response at 3 months. The overall cost of the testing and treatment intervention was £242 183, and the ICER for the service was £3689 per quality‐adjusted life year (QALY) gained. If screening had been restricted to just people with a history of injecting drug use (PWID) the ICER would have been £4865 per QALY gained. The service was effective at identifying people with HCV infection, and despite the additional cost of targeted testing, its cost‐effectiveness was below the commonly accepted thresholds. In this setting, restricting targeted testing to PWID would not improve the cost‐effectiveness.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

The testing of people with any risk factor for hepatitis C in community pharmacies is cost‐effective

Buchanan

Cooper

Grellier

et al. 2019

Journal of Viral Hepatitis

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show abstract

Section: Life Cycle and Pathogenicity Of Hcvmentioning

confidence: 99%

“…This polyprotein cleaves at the N-terminal side of three structural proteins, the nucleocapsid (core), envelope 1 (E1) and envelope 2 (E2), all of which are involved in the architectural organization of HCV. At the carboxylterminal side, the polyprotein cleaves to six nonstructural proteins, NS2, NS3, NS4 (NS4A and NS4B), NS5 (NS5A and NS5B) and NS6, which are responsible for the life cycle of the virus [9].After entering a susceptible host, HCV invades, infects and replicates within the blood stream, repeating the process in various tissues, as well as in peripheral B and T lymphocytes, as it proceeds to the liver by tropism, passing through various tissues such as those of the pancreas, thyroid, adrenal glands, spleen and bone marrow [10][11][12]. Since HCV can also directly infect the lymphatic tissue, its stimulation can lead to the development of B-cell lymphomas [13].…”

mentioning

confidence: 99%

Pathogenesis of hepatitis C: HCV consensus 2007

Viso¹

2007

Braz J Infect Dis

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The chronic hepatitis C virus (HCV) infects approximately 130 million people worldwide [1]. It is estimated that approximately 15% of HCV-infected individuals eliminate the virus spontaneously, that 25% develop a mild form of the disease, and that 60% develop the chronic progressive form [2]. The elimination or persistence of HCV infection depends on the balance between the effectiveness, specificity and rapidity of the innate and adaptive immune responses, as well as on the HCV replication rate [3]. Persistence of HCV can also be caused by infection at privileged (extrahepatic) sites, viral inhibition of antigen presentation, selective immune suppression, negative regulation of HCV gene expression, viral mutations, immune exhaustion of T cells and the incomplete differentiation of memory T cells [4,5].Fibrosis is the principal complication of chronic hepatitis C, and it is estimated that 20% of patients develop cirrhosis over a period of 10, 20 or 30 years [2,6]. The progression of fibrosis increases morbidity and mortality in chronic hepatitis C [7], since it can lead to death due to complications caused by cirrhosis or hepatocarcinoma [2].Various studies have associated the progression of fibrosis in hepatitis C with diverse factors such as: the kinetics and pathogenicity of HCV; host-HCV interaction; intrinsic host factors such as demographic profile, body mass index and diabetes mellitus; host exposure to external factors; and the form of HCV acquisition. Life Cycle and Pathogenicity of HCVBelonging to the Flaviviridae family, HCV is a small enveloped virus [8]. Its genome consists of one RNA molecule that is composed of two terminal regions, 5'-and 3'-untranslated regions, and between these there is a single open reading frame that encodes a polyprotein with approximately 3000 amino acids. This polyprotein cleaves at the N-terminal side of three structural proteins, the nucleocapsid (core), envelope 1 (E1) and envelope 2 (E2), all of which are involved in the architectural organization of HCV. At the carboxylterminal side, the polyprotein cleaves to six nonstructural proteins, NS2, NS3, NS4 (NS4A and NS4B), NS5 (NS5A and NS5B) and NS6, which are responsible for the life cycle of the virus [9].After entering a susceptible host, HCV invades, infects and replicates within the blood stream, repeating the process in various tissues, as well as in peripheral B and T lymphocytes, as it proceeds to the liver by tropism, passing through various tissues such as those of the pancreas, thyroid, adrenal glands, spleen and bone marrow [10][11][12]. Since HCV can also directly infect the lymphatic tissue, its stimulation can lead to the development of B-cell lymphomas [13]. It is known that the liver is the principal site of HCV replication, and various studies have shown that this virus infects approximately 10% of hepatic cells [5]. Infection with HCV at extrahepatic sites can promote the appearance of HCV variants [14,15], thereby decreasing the chance that the immune system will recognize the virus.To enter the host ...

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“…A poliproteína viral é clivada em seu pólo N-terminal e origina três proteínas estruturais (core, E1, E2), que estão envolvidas na organização arquitetural do HCV. No pólo C-terminal a poliproteína é clivada em seis proteínas não estruturais (NS2, NS3, NS4A, NS4B, NS5A, NS5B e NS6), responsáveis pelo ciclo biológico do vírus (McGarvey et al, 1998). …”

Section: Estrutura E Organização Genômica Do Hcvunclassified

Influência da infecção pelo vírus linfotrópico humano tipo 1 (HTLV-1) em parâmetros laboratoriais de pacientes com hepatite C crônica

Cardoso¹

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Structure and Molecular Virology

Cited by 5 publications

References 356 publications

The testing of people with any risk factor for hepatitis C in community pharmacies is cost‐effective

The testing of people with any risk factor for hepatitis C in community pharmacies is cost‐effective

Pathogenesis of hepatitis C: HCV consensus 2007

Influência da infecção pelo vírus linfotrópico humano tipo 1 (HTLV-1) em parâmetros laboratoriais de pacientes com hepatite C crônica

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