Carrier, chronic, HBsAg

For chronic HBsAg carriers (s. p. 425), there are no comprehensive regulations to follow with respect to professional conduct, everyday routine and family life. Yet they must be well informed about their condition and should be fully aware of the danger they pose. Provided the respective hygiene measures are observed, restrictions in professional life are generally not necessary. 

Acute viral hepatitis D/B is precipitated by an initially uncoated (incomplete, defective) human apathogenic viroid, which subsequently acquires HBsAg as its envelope protein. This hepatitis delta virus (HDV) becomes pathogenic as a result of two different infection modes (i.) simultaneous infection of HBV and HDV (= coinfection) and (2.) infection of a chronic HBsAg carrier with HDV (= superinfection). 

The HDV infection of a chronic HBsAg carrier leads to the suppression of HBV synthesis, so that HBsAg, HBcAg and HBeAg are no longer detectable. By contrast, anti-HDV can be identified earlier and at a higher titre. (s. fig. 22.19)... 

In terms of coinfection, prevention is only possible by means of passive or active immunization against HBV. It is imperative for chronic HBsAg carriers to avoid HDV endemic areas. However, should this not be possible, strict protective measures against HDV infection are called for. 

Pasture, G., Monno, L., Santantonlo, T., Angavano, G., Milella, M., GiannelU, A., Fiore, J.R. Hepatitis B virus clearance from serum and Uver after acute hepatitis delta superinfection in chronic HBsAg carriers. X Med. Virol. 1990 31 284-290... 

Plasma-derived hepatitis B virus vaccine is prepared from the plasma of chronic HBsAg carriers, and consists of purified, inactivated 20-nm HBsAg particles adsorbed on to an aluminium adjuvant. The use of a vaccine produced with plasma derived from infected individuals represented a major departure from conventional approaches, and safety testing has therefore been designed to cover all possibilities of risk and to ensure freedom from transmission of residual HBV and other blood-borne agents. Various clinical trials (SEDA-10, 289) (SEDA-11, 289) have confirmed the safety of plasma-derived hepatitis B virus vaccines produced by different manufacturers. Fears that plasma-derived vaccine may transmit AIDS can be considered unfounded. 

Hoofnagle, J. H et al. (1987). Chronic type B hepatitis and the healthy HBsAg carrier state. Hepatology 7,758-763. 

Approximately 350 million people worldwide are chronic carriers of HBV, with the majority living in Asia and Africa. In the United States approximately one million people have chronic HBV infection. Although chronically infected, individuals may remain asymptomatic for long periods. Spontaneous loss of HBeAg occurs in 7% to 20% of patients each year, but spontaneous loss of HBsAg occurs in only 1% to 2% per year [14]. Health experts estimate that 2% of patients with chronic HBV infection develop cirrhosis each year, and that 15% to 25% of patients with chronic HBV infection will die prematurely from cirrhosis or hepatocellular carcinoma (HCC). 

Anti-HBc IgM is the earliest immunological response of the body to HBV antigens. It is the most reliable marker, and once the disease is overcome, it can probably be demonstrated lifelong as anti-HBc IgG. In chronic hepatitis B carriers, low titre anti-HBc IgG may also be present. It is the most suitable marker for the HBV contamination rate of a population (more reliable than anti-HBs). The absence of HBsAg and anti-HBc IgM rules out acute HBV infection. In healthy patients who test positive for anti-HBc, latent viral replication is usually still to be found. This can be detected with the help of PCR. Active vaccination does not result in positive anti-HBc IgM. (s. p. 114)... 

Bonino, F., Rosina, F., Rizzetto, M., Rizzi, R., Chiaberge, E., Tardanico, R., Callea, F., Verme, G. Chronic hepatitis in HBsAg carriers with serum HBV-DNA and anti-HBe. Gastroenterology 1986 90 1268-1273... 

Chronic viral hepatitis Within a pieriod of 5-6 years, cirrhosis is caused by chronic viral hepatitis B in 15-30%, chronic viral hepatitis C in 20-50% and chronic viral hepatitis B/D in up to 60% of cases. The risk of cirrhosis is 4.2 times higher in HBsAg carriers and 2.3 times higher in carriers of anti-HCV than in pieople without these serum markers. (68, 78, 114, 144)... 

HBV is not considered a cytopathic virus in certain circumstances, however, it can cause direct cytotoxic liver injury. Direct cytopathic liver injury can occur when the viral load is very high, as in the rare fibrosing cholestatic hepatitis. After the HBV enters the vascular compartment, it migrates to the liver, where primary replication occurs. The incubation period of HBV is 1 to 6 months—much longer than HAV. HBV replication occurs in liver cell nuclei, with HBsAg produced in the cell cytoplasm and expressed on the cell surface. These particles are also found circulating in the plasma of patients with acute HBV, the chronic carrier state, and chronic HBV infection. ... 

Villa, E., Rubbiani, L., Barchi, T., Ferretti, I., Grisendi, A., de Palma, M., Bellentani, S., and Manenti, F., 1982, Susceptibility of chronic symptomless HBsAg carriers to ethanol-induced hepatic damage. Lancet ii 1243. 

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