The frequencies of HLA class I antigens and class II haplotypes were compared in subjects with previous (polymerase chain reaction [PCR]-negative) or with persistent (PCR-positive) hepatitis C virus (HCV) infection and in HCV patients with mild versus severe histologic activity scores on liver biopsy. The DRB1*11 allele group was found in 11 (31.4%) of 35 subjects with previous infection and in 11 (8.2%) of 135 subjects with persistent infection (P < .001). The DQB1*0301 allele was found in 18 (51.4%) of 35 subjects with previous infection and in 33 (24.4%) of 135 patients with persistent infection (P < .002). Both observations remained significant after correction for multiple testing. No significant association was shown between severity of disease and any HLA class I or II type. Thus, the HLA class II alleles DRB1*11 and DQB1*0301 are associated with clearance of circulating HCV.

Peripheral blood monocytes (PBM) are one site of persistence of human cytomegalovirus (HCMV) in healthy carriers. However, because PBM circulate only briefly before entering the tissues and are difficult to infect with HCMV, it has been suggested that they may acquire HCMV during development in the bone marrow. Consistent with this, we show evidence that bone marrow progenitors from healthy HCMV carriers contain endogenous HCMV DNA as detected by PCR. We also show that bone marrow precursors are readily infected by clinical isolates of HCMV in vitro but that no viral gene expression occurs until these cells become differentiated. In contrast, incubation of these cells at any developmental stage with the laboratory strain AD169 resulted in few cells expressing viral immediate-early genes, and this correlated with a lack of entry of AD169 virus. These observations are consistent with bone marrow progenitors acting as a reservoir for HCMV and transmitting the viral genome to PBM, in the absence of lytic-gene expression, until they leave the circulation and undergo tissue-specific differentiation to macrophages.

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Summary A 38 year old man developed meningitis following a dog bite. Pasteurella pneumotropica, usually an animal pathogen, was isolated from the cerebrospinal fluid. The patient made a complete recovery after antibiotic therapy. The relevant literature is reviewed.

Hepatitis G virus (HGV) is a flavivirus that can cause acute hepatitis and persistent infection but its role in chronic liver disease or primary liver cancer is unproven. In this study we have examined the prevalence of HGV RNA in the serum of patients with hepatitis C virus (HCV) infection and in patients with cryptogenic chronic liver disease, including non-alcoholic steatohepatitis (NASH), and in patients with HCV-related hepatocellular carcinoma (HCC) and HCC arising in patients with cryptogenic liver disease. One-hundred and thirty patients who were positive for antibody to HCV (anti-HCV), 54 patients with cryptogenic chronic liver disease (including 17 patients with NASH) and 46 patients with hepatitis C-related (n = 27) or cryptogenic liver disease-related HCC (n = 19) were studied. HGV RNA was detected using nested reverse transcriptase-polymerase chain reaction (RT-PCR) and was found in 16.1% of patients with HCV infection. HGV RNA was not detected in any patient with cryptogenic liver disease. In patients with HCC, 7/34 samples were positive for HGV RNA and six out of seven HGV-positive subjects also had HCV infection. Only one patient with HCC in cryptogenic liver disease was positive for HGV RNA. Hence, cryptogenic liver disease in the UK is not caused by HGV/GBVc infection. It seems unlikely that HGV plays a significant role in hepatocarcinogenesis.