Refine your search
Collections
Co-Authors
A B C D E F G H I J K L M N O P Q R S T U V W X Y Z All
Swaroop, Suchit
- Role of Interleukin-I Super Family in Progression of Osteoarthritis
Abstract Views :224 |
PDF Views:129
Authors
Amit Kumar
1,
Md Arshad
2,
Ajai Singh
3,
Asif Jafri
4,
Sabir Ali
5,
Manish Yadav
5,
Suchit Swaroop
1
Affiliations
1 Experimental and Public Health Laboratory, Department of Zoology, University of Lucknow, Lucknow – 226007, IN
2 Molecular Endocrinology Lab, Department of Zoology, University of Lucknow, Lucknow-226007, IN
3 Department of Orthopaedics, King George Medical University, Lucknow – 226003, IN
4 Molecular Endocrinology Lab, Department of Zoology, University of Lucknow, Lucknow – 226007, IN
5 Department of Orthopedics, King George Medical University, Lucknow – 226003, IN
1 Experimental and Public Health Laboratory, Department of Zoology, University of Lucknow, Lucknow – 226007, IN
2 Molecular Endocrinology Lab, Department of Zoology, University of Lucknow, Lucknow-226007, IN
3 Department of Orthopaedics, King George Medical University, Lucknow – 226003, IN
4 Molecular Endocrinology Lab, Department of Zoology, University of Lucknow, Lucknow – 226007, IN
5 Department of Orthopedics, King George Medical University, Lucknow – 226003, IN
Source
Journal of Ecophysiology and Occupational Health, Vol 17, No 1-2 (2017), Pagination: 9-16Abstract
Osteoarthritis (OA) is considered as multifactorial disorder characterized by erosion of articular cartilage, tightening of joint space, subchondral bone remodelling and internal synovial inflammation. OA reduces joint function progressively as a person gets older. The most important group of the cytokines or chemokines are pre-dominantly involving in the early progression of the disease includes IL-1, IL-6, IL-18 and TNF-a, etc. IL-1 family of cytokines are known to be strongest stimulus for progressive synthesis of Matrix Metallo Proteinases (MMPs). Large number of immune cells, chondrocytes and endothelial cells potentially secrete IL-1 with diverse effect on number of diseases. This review highlights the association of IL-1 family cytokine in OA.Keywords
Cytokine, IL-1 Family, Mode of Action, Osteoarthritis.- Association of Cytokine TNF-α in Development of Osteoarthritis: A Comprehensive Study
Abstract Views :242 |
PDF Views:119
Authors
Affiliations
1 Department of Zoology, Experimental and Public Health Laboratory, University of Lucknow, Lucknow − 226007, IN
2 Department of Zoology, Molecular Endocrinology Lab, University of Lucknow, Lucknow − 226007, IN
3 Department of Orthopaedics, King George Medical University, Lucknow − 226003, IN
1 Department of Zoology, Experimental and Public Health Laboratory, University of Lucknow, Lucknow − 226007, IN
2 Department of Zoology, Molecular Endocrinology Lab, University of Lucknow, Lucknow − 226007, IN
3 Department of Orthopaedics, King George Medical University, Lucknow − 226003, IN
Source
Journal of Ecophysiology and Occupational Health, Vol 18, No 3-4 (2018), Pagination: 117-121Abstract
Osteo-Arthritis (OA) is a disease of joints affecting the normal functions of joint and causes physical disability. Many factors are responsible for development of osteoarthritis including over age, obesity, gender, drug abuse, over load on joints and genetic factors. OA causes health problems and impairs the quality of life with increased economic burden across the world. Apart from the pro-inflammatory role of cytokine Interleukin-1 (IL-1) in osteoarthritis, Tumor necrosis factor-alpha (TNF-α) is also involved in the progression of osteoarthritis. Members of TNF family are secreted from lymphocytes and natural killer cells but in OA patients it is also secreted from chondrocyte cells to influence the catabolic processes in Extra Cellular Matrix (ECM) by inducing the activity of matrix metaloproteinases (MMPs). In promoter region, most of the Single nucleotide polymorphisms (SNPs) of TNF-α located on -863, -857, -308, and -238. These SNPs are involved in various diseases including OA, rheumatoid Arthritis, systemic lupus erythematosus etc. Significance association of SNP -G308A of the TNF-α gene in OA has been observed in various studies. Aim of this mini review is to conclude the fundamental roles of TNF-α cytokine in patients with OA.Keywords
Cytokine, Gene Variants, Osteoarthritis, Pathophysiology, TNF-α.References
- Kumar A, Arshad M, Singh A, Jafri A, Ali S, Yadav M, Swaroop S. Role of Interleukin-1 Super Family in Progression of Osteoarthritis, Journal of Ecophysiology and Occupational Health. 2017; 17:9−16.
- Galil SMA, Ezzeldin N, Fawzy F, El-Boshy M. The SingleNucleotide Polymorphism (SNP) of tumor necrosis factor α− 308G/A gene is associated with early-onset primary knee osteoarthritis in an Egyptian female population, Clinical Rheumatology. 2017; 36:2525−30. https://doi.org/10.1007/s10067-017-3727-1. PMid: 28695434.
- Aoki Y, Ohtori S, Ino H, Douya H, Ozawa T, Saito T, Takahashi K. Disc inflammation potentially promotes axonal regeneration of dorsal ischolar_main ganglion neurons innervating lumbar intervertebral disc in rats, Spine. 2004; 29:2621−26. https://doi.org/10.1097/01.brs.0000146051.11574.b4. PMid:15564910.
- Ji B, Shi J, Cheng X, Zhou J, Zhou Q, Cao C, Pang J. Association analysis of two candidate polymorphisms in the tumour necrosis factor-α gene with osteoarthritis in a Chinese population, International Orthopaedics. 2013; 37:2061−63. https://doi.org/10.1007/s00264-013-1931-4. PMid: 23748461, PMCid: PMC3779584.
- Bodmer JL, Schneider P, Tschopp J. The molecular architecture of the TNF superfamily, Trends in Biochemical Sciences. 2002; 27:19−26. https://doi.org/10.1016/S0968-0004(01)01995-8.
- Varfolomeev E, Goncharov T, Fedorova AV, Dynek JN, Zobel K, Deshayes K, Vucic D. c-IAP1 and c-IAP2 are critical mediators of tumor necrosis factor α (TNFα)-induced NF-κB activation, Journal of Biological Chemistry. 2008; 283:24295−99. https:// doi.org/10.1074/jbc.C800128200. PMid: 18621737, PMCid: PMC3259840.
- Farahat MN, Yanni G, Poston R, Panayi GS. Cytokine expression in syno-vial membranes of patients with rheumatoid arthritis and osteoarthritis, Annals of the Rheu-Matic Diseases. 1993; 52:870. https://doi.org/10.1136/ard.52.12.870.
- Fernandes JC, Martel‐Pelletier J, Pelletier JP. The role of cytokines in os-teoarthritis pathophysiology, Biorheology. 2002; 39:237−46. PMid: 12082286.
- Guerne PA, Carson DA, Lotz M. IL-6 production by human articular chon-drocytes.Modulation of its synthesis by cytokines, growth factors, and hormones in vitro, The Journal of Immunology. 1990; 144:499−505. PMid: 2104896.
- Joos H, Wildner A, Hogrefe C, Reichel H, Brenner RE. Interleukin-1 beta and tumor necrosis factor alpha inhibit migration activity of chondrogenic progenitor cells from non-fibrillated osteoarthritic cartilage, Arthritis Research and Therapy. 2013; 15:R119. https://doi.org/10.1186/ar4299. PMid: 24034344, PMCid: PMC3978440.
- Idriss HT, Naismith JH. TNFα and the TNF receptor superfamily: Struc-ture‐function relationship (s)”, Microscopy Research and Technique. 2000; 50:184−95. https://doi.org/10.1002/10970029(20000801)50:3<184::AID-JEMT2>3.0.CO;2-H.
- Hajeer AH, Hutchinson IV. TNF‐α gene polymorphism: Clinical and bio-logical implications, Microscopy Research and Technique. 2000; 50:216−28. https://doi.org/10.1002/10970029(20000801)50:3<216::AID-JEMT5>3.0.CO;2-Q.
- Han L, Song JH, Yoon JH, Park YG, Lee SW, Choi YJ, ... Park WS. TNF-α and TNF-β Polymorphisms are Associated with Susceptibility to Osteoarthri-tis in a Korean Population, Korean Journal of Pathology. 2012; 46:30. https://doi.org/10.4132/KoreanJPathol.2012.46.1.30. PMid: 23109975, PMCid: PMC3479703.
- Campbell J, Ciesielski CJ, Hunt AE, Horwood NJ, Beech JT, Hayes LA, ... Foxwell BM. A novel mechanism for TNF-α regulation by p38 MAPK: In-volvement of NF-κB with implications for therapy in rheumatoid arthritis, The Journal of Immunology. 2004; 173:6928−37. https://doi.org/10.4049/jimmunol.173.11.6928. PMid: 15557189.
- Xue J, Wang J, Liu Q, Luo A. Tumor necrosis factor-α induces ADAMTS-4 expression in human osteoarthritis chondrocytes, Molecular Medicine Reports. 2013; 8:1755−60. https://doi.org/10.3892/mmr.2013.1729. PMid: 24126638.
- Marcu BK, Otero M, Olivotto E, Maria Borzi R, Goldring BM. NF-κB sig-naling: Multiple angles to target OA, Current Drug Targets. 2010; 11:599−613. https://doi.org/10.2174/138945010791011938. PMid: 20199390, PMCid: PMC3076145
- Kalichman L, Hernández-Molina G. Hand osteoarthritis: An epidemiological perspective, In Seminars in Arthritis and Rheumatism. 2010; 39:465−76. https://doi.org/10.1016/j.semarthrit.2009.03.001. PMid: 19482338.
- Kapoor M, Martel-Pelletier J, Lajeunesse D, Pelletier JP, Fahmi H. Role of proinflammatory cytokines in the pathophysiology of osteoarthritis, Nature Reviews Rheu-matology. 2011; 7:33. https://doi.org/10.1038/nrrheum.2010.196. PMid: 21119608.
- Kou S, Wu Y. Meta-analysis of tumor necrosis factor alpha308 polymorphism and knee osteoarthritis risk, BMC Musculoskeletal Disorders. 2014; 15:373. https://doi.org/10.1186/1471-2474-15-373. PMid: 25398219, PMCid: PMC4289255.
- Krasnokutsky S, Attur M, Palmer G, Samuels J, Abramson SB. Current concepts in the pathogenesis of osteoarthritis, Osteoarthritis and Cartilage. 2008; 16:S1−S3. https://doi.org/10.1016/j.joca.2008.06.025. PMid: 18723377.
- O’Donnell MA, Legarda-Addison D, Skountzos P, Yeh WC, Ting AT. Ubiquitination of RIP1 regulates an NF-κB-independent cell-death switch in TNF signal-ing, Current Biology. 2007; 17:418−24. https://doi.org/10.1016/j.cub.2007.01.027. PMid: 17306544, PMCid: PMC1868513.
- Grell M, Douni E, Wajant H, Löhden M, Clauss M, Maxeiner B, ... Scheurich P. The transmembrane form of tumor necrosis factor is the prime activating ligand of the 80 kDa tumor necrosis factor receptor, Cell. 1995; 83:793−802. https://doi.org/10.1016/0092-8674(95)90192-2.
- Lopez-Armada MJ, Carames B, Martin MA, Cillero-Pastor B, Lires-Dean M, Fuentes-Boquete I, ... Blanco FJ. Mitochondrial activity is modulated by TNFα and IL-1β in normal human chondrocyte cells, Osteoarthritis and Cartilage. 2006;14:1011−22. https://doi.org/10.1016/j.joca.2006.03.008. PMid: 16679036.
- Rodríguez M, Cabal-Hierro L, Carcedo MT, Iglesias JM, Artime N, Darnay BG, Lazo PS. NF-κB signal triggering and termination by tumor necrosis factor re-ceptor 2, Journal of Biological Chemistry. 2011; 286:22814−24. https://doi.org/10.1074/jbc.M111.225631. PMid: 21558270, PMCid: PMC3123049.
- Steenvoorden MMC, Bank RA, Ronday HK, Toes REM, Huizinga TWJ, DeGischolar_main J. Fibroblast-like synoviocyte-chondrocyte interaction in cartilage degra-dation, Clinical and Experimental Rheumatology. 2007; 25:239. PMid: 17543148.
- Munoz-Valle JF, Oregón-Romero E, Rangel-Villalobos H, Martínez-Bonilla GE, Casta-eda-Saucedo E, Salgado-Goytia L, ...Parra-Rojas I. High expression of TNF alpha is associated with− 308 and− 238 TNF alpha polymorphisms in knee osteoarthri-tis, Clinical and Experimental Medicine. 2014; 14:61−67. https://doi.org/10.1007/s10238-012-0216-3. PMid: 23108479.
- Nakajima M, Takahashi A, Kou I, Rodriguez-Fontenla C, GomezReino JJ, Furuichi T, ... Kubo M. New sequence variants in HLA class II/III region associated with susceptibility to knee osteoarthritis identified by genome-wide association study, PloS One. 2010; 5:e9723. https://doi.org/10.1371/journal.pone.0009723. PMid: 20305777, PMCid: PMC28411.
- Micheau O, Tschopp J. Induction of TNF receptor I-mediated apoptosis via two sequential signaling complexes, Cell. 2003; 114:181−90. https://doi.org/10.1016/S0092-8674(03)00521-X.
- Verma P, Dalal K. ADAMTS‐4 and ADAMTS‐5: Key enzymes in osteoarthri-tis, Journal of Cellular Biochemistry. 2011; 112:3507−14. https://doi.org/10.1002/jcb.23298. PMid: 21815191.
- Thomas DP, King B, Stephens T, Dingle JT. In vivo studies of cartilage regeneration after damage induced by catabolin/interleukin-1, Annals of the Rheumatic Dis-eases. 1991; 50:75−80. https://doi.org/10.1136/ard.50.2.75.
- Hämäläinen S, Solovieva S, Vehmas T, Leino-Arjas P, Hirvonen A. Variations in the TNFα gene and their interactions with the IL4R and IL10 genes in relation to hand osteoarthritis, BMC Musculoskeletal Disorders. 2014; 15:311. https://doi.org/10.1186/1471-2474-15-311. PMid: 25252624, PMCid: PMC4181701.
- Schäfers M, Marziniak M, Sorkin LS, Yaksh TL, Sommer C. Cyclooxy-genase inhibition in nerve-injury-and TNFinduced hyperalgesia in the rat, Experimental Neurology. 2004; 185:160−68. https://doi.org/10.1016/j.expneurol.2003.09.015. PMid: 14697327
- Shi, D., Zheng, Q., Chen, D., Zhu, L., Qin, A., Fan, J., ...&Xu, J. (2010) “Association of sin-gle-nucleotide polymorphisms in HLA class II/III region with knee osteoarthri-tis”, Osteoarthritis and cartilage, 18, 1454-1457. https://doi.org/10.1016/j.joca.2010.07.009. PMid: 20691797.
- Sommer C, Kress M. Recent findings on how proinflammatory cytokines cause pain: peripheral mechanisms in inflammatory and neuropathic hyperalgesia, Neuroscience Letters. 2004; 361:184−87. https://doi.org/10.1016/j.neulet.2003.12.007. PMid: 15135924.
- Haas TL, Emmerich CH, Gerlach B, Schmukle AC, Cordier SM, Rieser E, ... Koschny R. Recruitment of the linear ubiquitin chain assembly complex stabilizes the TNF-R1 signaling complex and is required for TNF-mediated gene induction, Molecular Cell. 2009; 36:831−44. https://doi.org/10.1016/j.molcel.2009.10.013. PMid:20005846.
- Wilson AG, Symons JA, McDowell TL, McDevitt HO, Duff GW. Ef-fects of a polymorphism in the human tumor necrosis factor α promoter on transcriptional activation, Proceedings of the National Academy of Sciences. 1997; 94:3195−99. https://doi.org/10.1073/pnas.94.7.3195.
- Yoshihara Y, Nakamura H, Obata KI, Yamada H, Hayakawa T, Fujikawa K, Okada Y. Matrix metalloproteinases and tissue inhibitors of metalloproteinases in synovial fluids from patients with rheumatoid arthritis or osteoarthritis, Annals of the Rheu-Matic Diseases. 2000; 59:455−61. https://doi.org/10.1136/ard.59.6.455. PMCid:PMC1753174.
- Zhou Z, Connell MC, MacEwan DJ. TNFR1-induced NF-κB, but not ERK, p38MAPK or JNK activation, mediates TNF-induced ICAM-1 and VCAM-1 expression on endothelial cells, Cellular Signalling. 2007; 19:1238−48. https://doi.org/10.1016/j.cellsig.2006.12.013. PMid: 17292586.
- Sofosbuvir and Daclatasvir Bypassing Genotypic Investigation of Chronic Hepatitis C Infection: A Real-Life Experience at Tertiary care center in North Indian Population Sofosbuvir and Daclatasvir Bypassing Genotypic Investigation
Abstract Views :324 |
PDF Views:99
Authors
Affiliations
1 Experimental and Public Health Laboratory, Department of Zoology, University of Lucknow, Lucknow – 226007, Uttar Pradesh, IN
2 Department of Medicine, King George’s Medical University, Lucknow – 226003, Uttar Pradesh, IN
3 Department of Medical Gastroenterology, King George’s Medical University, Lucknow – 226003, Uttar Pradesh, IN
1 Experimental and Public Health Laboratory, Department of Zoology, University of Lucknow, Lucknow – 226007, Uttar Pradesh, IN
2 Department of Medicine, King George’s Medical University, Lucknow – 226003, Uttar Pradesh, IN
3 Department of Medical Gastroenterology, King George’s Medical University, Lucknow – 226003, Uttar Pradesh, IN
Source
Journal of Ecophysiology and Occupational Health, Vol 20, No 1&2 (2020), Pagination: 70-74Abstract
Background and Aims: The goal of Hepatitis C Virus infection treatment is to remove the virus, to avoid advancement of Hepatitis C Virus (HCV) infection and progression of related disease such as liver cirrhosis and hepatocellular carcinoma and to achieve End of Treatment Response (ETR) with 12-week therapy and Sustained Virological Response (SVR) at post-treatment week 12 (SVR-12), which is defined as undetectable HCV RNA at 12 weeks post ETR. In the Compassionate Use Program (CUP) in Europe, Sofosbuvir (SOF) and Daclatasvir (DCV) were used in all genotypes and achieved SVR-12. Aims: Our aim is to compare the efficacy and effectiveness of Sofosbuvir and Daclatasvir in the treatment of HCV infection in the patients who could not afford for the investigating of HCVGenotype and to those in whom genotyping was done. Methods: Group 1 includes ten patients, given Sofosbuvir and Daclatasvir without genotype and group 2 includes nine patients, given Sofosbuvir and Daclatasvir with genotype. The patient group selection was done using a randomized table generated by using excel. All the patients in the groups completed the twelve weeks treatment with twelve weeks and twenty-four weeks of follow up. All the nineteen patients were given Sofosbuvir and Daclatasvir for twelve weeks and the endpoint of therapy was marked by undetectable HCV-RNA in blood by ETR-12 (end of treatment response), Sustained Virological Response at post-treatment week 12 (SVR-12) and Sustained Virological Response at post-treatment week 24 (SVR- 24). Results: Quantitative HCV-RNA (IU/ml) by RT-PCR was undetectable in all the patients in both groups at the end of treatment (ETR-12) and SVR-12- and SVR-24-weeks follow-up after completion of treatment i.e. Sofosbuvir and Daclatasvir has 100% ETR-12, SVR-12 and SVR-24 in both the groups. Conclusion: If patients do not investigate for genotype and use the Sofosbuvir and Daclatasvir in HCV infected patients, there is no effect on outcome ETR. This will reduce the risk of late stage complications such as liver cirrhosis and hepatocellular carcinoma and will also leads to the economic benefits such as no extra burden on patients.Keywords
Cirrhosis, End of Treatment Response (ETR), Hepatocellular Carcinoma (HCC), Sofosbuvir and Daclatasvir (SOF+DCV), Steatosis, Sustained Virological Response (SVR).References
- Nazish B, Tariq M. An overview about Hepatitis C: A devastating virus. Crit Rev Microbiol. 2010; 36(2):91–133. PMid: 20345213.https://doi.org/10.3109/10408410903357455
- Alter MJ, Margolis HS, Krawczynski K, Judson FN, Mares A, Alexander WJ, et al. The natural history of communityacquired Hepatitis C in the United States. The Sentinel Counties Chronic non-A, non-B Hepatitis Study Team. N Engl J Med.1992; 327:1899–905. PMid: 1280771. https://doi.org/10.1056/ NEJM199212313272702
- Kim WR. The burden of Hepatitis C in the United States. Hepatology.2002; 36:S30–4. https://doi.org/10.1002/hep.1840360705
- Singh S, Malhotra V, Sarin SK. Distribution of Hepatitis C Virus genotypes in patients with chronic Hepatitis C infection in India.Indian J Med Res. 2004 Apr; 119:145–8.
- Prakash S, Jain A, Jain B. Development of novel triplex singlestep real-time PCR assay for detection of Hepatitis Virus B and C simultaneously. Virol. 2016 May; 492:101–7. PMid: 26914508.https://doi.org/10.1016/j.virol.2016.01.029
- Sievert W, Altraif I, Razavi HA, Abdo A, Ahmed EA, Alomair A, et al. A systematic review of Hepatitis C Virus epidemiology in Asia, Australia and Egypt. Liver Int. 2011; 31(sup 2):61–80. PMid: 21651703. https://doi.org/10.1111/j.1478-3231.2011.02540.x
- http://www.millenniumpost.in/india-lacks-accurate-data-totackle-hepatitis-155867
- American Association for the Study of Liver Diseases and the Infectious Diseases Society of America. Recommendations for testing, managing and treating hepatitis C. 2015. http://www.Hcvguidelines.org/full-Report-View
- European Association for Study of Liver. EASL Recommendations on Treatment of Hepatitis C 2015. J Hepatol. 2015; 63:199–236.PMid: 25911336. https://doi.org/10.1016/j.jhep.2015.03.025
- Majumdar A, Kitson MT, Roberts SK. Systematic review: Current concepts and challenges for the direct-acting antiviral era in Hepatitis C Cirrhosis. Aliment Pharmacol Ther. 2016; 43:1276– 92. PMid: 27087015. https://doi.org/10.1111/apt.13633
- Holmes JA, Thompson AJ. Interferon-free combination therapies for the treatment of Hepatitis C: Current insights. Hepat Med.2015; 7:51–70. PMid: 26586968 PMCid: PMC4636173. https:// doi.org/10.2147/HMER.S55864
- Gao M. Antiviral activity and resistance of HCV NS5A replication complex inhibitors. Curr Opin Virol. 2013; 3:514–20. PMid: 23896281. https://doi.org/10.1016/j.coviro.2013.06.014
- Sofia MJ, Bao D, Chang W, Du J, Nagarathnam D, Rachakonda S, et al. Discovery of a β-d-20-deoxy-20-α-fluoro-20-βCmethyluridine nucleotide prodrug (PSI-7977) for the treatment of Hepatitis C Virus. J Med Chem. 2010; 53:7202–18. PMid: 20845908. https://doi.org/10.1021/jm100863x
- Wyles DL, Ruane PJ, Sulkowski MS, et al. Daclatasvir plus Sofosbuvir for HCV inpatients coinfected with HIV-1. N Engl J Med. 2015; 373:714–25.
- Nelson DR, Cooper JN, Lalezari JP, Lawitz E, Pockros PJ, Gitlin N, et al. All-oral 12-week treatment with Daclatasvir plus Sofosbuvir in patients with Hepatitis C Virus genotype 3 infection: ALLY-3 phase III study. Hepatology. 2015; 61:1127–35. PMid: 25614962 PMCid: PMC4409820. https://doi.org/10.1002/hep.27726
- Poordad F, Schiff ER, Vierling JM, Landis C, Fontana RJ, Yang R, et al. Daclatasvir with Sofosbuvir and ribavirin for Hepatitis C Virus infection with advanced cirrhosis or post-liver transplant recurrence. Hepatology. 2016; 63:1493–505. PMid: 26754432 PMCid: PMC5069651. https://doi.org/10.1002/hep.28446
- Prakash S, Shukla S, Ramakrishna V, Jain A. Distribution of Hepatitis C genotypes in Uttar Pradesh, India; Rare genotype 4 detected. Journal of Medical Virology. 2018; 90:1875–81. PMid: 30085356. https://doi.org/10.1002/jmv.25277
- Lole KS, Jha JA, Shrotri1 SP, Tandon BN, Mohan Prasad VG, Vidya A. Arankalle VA. Comparison of Hepatitis C Virus genotyping by 5′ Noncoding Region- and Core-based reverse transcriptase PCR assay with sequencing and use of the assay for determining subtype distribution in India. J Clin Microbiol.2003 Nov; 41(11):5240–4. PMid: 14605173 PMCid: PMC262521.https://doi.org/10.1128/JCM.41.11.5240-5244.2003
- Deep A, Kumar A, Swaroop S. There is no need of investigating for genotype if we use Sofosbuvir and Daclatasvir for chronic Hepatitis C infection. Journal of Clinical and Experimental Hepatology. 2017; 7(2):S19. https://doi.org/10.1016/j.jceh.2017.05.043
- Welzel TM, Petersen J, Herzer K, Ferenci P, Gschwantler M, Wedemeyer H, et al. Daclatasvir plus Sofosbuvir, with or without ribavirin, achieved high sustained virological response rates in patients with HCV infection and advanced liver disease in a realworld cohort. Gut. 2016; 65:1861–70. PMid: 27605539 PMCid: PMC5099229. https://doi.org/10.1136/gutjnl-2016-312444