Different forms of hepatitis B virus DNA and expression of HBV antigens in peripheral blood mononuclear cells in chronic hepatitis B

Bouffard, Pascal; Lamelin, J P; Zoulim, Fabien; Pichoud, Christian; Trépo, Christian

doi:10.1002/jmv.1890310413

Cited by 34 publications

(14 citation statements)

References 23 publications

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“…Yet there is still a possibility that an altered glomerular permeability could account for the HBV DNA detectable in some patients. Another plausible way for virions to reach the urinary tract, besides the possible "leakage" of free viral particles into the urine, is by means of leukocytes and to a minor extent shed renal epithelial cells, where HBV DNA has been demonstrated as well as in hepatocytes [Bouffard et al, 1990;He et al, 1998]. In this way, a larger amount of HBV DNA would be expected during times of increased local epithelial and white cell count, such as during disease or inflammatory reactions in the urinary tract.…”

Section: Discussionmentioning

confidence: 99%

Urine from chronic hepatitis B virus carriers: Implications for infectivity

Knutsson

Kidd‐Ljunggren

2000

J. Med. Virol.

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Horizontal transmission of hepatitis B virus (HBV) without apparent sexual or parenteral exposure is common in hyperendemic areas. In most cases, the route of transmission is unknown. To investigate urine as a potential source of infection, serum and urine from 56 chronic hepatitis B surface antigen (HBsAg) carriers were examined for the presence of HBV DNA using the polymerase chain reaction (PCR). Thirty-four of the patients were anti-hepatitis B e antigen (anti-HBe) positive and 22 were hepatitis B e antigen (HBeAg) positive. HBV DNA was detected in serum from 46 patients (82%) and in urine from 28 patients (50%). Most HBeAg-positive patients had HBV DNA detectable in urine (91%), whereas urine samples from anti-HBe-positive patients were found to contain HBV DNA to a lesser extent (24%). When comparing HBV DNA from serum and urine by an end-point titration PCR, a titration difference averaging 10(3) was found between serum and urine. A significant female predominance was also noted among the positive urine samples (P < 0.05), which was not correlated to the presence of haematuria. Detection of HBV DNA may indicate active viral replication, and thereby infectivity. Because a high proportion of chronic HBV carriers were found to have HBV DNA in urine, it is suggested that irrespective of HBeAg/anti-HBe status, urine should be regarded as a potential route of transmission and therefore be investigated further as a means of horizontal and nosocomial transmission of HBV.

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Section: Discussionmentioning

confidence: 99%

Urine from chronic hepatitis B virus carriers: Implications for infectivity

Knutsson

Kidd‐Ljunggren

2000

J. Med. Virol.

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“…The results showed the objective evidence of existence of HBV in gastric cancer tissues. HBV DNA or HBV antigens had been detected in extra‐hepatic organs or tissues, including spleen, kidney, skin, pancreatic tissues, bile duct epithelium, and peripheral blood cells . HBcAg had been demonstrated to play an immunosuppressive role on T cells .…”

Section: Discussionmentioning

confidence: 99%

Hepatitis B virus infection is associated with younger median age at diagnosis and death in cancers

Xiao

Luo

et al. 2017

Intl Journal of Cancer

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Several non-hepatocellular cancers were linked with hepatitis B virus (HBV) infection. This study was aimed to quantify the potential associations between HBV infection and multiple non-hepatocellular cancers. Continuous cases, including 5,715 non-cancer and 40,963 cancer cases diagnosed from 2008 to 2014 in Sun Yat-sen University Cancer Center were analyzed. HBV DNA and hepatitis B core antigen (HBcAg) were examed in gastric cancer tissues by polymerase chain reaction and immunohistochemical staining. After adjusting for age, sex, year of diagnosis, smoking, drinking and family history of cancer, significant associations were found between serum HBsAg and frequently reported HBV-related non-hepatocellular cancers, including non-Hodgkin's lymphoma, cholangiocarcinoma and pancreatic cancer [adjusted odds ratio (AOR) and 95% confidence interval (CI): 1.89 (1.65-2.16)], as well as total other non-hepatocellular cancers [AOR and 95% CI: 1.12 (1.03-1.22)]. The median ages at diagnosis, all-cause death and cancer-specific death of serum HBsAg positive cancer patients were all significantly younger than those with serum HBsAg negative. HBV DNA was detected in 12.4% (34/275) gastric cancer tissues and HBcAg was most commonly detected in lymphocytes. This was the first report that HBV infection had a modest but significant nonspecific association with total non-hepatocellular cancers. Median age at diagnosis and death was significantly younger in serum HBsAg positive cancer patients. The underlying mechanism needs further investigation.

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“…Integrated HBV‐DNA was also occasionally detectable. The presence of HBV‐DNA in PBMCs has been associated with coexpression of HBV proteins in these cells, serum HBeAg and HBV‐DNA as well as disease activity [50,52]. These findings suggest that HBV infection of PBMCs is a common phenomenon during HBV infection.…”

Section: Molecular Analysis and Mechanisms Of Occult Hbv Infectionmentioning

confidence: 99%

Occult hepatitis B virus infection and its clinical implications

2002

Journal of Viral Hepatitis

289

272

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Occult hepatitis B virus (HBV) infection is characterized by presence of HBV infection with undetectable hepatitis B surface antigen (HBsAg). Serum HBV level is usually less than 104 copies/mL in these patients. Diagnosis of occult HBV infection requires sensitive HBV-DNA PCR assay. Several possibilities have been hypothesized as the mechanisms of occult HBV infection. These include: (i) mutations of HBV-DNA sequence; (ii) integration of HBV-DNA into host's chromosomes; (iii) infection of peripheral blood mononuclear cells by HBV; (iv) formation of HBV-containing immune complex; (v) altered host immune response; and (vi) interference of HBV by other viruses. The precise prevalence of occult HBV infection remains to be defined. The clinical implications of occult HBV infection involve different clinical aspects. First of all, occult HBV infection harbours potential risk of HBV transmission through blood transfusion, haemodialysis, and organ transplantation. Second, it may serve as the cause of cryptogenic liver disease, contribute to acute exacerbation of chronic hepatitis B, or even fulminant hepatitis. Third, it is associated with development of hepatocellular carcinoma. Fourth, it may affect disease progression and treatment response of chronic hepatitis C. Most of the previous studies utilized retrospective observation without control groups, and lacked direct association of occult HBV infection with specific pathological changes and disease progression. Highly sensitive, quantitative, and functional molecular analyses of HBV, combined with a well-designed prospective clinical assessment will provide the best approach for the future study of occult HBV infection.

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Different forms of hepatitis B virus DNA and expression of HBV antigens in peripheral blood mononuclear cells in chronic hepatitis B

Cited by 34 publications

References 23 publications

Urine from chronic hepatitis B virus carriers: Implications for infectivity

Urine from chronic hepatitis B virus carriers: Implications for infectivity

Hepatitis B virus infection is associated with younger median age at diagnosis and death in cancers

Occult hepatitis B virus infection and its clinical implications

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