Prevalence of Herpesviridae and Hepatitis B Virus Dna in the Liver of Patients With Non–A, Non–B Fulminant Hepatic Failure

Abstract

been linked with FHF in neonates, pregnancy, immunocomMembers of the herpes virus family and hepatitis B promised patients, and apparently healthy individuals. [5][6][7][8] Epvirus (HBV) have been implicated as etiologic agents in stein-Barr virus (EBV) infection may cause acute liver failure non-A, non-B (NANB) fulminant hepatic failure (FHF), in male infants with X-linked lymphoproliferative disease, but the frequency of infection with these agents has not immunocompromised patients, and those in whom it is acbeen established using appropriate controls. To examine quired sporadically. these findings. 4,18,19 To more accurately define the contribuand 14 of 104 control patients (13%) were positive for tion of the herpes viruses and cryptic HBV infection to NANB CMV DNA. Two of 50 FHF (4%) and 10 of 104 control FHF, we systematically assessed the livers of both patients patients (10%) had EBV DNA, and HBV DNA was obwith acute liver failure and representative controls for eviserved in 3 of 10 North American FHF patients (30%) dence of viral sequences using the polymerase chain reaction and 3 of 59 controls (5%) without serum markers for HBV (PCR). tion was diagnosed by evaluating serum for anti-hepatitis A virus Received March 8, 1996; accepted August 9, 1996. immunoglobulin M, hepatitis B surface antigen and hepatitis B core immunoglobulin G (CMV IMX, Abbott Laboratories, Chicago, IL) and

Hepatitis B Infection in Patients With Acute Liver Failure in the United States

“…Despite these limitations, our sample size of 19 liver specimens is larger than other published reports. 6,7,8,12 Thus, we believe that occult hepatitis B infection is extremely rare among patients with ALF in the US. Precore stop-codon variants had been previously reported to be rare in the US, because the predominant HBV genotype A precludes the development of the G 1896 A mutation.…”

“…[3][4][5] Available data on the prevalence of occult hepatitis B infection among patients with ALF in the US are conflicting and based on very few studies in a small number of patients. The prevalence of occult hepatitis B infection in patients with ALF was reported to be 30% to 50% in 3 studies that involved a total of 31 patients, [6][7][8] but absent in 2 other studies that involved a total of 23 patients. 13,14 Studies that examined both sera and liver tissues invariably reported higher rates of HBV detection in the liver.…”

“…[3][4][5][6][7][8] In these patients, the etiology of ALF may be related to occult hepatitis B infection. The prevalence of occult hepatitis B infection in patients with non-A, non-B ALF has been reported to vary from a low of 0% to 4% in Europe [9][10][11][12] to 50% in Japan.…”

Molecular basis for persistent hepatitis B virus infection in the liver after clearance of serum hepatitis B surface antigen

“…These 4 patients had no history or serological evidence of HBV infection, and HBV DNA was not detected by PCR in the total cellular DNA extracted from their native liver. 24 Additional control samples included DNA extracted from the HBsAg-producing hepatoma cell line, PLC/PRF/5, 22 and sucrose gradient-purified Dane particles (approximately 560 particles per PCR reaction) derived from pooled serum of patients with chronic HBV.…”

Infecção oculta pelo vírus da hepatite B em comunidade amazônica submetida a intenso fluxo migratório, estado do Pará, Brasil

“…A reativação da hepatite crônica B ou mesmo o surgimento de falência hepática fulminante foi relatada em pacientes com IOB submetidos à terapia citotóxica, a transplante autólogo de células-tronco, transplante alogênico de medula óssea, linfoma, anemia aplástica ou leucemia 12,13,14,15,16,17,18 .…”