Hepatitis virus infection through virus reactivation has a high risk of mortality in patients with hematological malignancies receiving chemotherapy. We examined the incidence of both hepatitis B virus (HBV) and hepatitis C virus (HCV) infection and severe liver dysfunction (alanine aminotransferase >ten times the normal upper limit and total bilirubin >5 mg/dl) during chemotherapy in 268 patients with hematological malignancies. Eight patients (3.0%) were infected with HBV and 22 patients (8.2%) were infected with HCV. One patient (0.4%) was infected with both HBV and HCV. HBV- or HCV-infected patients showed severe liver dysfunction at a significantly higher incidence than non-infected patients (11/31 (35.5%) vs. 0/237 (0%), p<0.0001). Furthermore, the incidence of severe liver dysfunction in HBV-infected patients was significantly higher than in HCV-infected patients (6/8 (75.0%) vs. 4/22 (18.2%), p<0.01). Three of eight HBV-infected patients were initially negative for hepatitis B surface antigen (HBsAg) by latex agglutination and became positive for HBsAg during chemotherapy. Furthermore, all three patients developed severe liver dysfunction and two developed fatal fulminant hepatitis. From an examination of the original stock of serum samples before chemotherapy, two patients were found to be positive for HBV-DNA by polymerase chain reaction (PCR). Although post-transfusion HBV infection was suspected in the one remaining patient, the cause of HBV infection could not be clarified due to the impossibility of examination in blood donors. Since HBV-infected patients develop severe liver dysfunction at a higher incidence than either patients not infected with virus or HCV-infected patients before chemotherapy for hematological malignancies, it is recommended that HBV-DNA should be tested by PCR to detect HBV marker-negative carriers and liver function tests should be carefully monitored.

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To investigate the clinical role of the soluble form of c‐kit receptor (s‐kit) in patients with acute myeloid leukemia (AML), we determined the levels of serum s‐kit and expression of c‐kit antigens and mRNA in leukemic cells. The serum s‐kit level was measured using ELISA assay in 30 AML patients and 20 normal controls. C‐kit antigens of leukemic blasts were stained immunohistologically, and c‐kit mRNA was detected by RT‐PCR. The serum s‐kit level in M1 and M2 were significantly increased (p<0.01) and that in M4 or M5 was significantly decreased (p<0.05) compared to that in the controls. In the comparisons among subtypes of FAB classification, M1 and M2 showed significantly higher levels than M4 or M5 (p<0.05 and p<0.01, respectively). Both expression of c‐kit antigens and mRNA were observed in M0 (1/4), M1 (2/4) and M2 (6/8), but neither was observed in M4 or M5. The serum s‐kit levels were correlated with the absolute number of AML blasts in peripheral blood (r=0.564, p<0.05). These results indicate that the serum s‐kit level is related to the stage of differentiation of AML blasts in accordance with the expression of c‐kit protein and mRNA in AML blasts, and is useful for assessment of leukemic cell burden.

The budding process and fine structure of lymphadenopathy-associated virus (LAV), were studied by indirect immunofluorescence (IF) and electron microscopy (EM). By IF, LAV antigen was seen to be distributed focally within infected CCRF-CEM cells. Consistent with this finding, electron micrographs showed that LAV particles occurred in a focally aggregated state in a restricted area of the surface of the infected cells. LAV particles possessed bar-shaped, dense and central or eccentric cores. In addition, two or more cores were occasionally observed in one virus particle, or the cores were sometimes absent when thin sections were examined. The envelope of the virus particles had an irregular structure, although LAV particles were approximately spherical.Previous studies have shown that a novel human retrovirus is the causative agent of acquired immunodeficiency syndrome (AIDS) and AIDS-related complex (ARC). Lymphadenopathy-associated-virus (LAV) was isolated initially from cultured T lymphocytes of a homosexual man with lymphadenopathy syndrome (1). Viruses antigenically and morphologically related to LAV were subsequently isolated from individuals with AIDS and ARC, and designated human T-lymphotropic virus type III (HTLV-III) (5) and AIDS-associated retrovirus (ARV) (10). These viruses were later found to be variants of the same virus as shown by comparison of their complete nucleotide sequences (12,15,16,19). The authorized nomenclature of the virus has not yet been decided. LAV has a cytopathic effect on OKT-4 positive lymphocytes (9) and an epitope of the OKT-4 antigen was recently shown to be a component of the receptor for LAV (2,8). Previous studies showed that LAV is released from infected cells by budding from the plasma membrane and that a unique feature of the virus is a cylindrical core observed in many mature virions (5). It is increasingly evident that LAV could be best classified within the lentivirus group of retroviruses (6,(17)(18)(19). However the budding process and fine structure of LAV have not been clearly defined. We report here the data on the budding process and fine structure of LAV obtained by indirect immunofluorescence (IF) and electron microscopy (EM).

We report a case of a 41-year-old man with acute myelogenous leukemia who developed fulminant hepatitis from reactivation of trace hepatitis B virus (HBV) 2 months after complete remission. Although he became positive for HB surface antigen at the onset of fulminant hepatitis, he had been negative for HBV serum markers, and only HBV DNA was detected by polymerase chain reaction (PCR) amplification on admission. The original stocks of serum samples from all blood donors were tested again for HBV DNA by PCR, and all samples were negative. This case demonstrates that testing for HBV DNA by PCR is necessary before chemotherapy, because silent HBV carriers are rare and fulminant hepatitis may be induced by chemotherapy in patients with hematologic malignancies.