Spontaneous Clearance and Reactivation of Hepatitis B Virus Infection Among Male Homosexuals with Chronic Type B Hepatitis

Abstract

Abrupt increases of alanine transaminase were observed in 6 of 23 non-treated, male homosexuals with chronic hepatitis associated with hepatitis B virus. Before this occurrence, all subjects had hepatitis B e antigen (HBeAg) and elevated DNA polymerase activity. Within 3 months, HBeAg was nondetectable in 3 subjects and elevated DNA polymerase disappeared in 4. These serologic events were not always sustained, however. In 3 subjects, reactivation of hepatitis B virus infection occurred within the subsequent 6-month period. Serologic testing for cytomegalovirus, Epstein-Barr virus, delta agent, and hepatitis B surface antigen (HBsAg) subtype showed that episodes of clearance and reactivation were not explainable by secondary infection with these agents or infection with a different HBsAg subtype. Spontaneous clearance and reactivation of hepatitis B virus infection may commonly occur among male homosexuals with chronic type B hepatitis. These phenomena should be considered when evaluating the need for treatment or interpreting the results of investigations that use anti-viral therapy.

Quantification of intrahepatic hepatitis B virus (HBV) DNA in patients with chronic HBV infection

“…6,24 We and others have previously reported the possible persistence of detectable levels of intrahepatic free viral genomes despite the absence of serum HBV DNA, 5,37,38 and we may suppose that such episomal forms persist as covalently closed circular DNA and represent the virus reservoir involved in the reactivation of the productive viral replication that may occur in patients with apparently extinguished HBV infection. [7][8][9][10][11][12]33,34 The discrepancy between the relatively high amount of liver HBV genomes and low levels of serum HBV DNA appears to be of particular interest in patients under lamivudine treatment. This therapy, enabling formation of new virions, induces a fall of viremia levels at values corresponding to the limit of sensitivity of a single step PCR assay.…”

“…Consequently, HBsAg-positive patients with suppressed viral replication and undetectable levels of viremia have usually low grade or absence of hepatocellular injury. [2][3][4] Nevertheless, several observations suggest that an undefined amount of free viral genomes may persist into the hepatocytes of these subjects, 5,6 and such episomal HBV forms might be implicated in the reactivation of silent infections that may occur either spontaneously [7][8][9] or in conditions of immunosuppression, [10][11][12] or, in patients treated with antiviral drugs, after stopping therapy. [13][14][15][16][17] Thus, analysis and quantification of intrahepatic HBV genomes appear to be of biological interest and may provide useful clinical information.…”

Acute Exacerbation of Chronic Hepatitis B: The Dilemma of Differentiation from Acute Viral Hepatitis B

“…It is more common in male homosexuals, patients who are infected with human immunodeficiency virus (HIV), concurrent with bacterial infections or surgery, when there is emotional or physical stress and in pregnancy. [52][53][54] Exacerbation of chronic HBV infection has been shown to occur after delivery, which may be due to a reactivation of the immune system after delivery. 55 Patients receiving highly active antiretroviral therapy (HAART) for HIV may develop HBV-associated severe hepatitis due to HAART-induced immune reconstitution.…”

Severe acute exacerbation in chronic hepatitis B virus infection in Sendai, Japan.

“…Six cases were suspected to result from spontaneous reactivation and 2 from drug-induced reactivation of chronic HBV infection, and the other 2 from superinfection with non-A, non-B hepatitis agent (s). These results suggest that the reactivation of chronic HBV infection is an important factor of severe acute exacerbations in chronic HBV infection in Japan.severe acute exacerbation ; HBsAg carrier ; reactivation of chronic HBV infection Patients with chronic type B hepatitis positive for hepatitis B e antigen (HBeAg) are considered to experience frequent acute exacerbations (Perrilo et al 1984;Liaw et al 1987). However, the exacerbations occasionally occur in hepatitis B surface antigen (HBsAg) carriers negative for HBeAg (Liaw et al 1987).…”

“…Patients with chronic type B hepatitis positive for hepatitis B e antigen (HBeAg) are considered to experience frequent acute exacerbations (Perrilo et al 1984; Liaw et al 1987). However, the exacerbations occasionally occur in hepatitis B surface antigen (HBsAg) carriers negative for HBeAg (Liaw et al 1987).…”