Songül Beskisiz¹, Omer Satici², Vatan Kavak³* and Kendal Yalcin⁴

¹Department of Internal Medicine, Gazi Yaşargil Training and Research Hospital, University of Health Sciences, Diyarbakir, Turkey
²Department of Bitoistatics, Faculty of Medicine, Dicle University, Diyarbakir, Turkey
³Department of Anatomy, Faculty of Medicine, Dicle University, Diyarbakir, Turkey
⁴Department of Hepatology, Faculty of Medicine, Dicle University, Diyarbakir, Turkey

*Corresponding Author: Vatan Kavak, Department of Anatomy, Facultey of Medicine, Dicle University, Diyarbakir, Turkey.

Received: May 18, 2021; Published: June 30, 2021

Abstract

Aim: Our aim in this study; Liver in the domain of hepatitis E virus infection; It is the largest organ in the body located in the upper right of the abdominal cavity. The liver organ is the organ in the domain of the hepatitis E virus. It is to retrospectively investigate the HEV seropositivity in patients with viral hepatitis who are 18 years of age and older who applied to Dicle University Faculty of Medicine, Department of Gastroenterology, and to determine the risk factors associated with HEV infection by evaluating the cases according to epidemiological, clinical and laboratory characteristics.

Material and Methods: Within the scope of this study, 1025 patients aged 18 and over who applied to Dicle University Faculty of Medicine Gastroenterology Department between May 2011 and March 2015 were included. Age, gender, biochemistry (ALT, AST, GGT, Total bilirubin, albumin), whole blood (hemoglobin, thrombocyte), coagulation (INR), demographic criteria (origin (urban/rural), educational status (primary school and below-low, middle school and above-high), marital status (married/single), pregnancy (yes/no), known family history of viral hepatitis (yes/no), contact with animals, substance abuse (yes/no), alcohol use (yes/no no), cirrhosis status (yes/no), time of infection in patients with viral hepatitis, and antiviral drug use were retrospectively investigated.

Statistical Analysis: The data were transferred from the Excel package program to the SPSS (Statistical Package for Social Sciences) 25 package program. Variables were defined as categorical, ordered, and continuous measurement variables, and appropriate tests were used for these variables.

Results: The mean age of the patients was 49.29 ± 15.39 years and Anti-HEV IgG seropositivity was determined 56,4% of all patients (578/1025). HEV seropositivity was 76,3% in patients with HCV (29/38), 50% in patients with HBV (142/284), 70,7% in patients with HDV (58/82) and 56.2% in control group (349/621). Highest mean age in the groups was detected in HCV patients as 51.84 ± 15.77 years ( P = 0.001). Rate of Anti-HEV IgG seropositivity according to age groups was highest in patients older than 61 years old ( 141/578, 24.4%) and lowest in patients between 18-30 years old (68/578, 11.8%) (P < 0.001). Advanced age, rural origin, low education level, being married, history of contact with animals, high ALT levels, high GGT levels, low platelet levels, anti-delta seropositivity, ani-HCV seropositivity and anti-HAV IgG seropositivity was found to be significant risk factors for HEV seropositivity in the logistic regression analysis.

Conclusion: In this study, it was found that HEV infection is more common in people with low education levels in our region, people living in rural areas, elderly people, married people, those who are engaged in animal husbandry, and cirrhotic patients. In addition, ALT and GGT elevation, low platelets, anti-delta positive, anti-HCV positive and anti-HAV IgG positive were determined as risk factors for seropositivity in logistic regression analysis. These demographic findings may contribute to the determination of risky patients and taking preventive measures in the control of HEV infection. Accurate and permanent anatomy education provides the ability to comment 85% on all diseases. Therefore, in studies belonging to researchers; anatomy is important.

Keywords: Hepatitis E Virus; Hepatitis B Virus; Hepatitis C Virus; Hepatitis D Virus; Etiology; Epidemiology; Liver Anatomy

References

1. Pilmane M., et al. “Embriology and Anatomy for Healthy Sciences”. Riga Stradins University, Riga, Latvia (2016).
2. Aggarwal R and Naik S. “Epidemiology of hepatitis E: Current status”. Journal of Gastroenterology and Hepatology 24 (2009): 1484-1493.
3. Thomas DL., et al. “Epidemiology of hepatitis E virus infection in Turkey”. Lancet 341 (1993): 1561-1562.
4. Khuroo MS. “Discovery of hepatitis E: the epidemic non-A, non-B hepatitis 30 years down the memory lane”. Virus Research1 (2011): 3-14.
5. Balayan MS., et al. “Evidence of a virus in non-A, non-B hepatitis transmitted via the fecal oral route”. Intervirology 1 (1983): 23-31.
6. Reyes GR., et al. “Isolation of a cDNA from the virus responsible for enterically transmitted non-A, non-B hepatitis”. Science4948 (1990): 1335-1339.
7. Tam AW., et al. “Hepatitis E virus (HEV): molecular cloning and sequencing of the full-length viral genome”. Virology 185 (1991): 120-131.
8. Vishwanathan R. “Infectious hepatitis in Delhi (1955-56): a critical study: epidemiology”. Indian Journal of Medical Research 45 (1957): 1-29.
9. Khuroo MS. “Study of an epidemic of non-A, non-B hepatitis: possibility of another human hepatitis virus distinct from post-transfusion non- A, non-B type”. American Journal of Medicine 68 (1980): 818-823.
10. Kamar N., et al. “Hepatitis E”. Lancet 9835 (2012): 2477-2488.
11. Panda SK and Varma SP. “Hepatitis E: molecular virology and pathogenesis”. Journal of Clinical and Experimental Hepatology2 (2013): 114-124.
12. Cao D and Meng XJ. “Molecular biology and replication of hepatitis E virus”. Emerging Microbes and Infections 8 (2012): e17.
13. Yamashita T., et al. “Biological and immunological characteristics of hepatitis E virus-like particles based on the crystal structure”. Proceedings of the National Academy of Sciences of the United States of America 106 (2009): 12986-12991.
14. Krain LJ., et al. “Host immune status and response to hepatitis E virus infection”. Clinical Microbiology Reviews1 (2014): 139-165.
15. Nan Y., et al. “Hepatitis E virus inhibits type I interferon induction by ORF1 products”. Journal of Virology 20 (2014): 11924-11932.
16. Ahmad I., et al. “Molecular virology of hepatitis E virus”. Virus Research 161 (2011): 47-58.
17. Lu L., et al. “Phylogenetic analysis of global hepatitisE virus sequences: genetic diversity, subtypes and zoonosis”. Reviews in Medical Virology 16 (2006): 5-36.
18. Huang CC., et al. “Molecular cloning and sequencing of the Mexico isolate of hepatitis E virus (HEV)”. Virology2 (1992): 550-558.
19. Kwo PY., et al. “Acute hepatitis E by a new isolate acquired in the United States”. Mayo Clinic Proceedings 72 (1997): 1133-1136.
20. Erker JC., et al. “A hepatitis E virus variant from the United States: molecular characterization and transmission in cynomolgus macaques”. Journal of General Virology 80 (1990): 681-690.
21. Wang Y., et al. “A divergent genotype of hepatitis Evirus in Chinese patients with acute hepatitis”. Journal of General Virology 80 (1990): 169-177.
22. Ahmed A., et al. “Mystery of hepatitis E virus: recent advances in its diagnosis and management”. International Journal of Hepatology 2015 (2015): 872431.
23. Purdy MA., et al. “The molecular epidemiology of hepatitis E virus infection”. Virus Research1 (2011): 31-39.
24. Kmush B., et al. “Epidemiology of hepatitis E in low- and middle-income countries of Asia and Africa”. Seminar on Liver Disease1 (2013): 15-29.
25. Dalton HR., et al. “Hepatitis E: an emerging infection in developed countries”. Lancet Infectious Disease11 (2008): 698-709.
26. Pischke S., et al. “Hepatitis E in Germany--an under-reported infectious disease”. Deutsches Ärzteblatt International 35-36 (2014): 577-583.
27. Kalia M., et al. “Heparan sulfate proteoglycans are required for cellular binding of the hepatitis E virus ORF2 capsid protein and for viral infection”. Journal of Virology24 (2009): 12714-12724.
28. Yamada K., et al. “ORF3 protein of hepatitis E virus is essential for virion release from infected cells”. Journal of General Virology 90 (2009): 1880-1891.
29. Chandra NS., et al. “Dynamics of HEV viremia, fecal shedding and its relationship with transaminases and antibody response in patients with sporadic acute hepatitis E”. Virology Journal 7 (2010): 213.
30. Chandra V., et al. “Molecular biology and pathogenesis of hepatitis E virus”. Journal of Bioscience4 (2008): 451-464.
31. Kamar N., et al. “Hepatitis E virus infection”. Clinical Microbiology Reviews1 (2014): 116-138.
32. Zhang S., et al. “Clinical significance of anti-HEV IgA in diagnosis of acute genotype 4 hepatitis E virus infection negative for anti-HEV IgM”. Digestive Diseases and Sciences11 (2009): 2512-2518.
33. Gu Y., et al. “Structural basis for the neutralization of hepatitis E virus by a cross-genotype antibody”. Cell Research 5 (2015): 604-620.
34. Wedermeyer H., et al. “Pathogenesis and treatment of hepatitis E virus infection”. Gastroenterology6 (2012): 1388-1397.e1.
35. Wu T., et al. “Specific cellular immune response in hepatitis E patients”. Intervirology5 (2008): 322-327.
36. Wedemeyer H., et al. “Immunopathogenesis of hepatitis E virus infection”. Seminars in Liver Disease 1 (2003): 71-78.
37. Pérez-Gracia MT., et al. “Hepatitis E: an emerging disease”. Infection, Genetics and Evolution 22 (2014): 40-59.
38. Khuroo MS., et al. “Acut sporadic Non-A, Non-B hepatitis in İndia”. American Journal of Epidemiology 118 (1983): 360-364.
39. Haagsma EB., et al. “Chronic hepatitis E virus infection in liver transplant recipients”. Liver Transplantation 4 (2008): 547-553.
40. Behrendt P., et al. “The impact of hepatitis E in the liver transplant setting”. Journal of Hepatology6 (2014): 1418-1429.
41. Teshale EH., et al. “Evidence of person-to person transmission of hepatitis E virus during a large outbreak in Northern Uganda”. Clinical Infectious Disease7 (2010): 1006-1010.
42. Browne LB., et al. “Notes from the field: Hepatitis E Outbreak Among Refugees from South Sudan — Gambella, Ethiopia, April 2014-January 2015”. MMWR19 (2015): 537.
43. Huang FF., et al. “Detection by reverse transcription-PCR and genetic characterization of field isolates of swine hepatitis E virus from pigs in different geographic regions of the United States”. Journal of Clinical Microbiology4 (2002): 1326-1332.
44. Kumar S., et al. “Molecular detection and sequence analysis of hepatitis E virus in patients with viral hepatitis from North India”. Diagnostic Microbiology and Infectious Disease 2 (2011): 110-117.
45. Darwish MA., et al. “High seroprevalance of hepatitis A, B, C and E viruses in residents in an Egyptian village in The Nil Delta: a pilot study”. American Society of Tropical Medicine and Hygiene 6 (1996): 554-558.
46. Clayson ET., et al. “Rates of hepatitis E virus infection and diseases among adolescents and adults in Kathmandu, Nepal”. The Journal of Infectious Diseases 3 (1997): 763-766.
47. Lewis HC., et al. “Transmission routes and risk factors for autochthonous hepatitis E virus infection in Europe: a systematic review”. Epidemiology Infection2 (2010): 145-166.
48. Wong KH., et al. “Epidemiology of hepatitis A and hepatitis E infection and their determinants in adult chinese community in Hong Kong”. Journal of Medical Virology 72 (2004): 538-544.
49. Tucker TJ., et al. “Hepatitis E şn South Africa: Evidence for sporadic spread and increased seroprevalence in rural areas”. Journal of Medical Virology 50 (1996): 117-119.
50. Houcine N., et al. “Seroprevalence of HEV infection in rural and urban populations, Tunisia”. Clinical Microbiology Infection I8 (2012): 119-121.

Citation

Citation: Vatan Kavak. “Determınation of Hepatıtıs E Vırus Infection Frequency and Risk Factors in Viral Hepatites in Diyarbakır Regıon”. Acta Scientific Neurology 4.7 (2021): 54-63.

Copyright

Copyright: © 2021 Vatan Kavak. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.