Epidemiological patterns of HCV genotypes in KPK region of Pakistan

Paper Details

Research Paper 01/09/2020
Views (349) Download (20)
current_issue_feature_image
publication_file

Epidemiological patterns of HCV genotypes in KPK region of Pakistan

Muhammad Arshad, Ismail Jalil, Fazle Raziq, Muhammad Rafiq, Muhammad Irfan
Int. J. Biosci.17( 3), 273-280, September 2020.
Certificate: IJB 2020 [Generate Certificate]

Abstract

Hepatitis C virus is a significant mediator for development of hepatitis and related cirrhosis and hepatocellular carcinoma. HCV has several genotypes and subtypes. Epidemiology of HCV genotypes is crucial to understand as they play a key role in defining the outcomes of HCV infection. This study was conducted to analyze the epidemiology of HCV genotypes and HCV viral loads in Charsada, Peshawar, Kohat and Frontier Region Peshawar of KPK Pakistan. A total of 1305 HCV infected patients visiting HMC Peshawar were included in this study. Blood samples were collected and HCV RNA quantification and genotyping were carried out through RT-PCR. Viral loads and hameto-biochemical markers were also analyzed for the studied patients. Chi square analysis and odds ratios were used to compare the differences in HCV genotypes prevalence. In total of 1305 samples, 55.7% were males and 44.2% were females. The most prevalent genotype was genotype 3a (44.2%) was highest in both genders followed by genotype 2a (25.4%), 1a (6%) and Untypable genotypes (6%) (p>0.05). Demographic analysis showed that HCV genotype 3a was the dominant genotype in all four regions with the prevalence of 48.2% in FR region, 44% in Peshawar, 44.2% in Charsada and 41.4% in Kohat region of KPK. Medium viral load of 6×105-8×105 IU/ml was the most prevalent load in 41% of the patients. Highly significant association (p<0.0001) was found among the levels of clinical parameter prevalence in studied patients. This study concludes that HCV genotype 3a is the most prevalent genotype in Peshawar, Kohat, Charsada and FR Peshawar regions of KPK. HCV genotype 2a is an emerging genotype in the KPK population.

VIEWS 14

Afridi SQ, Zahid MN, Shabbir MZ, Hussain Z, Mukhtar N, Tipu MY. 2013. Prevalence of HCV genotypes in district Mardan. Virology journal 10(1), 90-94. http://dx.doi.org/10.1186/1743-422X-10-90.

Ali A, Nisar M, Ahmad H, Saif N, Idrees M, Bajwa MA. 2011. Determination of HCV genotypes and viral loads in chronic HCV infected patients of Hazara Pakistan. Virology journal 8(1), 466-472. http://dx.doi.org/10.1186/1743-422X-8-466.

Ali M, Afzal S, Zia A, Hassan A, Khalil AT, Ovais M. 2016. A systematic review of treatment response rates in Pakistani hepatitis C virus patients; current prospects and future challenges. Medicine 95(50).

Ali S, Ali I, Azam S, Ahmad B. 2011. Frequency distribution of HCV genotypes among chronic hepatitis C patients of Khyber Pakhtunkhwa. Virology Journal 8(1), 193-197.

Arshad M, Jalil I, Raza A, Malik S, Dasti JI. 2019. Novel polymorphism in the promoter region of HLA-DQB1 is predictor of anti-HCV therapy response. Jundishapur Journal of Microbiology 12(6), e92217. http://dx.doi.org/10.5812/jjm.92217.

Attaullah S, Khan S, Ali I. 2011. Hepatitis C virus genotypes in Pakistan: a systemic review. Virology Journal 8(1), 433-439.

Cooke G, Lemoine M, Thursz M, Gore C, Swan T, Kamarulzaman A. 2013. Viral hepatitis and the G lobal B urden of D isease: a need to regroup. Journal of Viral Hepatitis 20(9), 600-601. http://dx.doi.org/10.1111/jvh.12123.

Doyle JS, Hellard ME, Thompson AJ. 2012. The role of viral and host genetics in natural history and treatment of chronic HCV infection. Best Practice & Research Clinical Gastroenterology 26(4), 413-427. http://dx.doi.org/10.1016/j.bpg.2012.09.004.

Fried MW, Shiffman ML, Reddy KR, Smith C, Marinos G, Gonçales J. 2002. Peginterferon alfa-2a plus ribavirin for chronic hepatitis C virus infection. New England Journal of Medicine 347(13), 975-982. http://dx.doi.org/10.1056/NEJMoa020047.

Idrees M, Riazuddin S. 2008. Frequency distribution of hepatitis C virus genotypes in different geographical regions of Pakistan and their possible routes of transmission. BMC infectious diseases 8(1), 69-78. http://dx.doi.org/10.1186/1471-2334-8-69.

Inamullah I, Idrees M, Ahmed H, Ali M, Ali L, Ahmed A. 2011. Hepatitis C virus genotypes circulating in district Swat of Khyber Pakhtoonkhaw, Pakistan. Virology journal 8(1), 16-21. http://dx.doi.org/10.1186/1743-422X-8-16.

Jacobson IM, McHutchison JG, Dusheiko G, Di Bisceglie AM, Reddy KR, Bzowej NH. 2011.Telaprevir for previously untreated chronic hepatitis C virus infection. New England Journal of Medicine 364(25), 2405-2416. http://dx.doi.org/ 10.1056/NEJMoa1012912.

Khan N, Akmal M, Hayat M, Umar M, Ullah A, Ahmed I. 2014. Geographic distribution of hepatitis C virus genotypes in pakistan. Hepatitis monthly 14(10), http://dx.doi.org/10.5812/hepatmon.20299.

Koike K. 2014. The oncogenic role of hepatitis C virus. Viruses and Human Cancer, 97-111. http://dx.doi.org/10.1007/978-3-642-38965-8_6.

Lavanchy D. 2009. The global burden of hepatitis C. Liver international 29, 74-81. http://dx.doi.org/ 10.1111/j.1478-3231.2008.01934.x.

Lawitz E, Lalezari JP, Hassanein T, Kowdley KV, Poordad FF, Sheikh AM. 2013. Sofosbuvir in combination with peginterferon alfa-2a and ribavirin for non-cirrhotic, treatment-naive patients with genotypes 1, 2, and 3 hepatitis C infection: a randomised, double-blind, phase 2 trial. The Lancet infectious diseases 13(5), 401-408.

Manns MP, McHutchison JG, Gordon SC, Rustgi VK, Shiffman M, Reindollar R. 2001. Peginterferon alfa-2b plus ribavirin compared with interferon alfa-2b plus ribavirin for initial treatment of chronic hepatitis C: a randomised trial. The Lancet 358 (9286), 958-965.

Mohd Hanafiah K, Groeger J, Flaxman AD, Wiersma ST. 2013. Global epidemiology of hepatitis C virus infection: new estimates of age‐specific antibody to HCV seroprevalence. Hepatology 57(4), 1333-1342. http://dx.doi.org/10.1002/hep.26141.

Neumann AU, Lam NP, Dahari H, Gretch DR, Wiley TE, Layden TJ. 1998. Hepatitis C viral dynamics in vivo and the antiviral efficacy of interferon-α therapy. Science 282(5386), 103-107. http://dx.doi.org/10.1126/science.282.5386.103.

Pradat P, Alberti A, Poynard T, Esteban JI, Weiland O, Marcellin P. 2002. Predictive value of ALT levels for histologic findings in chronic hepatitis C: a European collaborative study. Hepatology 36(4), 973-977. http://dx.doi.org/10.1053/jhep.2002.35530

Smith DB, Bukh J, Kuiken C, Muerhoff AS, Rice CM, Stapleton JT. 2014. Expanded classification of hepatitis C virus into 7 genotypes and 67 subtypes: updated criteria and genotype assignment web resource. Hepatology 59(1), 318-327. http://dx.doi.org/10.1002/hep.26744.

Thrift AP, El-Serag HB, Kanwal F. 2017. Global epidemiology and burden of HCV infection and HCV-related disease. Nature reviews Gastroenterology & hepatology 14(2), 122-130. http://dx.doi.org/ 10.1038/nrgastro.2016.176.

Umer M, Iqbal M. 2016. Hepatitis C virus prevalence and genotype distribution in Pakistan: Comprehensive review of recent data. World journal of gastroenterology 22(4), 1684-1700. http://dx.doi. org/ 10.3748/wjg.v22.i4.1684.

Vilarinho S, Lifton RP. 2016. Pioneering a global cure for chronic hepatitis C virus infection. Cell 167(1), 12-15. http://dx.doi.org/10.1016/j.cell.2016.08.038.

Wasitthankasem R, Vongpunsawad S, Siripon N, Suya C, Chulothok P, Chaiear K. 2015. Genotypic distribution of hepatitis C virus in Thailand and Southeast Asia. PloS one 10(5), e0126764. http://dx.doi.org/10.1371/journal.pone.0126764.