Significance of serum hepatitis C virus RNA levels in chronic hepatitis C

Hepatitis C virus (HCV) is the main cause of parenteral non-A, non-B hepatitis and serum can be tested for the virus itself by reverse-transcription polymerase chain amplificaton. What of the level of this viraemia? To find out if quantitative study of H CV RNA might be useful clinically we took adv...

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Published inThe Lancet (British edition) Vol. 341; no. 8859; pp. 1501 - 1504
Main Authors Lau, J.Y.N, Davis, G.L, Kniffen, J, Qian, K.-P, Urdea, M.S, Chan, C.S, Neuwald, P.D, Wilber, J.C, Mizokami, M
Format Journal Article
LanguageEnglish
Published London Elsevier Ltd 12.06.1993
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Elsevier Limited
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Abstract Hepatitis C virus (HCV) is the main cause of parenteral non-A, non-B hepatitis and serum can be tested for the virus itself by reverse-transcription polymerase chain amplificaton. What of the level of this viraemia? To find out if quantitative study of H CV RNA might be useful clinically we took advantage of participation in trials of interferon-α in patients with chronic HCV infection and applied a new assay, branched DNA (bDNA) signal amplification. Paired serum and liver biopsy specimens from 47 patients with confirmed chronic HCV infection and evidence of HCV RNA in their serum were studied. The quantitative bDNA assay (detection limit 350000 equivalents/mL [eq/mL]) was positive in 34 sera (sensitivity 72%). Patients who acquired HCV infection by blood transfusion had a higher viraemia (median 2701 000 eq/mL, n=29) than health workers and intravenous drug users (635 000 eq/mL, n=13; p<0·01). Patients with a sustained complete response to interferon-α therapy had lower pre-treatment viraemia levels (median at bDNA cut-off, n=11) than complete responders who relapsed after the drug was stopped (1613 000 eq/mL, n=15; p<0·01) and non-responders (3066 000 eq/mL, n=20; p<0·01). High viraemia levels were not related to the histological diagnosis but were associated with lobular inflammation, lymphoid aggregates, and bileduct lesions. These findings indicate that mode of acquisition is an important determinant of HCV viraemia and that patients with low HCV viraemia levels are more likely to respond to interferon in a sustained fashion.
AbstractList Hepatitis C virus (HCV) is the main cause of parenteral non-A, non-B hepatitis and serum can be tested for the virus itself by reverse-transcription polymerase chain amplificaton. What of the level of this viraemia? To find out if quantitative study of H CV RNA might be useful clinically we took advantage of participation in trials of interferon-α in patients with chronic HCV infection and applied a new assay, branched DNA (bDNA) signal amplification. Paired serum and liver biopsy specimens from 47 patients with confirmed chronic HCV infection and evidence of HCV RNA in their serum were studied. The quantitative bDNA assay (detection limit 350000 equivalents/mL [eq/mL]) was positive in 34 sera (sensitivity 72%). Patients who acquired HCV infection by blood transfusion had a higher viraemia (median 2701 000 eq/mL, n=29) than health workers and intravenous drug users (635 000 eq/mL, n=13; p<0·01). Patients with a sustained complete response to interferon-α therapy had lower pre-treatment viraemia levels (median at bDNA cut-off, n=11) than complete responders who relapsed after the drug was stopped (1613 000 eq/mL, n=15; p<0·01) and non-responders (3066 000 eq/mL, n=20; p<0·01). High viraemia levels were not related to the histological diagnosis but were associated with lobular inflammation, lymphoid aggregates, and bileduct lesions. These findings indicate that mode of acquisition is an important determinant of HCV viraemia and that patients with low HCV viraemia levels are more likely to respond to interferon in a sustained fashion.
Hepatitis C virus (HCV) is the main cause of parenteral non-A, non-B hepatitis and serum can be tested for the virus itself by reverse-transcription polymerase chain amplification. What of the level of this viraemia? To find out if quantitative study of HCV RNA might be useful clinically we took advantage of participation in trials of interferon-alpha in patients with chronic HCV infection and applied a new assay, branched DNA (bDNA) signal amplification. Paired serum and liver biopsy specimens from 47 patients with confirmed chronic HCV infection and evidence of HCV RNA in their serum were studied. The quantitative bDNA assay (detection limit 350,000 equivalents/mL [eq/mL]) was positive in 34 sera (sensitivity 72%). Patients who acquired HCV infection by blood transfusion had a higher viraemia (median 2,701,000 eq/mL, n = 29) than health workers and intravenous drug users (635,000 eq/mL, n = 13; p < 0.01). Patients with a sustained complete response to interferon-alpha therapy had lower pre-treatment viraemia levels (median at bDNA cut-off, n = 11) than complete responders who relapsed after the drug was stopped (1,613,000 eq/mL, n = 15; p < 0.01) and non-responders (3,066,000 eq/mL, n = 20; p < 0.01). High viraemia levels were not related to the histological diagnosis but were associated with lobular inflammation, lymphoid aggregates, and bile-duct lesions. These findings indicate that mode of acquisition is an important determinant of HCV viraemia and that patients with low HCV viraemia levels are more likely to respond to interferon in a sustained fashion.
Hepatitis C virus (HCV) is the main cause of parenteral non-A, non-B hepatitis and serum can be tested for the virus itself by reverse-transcription polymerase chain amplificaton. What of the level of this viraemia? To find out if quantitative study of H CV RNA might be useful clinically we took advantage of participation in trials of interferon-α in patients with chronic HCV infection and applied a new assay, branched DNA (bDNA) signal amplification. Paired serum and liver biopsy specimens from 47 patients with confirmed chronic HCV infection and evidence of HCV RNA in their serum were studied. The quantitative bDNA assay (detection limit 350000 equivalents/mL [eq/mL]) was positive in 34 sera (sensitivity 72%). Patients who acquired HCV infection by blood transfusion had a higher viraemia (median 2701 000 eq/mL, n=29) than health workers and intravenous drug users (635 000 eq/mL, n=13; p<0·01). Patients with a sustained complete response to interferon-α therapy had lower pre-treatment viraemia levels (median at bDNA cut-off, n=11) than complete responders who relapsed after the drug was stopped (1613 000 eq/mL, n=15; p<0·01) and non-responders (3066 000 eq/mL, n=20; p<0·01). High viraemia levels were not related to the histological diagnosis but were associated with lobular inflammation, lymphoid aggregates, and bileduct lesions. These findings indicate that mode of acquisition is an important determinant of HCV viraemia and that patients with low HCV viraemia levels are more likely to respond to interferon in a sustained fashion.
Hepatitis C virus (HCV) is the main cause of parenteral non-A, non-B hepatitis and serum can be tested for the virus itself by reverse-transcription polymerase chain amplification. What of the level of this viraemia? To find out if quantitative study of HCV RNA might be useful clinically we took advantage of participation in trials of interferon-alpha in patients with chronic HCV infection and applied a new assay, branched DNA (bDNA) signal amplification. Paired serum and liver biopsy specimens from 47 patients with confirmed chronic HCV infection and evidence of HCV RNA in their serum were studied. The quantitative bDNA assay (detection limit 350,000 equivalents/mL [eq/mL]) was positive in 34 sera (sensitivity 72%). Patients who acquired HCV infection by blood transfusion had a higher viraemia (median 2,701,000 eq/mL, n = 29) than health workers and intravenous drug users (635,000 eq/mL, n = 13; p &lt; 0.01). Patients with a sustained complete response to interferon-alpha therapy had lower pre-treatment viraemia levels (median at bDNA cut-off, n = 11) than complete responders who relapsed after the drug was stopped (1,613,000 eq/mL, n = 15; p &lt; 0.01) and non-responders (3,066,000 eq/mL, n = 20; p &lt; 0.01). High viraemia levels were not related to the histological diagnosis but were associated with lobular inflammation, lymphoid aggregates, and bile-duct lesions. These findings indicate that mode of acquisition is an important determinant of HCV viraemia and that patients with low HCV viraemia levels are more likely to respond to interferon in a sustained fashion.
Author Chan, C.S
Urdea, M.S
Kniffen, J
Wilber, J.C
Qian, K.-P
Lau, J.Y.N
Davis, G.L
Neuwald, P.D
Mizokami, M
Author_xml – sequence: 1
  givenname: J.Y.N
  surname: Lau
  fullname: Lau, J.Y.N
  organization: Section of Hepatobiliary Diseases, Division of Gastroenterology, Hepatology and Nutrition, Department of Medicine, University of Florida, Gainesville, Florida 32610, U.S.A
– sequence: 2
  givenname: G.L
  surname: Davis
  fullname: Davis, G.L
  organization: Section of Hepatobiliary Diseases, Division of Gastroenterology, Hepatology and Nutrition, Department of Medicine, University of Florida, Gainesville, Florida 32610, U.S.A
– sequence: 3
  givenname: J
  surname: Kniffen
  fullname: Kniffen, J
  organization: Section of Hepatobiliary Diseases, Division of Gastroenterology, Hepatology and Nutrition, Department of Medicine, University of Florida, Gainesville, Florida 32610, U.S.A
– sequence: 4
  givenname: K.-P
  surname: Qian
  fullname: Qian, K.-P
  organization: Section of Hepatobiliary Diseases, Division of Gastroenterology, Hepatology and Nutrition, Department of Medicine, University of Florida, Gainesville, Florida 32610, U.S.A
– sequence: 5
  givenname: M.S
  surname: Urdea
  fullname: Urdea, M.S
  organization: Chiron Corporation, Emeryville, California, United States
– sequence: 6
  givenname: C.S
  surname: Chan
  fullname: Chan, C.S
  organization: Chiron Corporation, Emeryville, California, United States
– sequence: 7
  givenname: P.D
  surname: Neuwald
  fullname: Neuwald, P.D
  organization: Chiron Corporation, Emeryville, California, United States
– sequence: 8
  givenname: J.C
  surname: Wilber
  fullname: Wilber, J.C
  organization: Chiron Corporation, Emeryville, California, United States
– sequence: 9
  givenname: M
  surname: Mizokami
  fullname: Mizokami, M
  organization: Second Department of Medicine, Nagoya City University Medical School, Nagoya, Japan
BackLink http://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=4786075$$DView record in Pascal Francis
https://www.ncbi.nlm.nih.gov/pubmed/8099380$$D View this record in MEDLINE/PubMed
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Sat Sep 28 08:34:25 EDT 2024
Sun Oct 29 17:10:06 EDT 2023
Fri Feb 23 02:26:41 EST 2024
IsPeerReviewed true
IsScholarly true
Issue 8859
Keywords Infection
Virus
Human
Chronic
RNA
Viral disease
Digestive diseases
Exploration
Hepatic disease
Serum
Hepatitis C virus
Viral hepatitis C
Language English
License CC BY 4.0
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Lancet
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Chomczynski (10.1016/0140-6736(93)90635-T_BIB16) 1987; 162
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Mishiro (10.1016/0140-6736(93)90635-T_BIB13) 1990; 336
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Snippet Hepatitis C virus (HCV) is the main cause of parenteral non-A, non-B hepatitis and serum can be tested for the virus itself by reverse-transcription polymerase...
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SubjectTerms Adult
Aged
Amplification
Base Sequence
Biological and medical sciences
Biopsy
Blood transfusion
Chronic infection
Clinical trials
Deoxyribonucleic acid
DNA
Drug abuse
Female
Hepacivirus - genetics
Hepacivirus - isolation & purification
Hepatitis
Hepatitis C
Hepatitis C - blood
Hepatitis C - drug therapy
Hepatitis C - microbiology
Hepatitis, Chronic - blood
Hepatitis, Chronic - drug therapy
Hepatitis, Chronic - microbiology
Human viral diseases
Humans
Infections
Infectious diseases
Interferon
Interferon alpha-2
Interferon-alpha - therapeutic use
Intravenous administration
Lesions
Liver
Male
Medical personnel
Medical research
Medical sciences
Middle Aged
Molecular Sequence Data
Non-A, non-B hepatitis
Patients
Quantitative research
Recombinant Proteins
Ribonucleic acid
RNA
RNA viruses
RNA, Viral - blood
Viral diseases
Viral hepatitis
Viremia
Viremia - microbiology
Viruses
Workers
α-Interferon
Title Significance of serum hepatitis C virus RNA levels in chronic hepatitis C
URI https://dx.doi.org/10.1016/0140-6736(93)90635-T
https://www.ncbi.nlm.nih.gov/pubmed/8099380
https://www.proquest.com/docview/198946895
https://www.proquest.com/docview/2148913741
https://search.proquest.com/docview/75776608
Volume 341
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