Acute demyelination in mice inoculated intraspinally with mouse hepatitis virus, JHM strain

After intracerebral or intralumbar inoculation of mouse hepatitis virus, JHM strain, into weanling mice, viral growth and lesions in the central nervous system were comparatively studied for 5 days postinoculation. In the intralumbar group the virus titer of the spinal cord exceeded that of the brain until 24 hr postinoculation, and declined later. In the intracerebral group the brain virus titer was always higher, and the cord titer attained the same level as that of intralumbar group at 72 hr. Demyelinating lesions in the spinal cord appeared 48 hr after intralumbar inoculation, that is, 36 hr earlier than after intracerebral inoculation. Virus-specific fluorescence was detected within glia cells in the cord white matter 48 hr intralumbar inoculation. Electron microscopy revealed a number of virions within oligodendroglia cells, suggesting that the acute phase demyelination might be due to viral growth within this type of cells.     

已接种甲肝疫苗的HIV感染者出现急性甲型肝炎病毒感染:田纳西州,2018

完全免疫甲肝病毒(HAV)需要接种2剂单价疫苗或3剂甲肝和乙肝联合疫苗,约90%的人在接种单剂疫苗后体内抗体可达保护水平。然而,人类免疫缺陷病毒(HIV)感染者可能不会产生相同水平的免疫力。在HAV暴发期间,评估HIV感染者疫苗应答因子(第一次疫苗接种时的CD4计数和HIV病毒载量)通常并不可行。卫生部门使用HAV疫苗接种史指导HAV暴露后预防(PrEP)相关的管理决策,然而,接种甲肝疫苗的HIV感染者可能无法在高风险暴露后获得可靠的保护性预防。     

Hepatitis B virus,hepatitis C virus

Medical workers should have anti-HBV antibody to protect HBV infection in the hospital. If they have not anti-HBV antibody, they should receive HBV vaccination. HBV vaccination program is as follows: 10 micrograms, s.c., 0, 1, 6 months. In case of HBV contamination, 1,000 IU hepatitis B immune globulin(HBIG) and/or 10 micrograms HB vaccine should be administered judging from HBV markers of contaminated subjects and HBV load of patients. The HCV vaccine is not available. In case of HCV contamination, it is unnecessary to treat just after accident. If acute hepatitis C is evolved in those subjects during follow-up, it is recommended to treat with interferon. Eradication of HCV by interferon among patients with acute hepatitis C will be almost 100%.     

Prevention of mother-to-child transmission of hepatitis B virus and hepatitis C virus

About 240 million people worldwide are chronically infected with hepatitis B virus (HBV). Vertical transmission is the most important mechanism of infection persistence in endemic areas. About 150 million people worldwide are chronically infected with hepatitis C virus (HCV). Mother-to-child transmission of HCV, which occurs in 3–10% of cases, is the leading route of infection in childhood. This review focuses on strategies to reduce the vertical transmission of HBV and HCV. The at-birth prophylaxis of newborns of HBV-infected mothers with specific immunoglobulin and vaccine plus administration of antivirals (tenofovir or telbivudine) in the third trimester of pregnancy (in case of high maternal viral load) greatly reduces the risk of transmission. In contrast, currently there is no drug able to reduce the vertical transmission of HCV infection. We discuss the possibility of reducing mother-to-child HCV transmission using newly available antivirals or antivirals in the pipeline for the treatment of hepatitis C.     

Acute hepatitis after amiodarone infusion

Acute hepatitis is a very rare, but potentially fatal, adverse effect of intravenous amiodarone. We present a case of an 88-year-old man with history of ischemic dilated cardiomyopathy and severely depressed left ventricular function that was admitted to our coronary care unit with diagnosis of decompensated heart failure and non-sustained ventricular tachycardia. A few hours after the beginning of intravenous amiodarone he developed an acute hepatitis. There was a completely recovery within the next days after amiodarone withdrawn and other causes of acute hepatitis have been ruled out. This case highlights the need for close monitoring of hepatic function during amiodarone infusion in order to identify any potential hepatotoxicity and prevent a fatal outcome. Oral amiodarone is, apparently, a safe option in these patients.     

Acute hepatitis associated with mouse leukemia. IV. The relationship of Eperythrozoon coccoides to the hepatitis virus of Princeton mice

The hepatitis of Princeton weanlings was not prevented by the prior injection of terramycin nor was the virus inactivated by exposure to room temperature. Eperythrozoon coccoides was not demonstrable in blood films from Swiss and Princeton mice infected with the corresponding type of hepatitis virus. Combined infection with this virus and eperythrozoa, originally obtained by Dr. R. B. McGhee from mice in association with Plasmodium berghei, was attended by the appearance of numerous organisms in the blood. The development of eperythrozoa in dually infected Princeton mice had no effect on the outcome of the hepatitis. In Swiss mice, animals with high natural resistance to hepatitis virus, the pathogenicity of this agent was markedly enhanced by combined infection with eperythrozoa. Eperythrozoa were maintained throughout 18 successive passages in normal Princeton and Swiss weanlings with intact spleens. The combined infection of Princeton mice with eperythrozoa and the virus component of Gledhill, Dick, and Andrewes, which is nearly inactive when injected alone, resulted in acute hepatitis with fatal outcome.     

Acute hepatitis associated with mouse leukemia. V. The neurotropic properties of the causal virus

Observations on the behavior of MHV (Pr) in the cerebral tissue of Princeton and Swiss weanling mice indicated a limited neurotropism. The virus migrated to the brain on intraperitoneal injection and was established there by cranial passage, though with difficulty in Swiss mice. Intracerebral multiplication was rarely followed by outward signs of nervous disorder. A slight pathologic reaction occurred in the brains of intracerebrally injected Princeton mice, but it was negligible compared with that of the ensuing hepatitis. In Swiss mice, injected intracerebrally with a mixture of MHV (Pr) and Eperythrozoon coccoides, a related virus with restricted pathogenicity and host range, possibly a mutant, was isolated from the liver and brain. MHV (C), an actively hepatotropic virus recovered from leukemic Balb C mice, was much more neurotropic than MHV (Pr). Intracerebral injection of Balb C and Swiss weanling mice was attended by marked leptomeningeal and encephalitic lesions. Paralysis of the extremities occurred in some of the animals. The virus was essentially inactive in Princeton mice. During the intracerebral passage of MHV (C) in Swiss mice a pleuropneumonia-like organism was isolated from the brain. In conjunction with the virus this organism produced a vigorous leukocytic reaction.     

Transmission of serologically silent hepatitis B virus along with hepatitis C virus in two cases of posttransfusion hepatitis

The polymerase chain reaction (PCR) was used to investigate the presence of hepatitis B virus (HBV)-related DNA sequences in blood from three blood donors and two transfusion recipients who developed posttransfusion non-A, non-B hepatitis (NANBH). In the first case, the sole donor was positive for antibody to hepatitis B surface (HBs) and core (HBc) antigens and had elevated alanine aminotransferase (ALT) levels, while the recipient had no HBV serologic markers. Both the donor and the recipient had serologic markers of hepatitis C virus (HCV) and were found positive for HBV DNA and HCV RNA sequences by PCR. The second case involved two donors and one recipient. Serologic tests for conventional HBV markers were negative in all three individuals, but one of the donors had elevated ALT. HBV DNA sequences were detected by PCR in the serum of the recipient and of the donor with high ALT, but not in the serum of the donor with normal ALT. Anti-HCV was detected in the serum of the recipient and of the suspect donor but not in that of the donor with normal ALT. The sequences amplified in the S region and determined after cloning of PCR products for both donor-recipient pairs were indistinguishable from each other and identical to the sequence of the major HBV subtype of adw in the first case and ayw in the second case. Furthermore, for the second case, an identical single-point mutation was found in both the donor and the recipient. These data confirm the transmission of conserved HBV sequences together with HCV in posttransfusion NANBH.(ABSTRACT TRUNCATED AT 250 WORDS)     

Classifying hepatitis B virus genotypes

In 1988, hepatitis B virus (HBV) was classified into four genotypes by a sequence divergence in the entire genome exceeding 8%, and designated by capital letters of the alphabet from A to D. There are seven genotypes of HBV (A-G) at present, and an eighth is on the horizon. They have an uneven geographical distribution, and only a few of them are prevalent in a given area of the world. Thus genotype A is frequent in northwest Europe, Sub-Saharan Africa, India and the North, Central and South America, B as well as C are common in Southeast Asia and Oceania, and D is prevalent in the Mediterranean area, Central Asia and South America. Genotype E is restricted to West Africa, and F is localized in Central and South America. The distribution of genotype G added to the alphabet list very recently has yet to be determined. Coinfection with HBV of distinct genotypes is not infrequent and found in about 10% of infected individuals, and is responsible for intertypic recombination of HBV genomes. The mutation for a stop codon in the precore region (G1896A) for aborting the translation of hepatitis B e antigen (HBeAg) is prohibited in HBV genomes of genotype A, as well as some of genotypes C and F, because they possess C at position 1858 that makes a Watson-Crick pair with G at position 1896. Hence, seroconversion to antibody to HBeAg is forbidden or delayed in individuals who carry them. Evidence is accumulating as regards the influence of HBV genotypes on the progression of chronic hepatitis B and response to antiviral therapies. HBV isolates even of the same genotype can differ in virological and clinical characteristics, and therefore, the genotype needs to be classified further into subtypes, especially if they are clinically relevant.     

Acute cholestatic hepatitis associated with celecoxib

OBJECTIVE: To report a case of acute cholestatic hepatitis associated with the selective cyclooxygenase-2 inhibitor celecoxib. CASE SUMMARY: A 41-year-old white man was hospitalized for jaundice after 2 doses of celecoxib 200 mg for pain associated with right-knee trauma. Laboratory workup showed hyperbilirubinemia, mildly elevated serum transaminase concentrations, and cholestasis. Abdominal imaging showed no dilation of the biliary tree. Histology showed cholestasis, with bile plugs in dilated bile canaliculi and a mild portal infiltrate that are highly suggestive of drug-induced cholestasis. DISCUSSION: This is the fourth report in the English-language literature describing cholestatic hepatitis temporally related to celecoxib use, the second supported by histologic findings typical of drug-induced cholestasis, and the first in a patient who denied use of alcoholic beverages and was taking no other drugs or herbal products at the time of the reaction. The Naranjo probability scale indicated that celecoxib was a probable cause of acute cholestatic hepatitis in this patient. CONCLUSIONS: Cholestatic hepatitis is a well-recognized adverse effect of several drugs. Although celecoxib is considered to have a very low potential for hepatic toxicity, well-documented reports of adverse reactions can contribute significantly to the definition of more accurate safety profiles for new drugs introduced into clinical practice.     

Persistent infection mechanism of GB virus C/hepatitis G virus differs from that of hepatitis C virus

OBJECTIVE: Changes in the deduced amino acid sequence of the envelope 2 (E2) region of the GB virus C/hepatitis G virus (GBV-C/HGV) were analyzed to investigate whether or not the region contributes to persistent infection with the virus. METHODS: Eight patients with acute hepatitis C and 1 patient with acute hepatitis of unknown etiology were included in the study. GBV-C/HGV RNA was detected in 6 patients, including the patient with hepatitis of unknown origin. The nucleotide sequence of the E2 region of hepatitis C virus (HCV) and GBV-C/HGV was determined by direct sequencing of polymerase chain reaction products in 5 patients with HCV infection and in 6 patients with GBV-C/HGV infection twice during the period of early infection and several months or years later in each patient. RESULTS: The mean substitution rate of the deduced amino acid sequence in the E2 region was over 100 times lower (p < 0.001) in GBV-C/HGV (0.01 +/- 0.04/month/100 sites) than in HCV (2.4 +/- 1.7/month/100 sites). The amino acid sequence of the loop domain of GBV-C/HGV-E2 did not change in any of the 6 patients. On the other hand, the sequence of the hypervariable region of HCV-E2 changed remarkably (5.9 +/- 4.3/month/100 sites). No amino acid substitution in the loop domain was observed in 7 additional patients who showed persistent GBV-C/HGV viremia for more than 2 years. CONCLUSION: These results indicate that changes in the amino acid sequence of the E2 region are not involved in the mechanism of persistent GBV-C/HGV infection.     

Acute cholestatic hepatitis induced by fenofibrate

We report a case of acute liver injury probably due to fenofibrate. A 50-year-old female without a history of liver disease developed cholestatic hepatitis during her second week of fenofibrate treatment. Laboratory tests on admission showed serum bilirubin 534·0 mcmol/L (conjugated 444·0), alkaline phosphatase (AP) 8·76, gamma-glutamyl traspeptidase (GGT) 20·92, alanine aminotransferase (ALT) 2·6, aspartate aminotransferase (AST) 3·64 mckat/L. Fenofibrate withdrawal and ursodeoxycholic acid (750 mg daily) administration was rapidly followed by a favourable outcome.