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OKÜLT HEPATİT B VİRUS ENFEKSİYONU: MOLEKÜLER MEKANİZMALAR VE KLİNİK ÖNEMİ

Yıl 2017, Cilt: 80 Sayı: 2, 71 - 81, 30.06.2017
https://doi.org/10.18017/iuitfd.330044

Öz

Okült Hepatitis B Virüs (HBV) infeksiyonu
(OBİ) serum HBV DNA statüsü dikkate alınmaksızın mevcut serolojik testler ile
HBV yüzey antijeni (HBsAg) negatif tespit edilen bireylerin karaciğerin de HBV
genomunun uzun süreli persistan varlığı olarak tanımlanır. OBİ virüse ve infekte
bireye ait faktörler ile çevresel faktörlerin zemininde gelişen genetik,
epigenetik ve immünolojik mekanizmaların karşılıklı etkileşimi ile şekillenen,
HBV infeksiyonunun doğal seyri içerisinde yer alan muhtemel safhalarından biri
olarak kabul edilir. OBİ klinik açıdan; okült virüsün kan transfüzyonu, doğum,
hemodiyaliz ve ortotopik karaciğer gibi organ nakli yolu ile bulaşını takiben
alıcıda tipik yeni HBV infeksiyonuna neden olabilmesi, immünsüpresyon
koşullarında OBİ reaktivasyonu ve takiben HBV ilişkili (akut ve fulminan
hepatit) karaciğer hastalıkları, kronik karaciğer hastalıklarının (KKH)
progresyonu üzerine etkisi ile özellikle
hepatoselüler karsinoma (HSK) için artan bir risk faktörü olduğu yönünde hipotez
uyarınca yoğun bir tartışma ve araştırma konusudur. Buna karşın gerek HBV infeksiyonunun
bu özgün formuna neden olan gerekse ilişkili olduğu karaciğer hastalıklarının
patogenezinde rol alan moleküler mekanizmalar henüz tam olarak
aydınlatılamamıştır. Bu derlemede OBİ’nin klinik önemi, epidemiyolojik
özellikleri ve laboratuar tanısına yönelik bilimsel literatürün gözden
geçirilmesi amaçlanmıştır.



Anahtar
Kelimeler:
Hepatit B virüs; okült hepatit B virüs infeksiyonu; bulaş;
reaktivasyon; kronik karaciğer hastalığı;
hepatoselüler karsinoma.

Kaynakça

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OCCULT HEPATITIS B VIRUS INFECTION: MOLECULAR MECHANISMS AND CLINICAL SIGNIFICANCE

Yıl 2017, Cilt: 80 Sayı: 2, 71 - 81, 30.06.2017
https://doi.org/10.18017/iuitfd.330044

Öz

Occult Hepatitis B Virus (HBV) infection
(OBI) is defined as the long-lasting persistence of HBV genomes in the
hepatocytes of individuals testing negative for HBV surface antigen (HBsAg) by
currently available assays and usually for serum HBV DNA. OBI is considered as
the possible phase in the natural history of chronic HBV infection that the
host’s immune surveillance and epigenetic mechanisms are likely involved.
Clinical impact of OB is that it can be transmitted (i.e., through blood
transfusion,
by liver organ
transplantation, hemodialysis and parturition) causing classic forms of
hepatitis B in newly infected individuals. The development of an
immunosuppressive status may induce OBI reactivation and development of acute
and often severe hepatitis. OBI can favor the progression of liver fibrosis.
Also OBİ infection has been hypothesized to be a significant risk factor
contributing to the progression of chronic liver diseases (CLD) with increased
risk for hepatocellular carcinoma (HCC) which may lead to an increased
progression of liver diseases. Although OBI is considered a phase in the natural
history of HBV, the molecular mechanisms leading to its occurrence and its contribution
to HCC development are yet poorly understood. In this review, it is aimed to examine
clinical importance, epidemiological aspects and laboratory diagnosis of OBI in
recent literature.



Keywords: Hepatitis B virüs;
occult hepatitis B virus infection; transmission; reactivation; chronic liver
disease; hepatocellular carcinoma.

Kaynakça

  • 1. World Health Organization. http://www.who.int/mediacentre/factsheets/fs204/en/ erişim 12 Ocak 2015.
  • 2. World Health Organization. http://www.who.int/mediacentre/factsheets/fs297/en/ erişim 12 Ocak 2015.
  • 3. Shi J, Zhu L, Liu S, Xie WF. A Metaanalysis of case-control studies on the combined effect of hepatitis B and C virus infections in causing hepatocellular carcinoma in China. Br J Cancer 2005;92:607–12.
  • 4. Chang MH. Cancer prevention by vaccination against hepatitis B. Recent Results. Cancer Res 2009; 181: 85-94.
  • 5. Kew MC. Epidemiology of hepatocellular carcinoma. Toxicology 2002; 181–182: 35–8.
  • 6. Lai CL, Ratziu V, Yuen MF, Poynard T. Viral hepatitis B. Lancet 2003; 62: 2089–94.
  • 7. Ganem D, Prince AM. Hepatitis B virus infection natural history and clinical consequences. N Engl J Med 2004;350: 1118–29.
  • 8. Fattovich G, Giustina G, Sanchez-Tapias J, Quero C, Mas A, et al. Delayed clearance of serum HBsAg in compensated cirrhosis B: relation to interferon alpha therapy and disease prognosis. European Concerted Action on Viral Hepatitis (EUROHEP). Am J Gastroenterol 1998; 93: 896–900.
  • 9. Raimondo G, Allain JP, Brunetto MR, Buendia MA, Chen DS, Colombo M, et al. Statements from the Taormina expert meeting on occult hepatitis B virus infection. J Hepatol 2008; 49: 652-7.
  • 10. Torbenson M, Thomas DL. Occult hepatitis B. Lancet Infect Dis. 2002; 2: 479-86.
  • 11. Pollicino T, Saitta C. Occult hepatitis B virus and hepatocellular carcinoma. World J Gastroenterol 2014; 20(20): 5951-61.
  • 12. Samal J, Kandpal M, Vivekanandan P. Molecular mechanisms underlying occult hepatitis B virus infection. Clin Microbiol Rev 2012;25:142-63.
  • 13. Raimondo G, Pollicino T, Cacciola I, Squadrito G. Occult hepatitis B virus infection. J Hepatol 2007; 46:160–70.
  • 14. Fang Y, Shang QL, Liu JY, Li D, Xu WZ, Teng X, et al. Prevalence of occult hepatitis B virus infection among hepatopathy patients and healthy people in China. J Infect 2009; 58: 383–8.
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  • 101. Transy C, Fourel G, Robinson WS, Tiollais P, Marion PL, Buendia MA. Frequent amplification of c-myc in ground squirrel liver tumors associated with past or ongoing infection with a hepadnavirus. Proc Natl Acad Sci U S A 1992; 89: 3874-8.
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  • 104. Shafritz DA, Shouval D, Sherman HI, Hadziyannis SJ, Kew MC. Integration of hepatitis B virus DNA into the genome of liver cells in chronic liver disease and hepatocellular carcinoma. Studies in percutaneous liver biopsies and post-mortem tissue specimens. N Engl J Med 1981; 305: 1067–73.
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  • 106. Makvandi M. Update on occult hepatitis B virus infection. World J Gastroenterol 2016; 22(39): 8720-87.
Toplam 106 adet kaynakça vardır.

Ayrıntılar

Bölüm Derleme
Yazarlar

Bülent Çakal

Yayımlanma Tarihi 30 Haziran 2017
Gönderilme Tarihi 21 Temmuz 2017
Yayımlandığı Sayı Yıl 2017 Cilt: 80 Sayı: 2

Kaynak Göster

APA Çakal, B. (2017). OCCULT HEPATITIS B VIRUS INFECTION: MOLECULAR MECHANISMS AND CLINICAL SIGNIFICANCE. Journal of Istanbul Faculty of Medicine, 80(2), 71-81. https://doi.org/10.18017/iuitfd.330044
AMA Çakal B. OCCULT HEPATITIS B VIRUS INFECTION: MOLECULAR MECHANISMS AND CLINICAL SIGNIFICANCE. İst Tıp Fak Derg. Haziran 2017;80(2):71-81. doi:10.18017/iuitfd.330044
Chicago Çakal, Bülent. “OCCULT HEPATITIS B VIRUS INFECTION: MOLECULAR MECHANISMS AND CLINICAL SIGNIFICANCE”. Journal of Istanbul Faculty of Medicine 80, sy. 2 (Haziran 2017): 71-81. https://doi.org/10.18017/iuitfd.330044.
EndNote Çakal B (01 Haziran 2017) OCCULT HEPATITIS B VIRUS INFECTION: MOLECULAR MECHANISMS AND CLINICAL SIGNIFICANCE. Journal of Istanbul Faculty of Medicine 80 2 71–81.
IEEE B. Çakal, “OCCULT HEPATITIS B VIRUS INFECTION: MOLECULAR MECHANISMS AND CLINICAL SIGNIFICANCE”, İst Tıp Fak Derg, c. 80, sy. 2, ss. 71–81, 2017, doi: 10.18017/iuitfd.330044.
ISNAD Çakal, Bülent. “OCCULT HEPATITIS B VIRUS INFECTION: MOLECULAR MECHANISMS AND CLINICAL SIGNIFICANCE”. Journal of Istanbul Faculty of Medicine 80/2 (Haziran 2017), 71-81. https://doi.org/10.18017/iuitfd.330044.
JAMA Çakal B. OCCULT HEPATITIS B VIRUS INFECTION: MOLECULAR MECHANISMS AND CLINICAL SIGNIFICANCE. İst Tıp Fak Derg. 2017;80:71–81.
MLA Çakal, Bülent. “OCCULT HEPATITIS B VIRUS INFECTION: MOLECULAR MECHANISMS AND CLINICAL SIGNIFICANCE”. Journal of Istanbul Faculty of Medicine, c. 80, sy. 2, 2017, ss. 71-81, doi:10.18017/iuitfd.330044.
Vancouver Çakal B. OCCULT HEPATITIS B VIRUS INFECTION: MOLECULAR MECHANISMS AND CLINICAL SIGNIFICANCE. İst Tıp Fak Derg. 2017;80(2):71-8.

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