Hepatitis B Antigen Inhibitor in Human Faeces and Intestinal Mucosa

Piazza, Marcello; Stasio, G. Di; Maio, Giuseppe Di; Marzano, Luca

doi:10.1136/bmj.2.5862.334

Cited by 32 publications

(12 citation statements)

References 23 publications

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“…Such sera were from haemophilic (Cossart and Vahrmarn, 1970) or other patients, in some instances standardized by comparison with reference sera provided by Drs A. M. Prince and B. S. Blumberg (Grob and Jemelka, 1971;Cossart and Vahrman, 1970;Gust, Kaldor, and Nastasi, 1971). In two reports (Grabow andProzesky, 1973a and1973b) use was made of baboon antiserum to human HB Ag from human serum and in another a commercially prepared antiserum distributed in a diagnostic kit (Piazza, Di Stasio, Maio, and Marzano 1973).…”

Section: Discussionmentioning

confidence: 99%

“…Piazza, di Stasio, Maio, and Marzano (1973) showed that homogenates of human faeces or intestinal mucosa incubated with HB antigen for two hours at 37°C (but not at 2°C) were able to render antigen inactive in the complement-fixation test. It was found by Grabow and Prozesky (1973a) that the addition of HB Ag to faecal extracts resulted in the conversion of a positive serological test for HB Ag to a negative one by a heat-labile agent active at 37°C but not at 4°C.…”

Section: Discussionmentioning

confidence: 99%

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The problem of the demonstration of hepatitis B antigen in faeces and bile

1974

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SYNOPSIS Attempts to detect hepatitis B antigen in faeces and bile should take into account the degradation and disappearance of the surface antigens in an environment containing proteolytic enzymes in the presence of bile salts as in the intestinal lumen. The cores of the Dane particles are much more stable than the surface antigens and these may best be identified by immune electron microscopy using core antibody.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

The problem of the demonstration of hepatitis B antigen in faeces and bile

1974

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“…In contrast, other studies failed to identify HBsAg in the feces [ 25 , 30 , 33 ]. It was hypothesized that intestinal mucosa containing an inhibitor of HBsAg and bile salts could damage HBV in the gastrointestinal tract [ 26 , 27 , 29 , 32 ]. However, these investigations were conducted in the 1970s, and the infectivity of feces had not yet been determined.…”

Section: Introductionmentioning

confidence: 99%

Lack of infectivity of HBV in feces from patients with chronic hepatitis B virus infection, and infection using chimeric mice

et al. 2015

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BackgroundBody fluids such as saliva and tears from patients with hepatitis B virus (HBV) infection are known as infectious agents. The infectivity of feces from patients with HBV infection has not been established. The aim of this study was to determine whether feces from HBV carriers can be a source of HBV infection.MethodsThirty-three children and 17 adults (ages 0–49 years, median age 13 years) who were chronically infected with HBV were enrolled. The levels of HBV DNA in the feces from these patients were quantified by real-time PCR, and the levels of fecal HBsAg were measured. Isolated human hepatocytes from chimeric mice with humanized livers were co-cultured with serum, tears and feces from the HBV carriers. Four chimeric mice were inoculated intravenously with sterilized feces from HBV carriers.ResultsHBV DNA was detected in the feces of 37 (74 %) of the 50 patients. The fecal HBV DNA levels ranged from 2.8 to 8.4 log copies/mL (mean ± SD = 5.6 ± 1.2 log copies/mL). A significant correlation was observed in the levels of HBV DNA between serum and feces (r = 0.54, p < 0.05). Of the 13 HBV carries, 7 (54 %) were positive for fecal HBsAg. The fecal HBsAg levels ranged from 0.06 to 1.0 IU/mL (median 0.28 IU/mL). Immunogold electron microscopy showed Dane particles in feces. HBV DNA was detected in the human hepatocytes co-cultured with serum and tears, but not in those co-cultured with feces. HBV DNA was not detected in the serum of the chimeric mice after oral or intravenous inoculation with sterilized fecal samples, which contained 5 log copies/mL of HBV DNA levels.ConclusionsAlthough the positive rate of fecal HBV DNA was high, the fecal HBsAg levels were extremely low. The chimeric mice were not infected with HBV after oral or intravenous inoculation with sterilized fecal samples. Therefore, feces from HBV carriers seem not to serve as an infectious vehicle for the transmission of HBV.

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“…Determination of HB^Ag was performed on the various samples by IEOP according to Pesendorfer et al [6] and Prince and Burke [7], Only for some of the samples was the presence of HBsAg tested by solid phase radioimmunoassay [8] and by Ausria 11-125 [9], Dosage of biliary bilirubin was done according to the method of J endrassik and G rof [10]. The inhibitor was prepared from human feces according to the methods previously described [11], Partial purification was achieved by ultracentrifugation and con centration procedures.…”

Section: Methodsmentioning

confidence: 99%

Presence of HBsAg in the Bile of Subjects with Acute HBsAg Viral Hepatitis

Piazza¹,

Cacciatore²,

Molinari³

et al. 1975

Pathobiology

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During acute HB_sAg serum positive viral hepatitis, the surface antigen was not detectable in duodenal bile but was almost always present in gallbladder and hepatic bile when cholecystokinin was intravenously administered. The immunologic nondemonstrability of HB_sAg in duodenal bile is probably due to the presence of a factor elaborated by the intestinal mucosa. The possible role played by this factor in the non transmission of type B viral hepatitis via faecal-oral route is suggested.

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Hepatitis B Antigen Inhibitor in Human Faeces and Intestinal Mucosa

Cited by 32 publications

References 23 publications

The problem of the demonstration of hepatitis B antigen in faeces and bile

The problem of the demonstration of hepatitis B antigen in faeces and bile

Lack of infectivity of HBV in feces from patients with chronic hepatitis B virus infection, and infection using chimeric mice

Presence of HBsAg in the Bile of Subjects with Acute HBsAg Viral Hepatitis

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