Analysis of the HCV genome has demonstrated extremely high heterogeneity in both structural and nonstructural coding regions and there are at least six different genotypes that have generally been divided into several subtypes. Of the 6 different Hepatitis genotypes, genotypes 1-3 is common worldwide, type 1a and 1b are the most common, accounting for about 60% of global infections. They predominate in Northern Europe, Southern and Eastern Europe, North America, and Japan respectively. Type 2 is less frequently represented than type 1. Type 3 is endemic in south-east Asia and is variably distributed in different countries. The determination of the infecting genotype is important for the prediction of response to antiviral treatment; genotype 1 is generally associated with a poor response to interferon alone, unlike genotypes 2 and 3 which are associated with better responses. A total of 238 plasma samples were received from patients attending gastroenterology department across India for treatment from March 2008 – Aug 2010. The samples were analyzed for viral load by real time PCR by Taqman principle. HCV genotyping was carried out on the samples whose viral load was more than 300IU/ml (limit of detection as per the kit). Qiagen RNA columns were used for RNA extraction, followed by reverse transcription (Promega) and genotyping was performed by conventional PCR. Out of 238 samples, 117 were positive for 3a, 44 samples were load negative, 43 samples were non- typable due to less viral load i.e. less than 1000 IU/ml. 26 were type 1a, 107 were 3a, and 11 were 2a.
| DOI | 10.11648/j.cmr.20150405.13 |
| Published in | Clinical Medicine Research (Volume 4, Issue 5, September 2015) |
| Page(s) | 139-142 |
| Creative Commons |
This is an Open Access article, distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution and reproduction in any medium or format, provided the original work is properly cited. |
| Copyright |
Copyright © The Author(s), 2024. Published by Science Publishing Group |
HCV, PCR, Reverse Transcription, Genotyping
| [1] | Ulrike Seifert, Heike Liermann, Vito Racanelli, Anne Halenius, Manfred Wiese, Heiner Wedemeyer, Thomas Ruppert, Kay Rispeter, Peter Henklein, Alice Sijts, Hartmut Hengel, Peter-M. Kloetzel and Barbara Reherm. Hepatitis C virus mutation affects proteasomal epitope processing. J Clin Invest. 2004:114 (2):250–259. |
| [2] | Houghton M. Hepatitis C viruses. In: Fields BN, Knipe DM, Howley PM, eds. Fields Virology, 3rd ed. Philadelphia, Lippincott - Raven, 1996:1035-105. |
| [3] | Jean-Franc¸ois Cantaloube, Pierre Gallian, Houssam Attoui, Philippe Biagini, Philippe De Micco, and Xavier de Lamballerie. Genotype Distribution and Molecular Epidemiology of Hepatitis C Virus in Blood Donors from Southeast France. Journal of Clinical Microbiology, Aug. 2005: 3624–3629. |
| [4] | Yi-Wei Tang a,b, Haijing Li a, Ann Roberto c Diane Warner c, Belinda Yen-Lieberman. Detection of hepatitis C virus by a user-developed reverse transcriptase-PCR and use of amplification products for subsequent genotyping. Journal of Clinical Virology 2004, 31: 148–152. |
| [5] | Amjad Ali1, Habib Ahmed, Muhammad Idrees. Molecular epidemiology of Hepatitis C virus genotypes in Khyber Pakhtoonkhaw of Pakistan. Virology Journal 2010: 7:203. |
| [6] | Sandra S. Richter Journal Clinical Microbiology December 2002, vol. 40 no. 12: 4407-4412. |
| [7] | Ping Qiu, Xiao-Yan Cai, Wei Ding, Qing Zhang, Ellie D Norris and Jonathan R Greene HCV genotyping using statistical classification approach. Journal of Biomedical Science 2009, 16:62 doi:10.1186/1423-0127-16-62. |
| [8] | Raymond P. Podzorski, PhD. Molecular Testing in the Diagnosis and Management of Hepatitis C Virus Infection. Arch Pathol Lab Med - 2002;126:285 – 290. |
| [9] | Stephen L. Chen 1 2 and Timothy R. Morgan. The Natural History of Hepatitis C Virus (HCV) Infection Int J Med Sci. 2006; 3(2): 47 – 52. |
| [10] | Yoann Morice, Jean-Franc¸ois Cantaloube, Ste´phanie Beaucourt, Laetitia Barbotte, Sija De Gendt, Fernando Lopes Goncales, Lesley Butterworth, Graham Cooksley, Robert G. Gish, Michel Beaugrand, Fabian Fay, Oscar Fay, Jorge E. Gonzalez, Regina Maria Bringel Martins, Daniel Dhumeaux, Bart Vanderborght, Lieven Stuyver, Erwin Sablon, Xavier de Lamballerie, and Jean-Michel Pawlotsky. Molecular Epidemiology of Hepatitis C Virus Subtype 3a in Injecting Drug Users.Journal of Medical Virology 2006, 78:1296–1303. |
| [11] | S. Chaudhuria, S. Dasa, A. Chowdhuryc, A. Santrac,S.K. Bhattacharyab,d, T.N. Naik Molecular epidemiology of HCV infection among acute and chronic liver disease patients in Kolkata, India. Journal of Clinical Virology 2005, 32: 38–46. |
| [12] | Tomoyoshi ohno, Masashi Mizokami, Rong-Rong Wu, Mohamed G. Saleh, Ken-Ichi ohba, Etsuro Orito, Motokazu Mukaide, Roger Williams, and Johnson Y. N. Lau. New Hepatitis C Virus (HCV) Genotyping System That Allows for Identification of HCV Genotypes 1a, 1b, 2a, 2b, 3a, 3b, 4, 5a, and 6a. Journal of Clinical Microbiology. Jan. 1997, Vol. 35, No. 1: 201–207. |
| [13] | Gower E, Estes C, Blach S, Razavi-Shearer K, Razavi H. Global epidemiology and genotype distribution of the hepatitis C virus infection. J Hepatol. 2014 Nov;61(1 Suppl):S45-57. |
| [14] | Mohd Hanafiah K, Groeger J, Flaxman AD, Wiersma ST. Global epidemiology of hepatitis C virus infection: new estimates of age-specific antibody to HCV seroprevalence. Hepatology. 2013 Apr;57(4):1333-42. |
| [15] | Scott D. Holmberg, Hepatitis C Virus and the Infectious Diseases Community. Clinical Infectious Diseases 2012;55(S1):S10–15. |
APA Style
Pushpalatha Manjunatha, Satish Kumar Amarnath, P. K. Menon, Arun Kumar H. R., Bala Satish M., et al. (2015). Molecular Epidemiology of Hepatitis C Virus and Predominant Genotype in India. Clinical Medicine Research, 4(5), 139-142. https://doi.org/10.11648/j.cmr.20150405.13
ACS Style
Pushpalatha Manjunatha; Satish Kumar Amarnath; P. K. Menon; Arun Kumar H. R.; Bala Satish M., et al. Molecular Epidemiology of Hepatitis C Virus and Predominant Genotype in India. Clin. Med. Res. 2015, 4(5), 139-142. doi: 10.11648/j.cmr.20150405.13
AMA Style
Pushpalatha Manjunatha, Satish Kumar Amarnath, P. K. Menon, Arun Kumar H. R., Bala Satish M., et al. Molecular Epidemiology of Hepatitis C Virus and Predominant Genotype in India. Clin Med Res. 2015;4(5):139-142. doi: 10.11648/j.cmr.20150405.13
Share This Article
Twitter
Linked In
Facebook
Copy
Download@article{10.11648/j.cmr.20150405.13,
author = {Pushpalatha Manjunatha and Satish Kumar Amarnath and P. K. Menon and Arun Kumar H. R. and Bala Satish M. and S. J. Sabarish Babu},
title = {Molecular Epidemiology of Hepatitis C Virus and Predominant Genotype in India},
journal = {Clinical Medicine Research},
volume = {4},
number = {5},
pages = {139-142},
doi = {10.11648/j.cmr.20150405.13},
url = {https://doi.org/10.11648/j.cmr.20150405.13},
eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.cmr.20150405.13},
abstract = {Analysis of the HCV genome has demonstrated extremely high heterogeneity in both structural and nonstructural coding regions and there are at least six different genotypes that have generally been divided into several subtypes. Of the 6 different Hepatitis genotypes, genotypes 1-3 is common worldwide, type 1a and 1b are the most common, accounting for about 60% of global infections. They predominate in Northern Europe, Southern and Eastern Europe, North America, and Japan respectively. Type 2 is less frequently represented than type 1. Type 3 is endemic in south-east Asia and is variably distributed in different countries. The determination of the infecting genotype is important for the prediction of response to antiviral treatment; genotype 1 is generally associated with a poor response to interferon alone, unlike genotypes 2 and 3 which are associated with better responses. A total of 238 plasma samples were received from patients attending gastroenterology department across India for treatment from March 2008 – Aug 2010. The samples were analyzed for viral load by real time PCR by Taqman principle. HCV genotyping was carried out on the samples whose viral load was more than 300IU/ml (limit of detection as per the kit). Qiagen RNA columns were used for RNA extraction, followed by reverse transcription (Promega) and genotyping was performed by conventional PCR. Out of 238 samples, 117 were positive for 3a, 44 samples were load negative, 43 samples were non- typable due to less viral load i.e. less than 1000 IU/ml. 26 were type 1a, 107 were 3a, and 11 were 2a.},
year = {2015}
}
TY - JOUR T1 - Molecular Epidemiology of Hepatitis C Virus and Predominant Genotype in India AU - Pushpalatha Manjunatha AU - Satish Kumar Amarnath AU - P. K. Menon AU - Arun Kumar H. R. AU - Bala Satish M. AU - S. J. Sabarish Babu Y1 - 2015/08/03 PY - 2015 N1 - https://doi.org/10.11648/j.cmr.20150405.13 DO - 10.11648/j.cmr.20150405.13 T2 - Clinical Medicine Research JF - Clinical Medicine Research JO - Clinical Medicine Research SP - 139 EP - 142 PB - Science Publishing Group SN - 2326-9057 UR - https://doi.org/10.11648/j.cmr.20150405.13 AB - Analysis of the HCV genome has demonstrated extremely high heterogeneity in both structural and nonstructural coding regions and there are at least six different genotypes that have generally been divided into several subtypes. Of the 6 different Hepatitis genotypes, genotypes 1-3 is common worldwide, type 1a and 1b are the most common, accounting for about 60% of global infections. They predominate in Northern Europe, Southern and Eastern Europe, North America, and Japan respectively. Type 2 is less frequently represented than type 1. Type 3 is endemic in south-east Asia and is variably distributed in different countries. The determination of the infecting genotype is important for the prediction of response to antiviral treatment; genotype 1 is generally associated with a poor response to interferon alone, unlike genotypes 2 and 3 which are associated with better responses. A total of 238 plasma samples were received from patients attending gastroenterology department across India for treatment from March 2008 – Aug 2010. The samples were analyzed for viral load by real time PCR by Taqman principle. HCV genotyping was carried out on the samples whose viral load was more than 300IU/ml (limit of detection as per the kit). Qiagen RNA columns were used for RNA extraction, followed by reverse transcription (Promega) and genotyping was performed by conventional PCR. Out of 238 samples, 117 were positive for 3a, 44 samples were load negative, 43 samples were non- typable due to less viral load i.e. less than 1000 IU/ml. 26 were type 1a, 107 were 3a, and 11 were 2a. VL - 4 IS - 5 ER -
Information
Email: