Cases reported "Superinfection"

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1/10. Clearance of HCV rna in a chronic hepatitis c virus-infected patient during acute hepatitis b virus superinfection.

    The routes of hepatitis b virus and hepatitis c virus transmission are quite similar and coexistence of both viruses in one patient is not a rare phenomenon. Until now, the natural course of liver diseases induced by coinfections has not been well documented and the mechanisms of interaction between the two viruses and the human host have not been fully clarified. We report the case of a patient suffering from chronic hepatitis due to hepatitis c virus who developed an acute hepatitis b virus superinfection. serum hepatitis c virus ribonucleic acid became undetectable by reverse transcriptase/polymerase chain reaction at diagnosis of acute hepatitis b virus infection. At the same time, there was a striking increase in the serum concentrations of the antibodies against C22 and C33c hepatitis c virus antigens. Four months after clinical resolution of the acute hepatitis, hepatitis B surface antigen was undetectable in serum and three months later antibodies against hepatitis B surface antigen appeared. Two years after acute hepatitis b virus infection, the patient has had no relapse of markers for viral replication of hepatitis b virus. transaminases are within the reference range and hepatitis c virus ribonucleic acid is undetectable in both serum and liver tissue. We hypothesize that acute hepatitis b virus infection stimulated a specific humoral response against hepatitis c virus as well as triggering non-specific defense mechanisms which finally eliminated both viruses.
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2/10. In vivo down regulation of HIV replication after hepatitis c superinfection.

    There are increasing molecular and clinical evidences that the effects of human immunodeficiency virus (HIV) infection can be modified by coinfection with other viruses. The objective was to investigate the viral interaction between HIV and hepatitis c virus (HCV) after HCV superinfection. A 16 year-old pregnant woman was evaluated because of icteric acute hepatitis. Admission laboratory tests showed the following results: ALT 877 IU/L; AST 1822 IU/L; bilirubin 6.79 mg/dl. diagnosis of acute HCV was based on detection of serum HCV rna by PCR and anti-HCV seroconversion. ELISA for anti HIV testing was positive and confirmed by western blot. serum markers for other viruses were negative. The patient was followed during 19 months; serum samples were taken monthly during this period for detection of plasma HIV and HCV rna. Levels of plasma HIV-rna were positive in all samples tested before and after the onset of acute hepatitis c. Six months later and a for two month period, and 13 months later for a period of one month HIV viremia was undetectable; then HIV-rna in plasma was detectable again. In conclusion, HCV superinfection may have temporarily interfered with HIV replication in our patient. The following observations support our hypothesis: it has been demonstrated that hiv-1 replication is suppressed by HCV core protein which has transcriptional regulation properties of several viral and cellular promoters. Clinical implications of this event are not generally known and the interaction between these two viruses in dual infections is worth considering.
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3/10. Reactivation of hepatitis c virus superinfection in a patient seropositive for hepatitis B e antigen.

    During the course of chronic hepatitis b virus (HBV) infection, a patient seropositive for hepatitis B e antigen experienced four episodes of acute hepatic necroinflammation. serum HBV-dna concentration elevated immediately before the first and third exacerbations, whereas serum hepatitis c virus (HCV) rna was detected during the second and fourth exacerbations. The nucleotide sequences of HCV hypervariable region derived from samples of the two exacerbations were identical. Interestingly, "de novo" seroconversion of anti-HCV antibody (Abbott HCV EIA 3.0) followed by reversion occurred in both the second and fourth exacerbations with low sample/cutoff ratios. Immunoblot analysis using a line-immunoassay (Inno-LIA HCV Ab III) revealed a single positive band (C1) developing after the second exacerbation. These data indicate that the second exacerbation in this patient was caused by newly acquired acute HCV superinfection, whereas the fourth exacerbation was likely due to reactivation of the previous HCV infection. Recognition of such a case suggests that the presence of de novo seroconversion of anti-HCV may indicate either reactivation or acute superinfection of HCV in a patient seropositive for hepatitis B e antigen.
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4/10. hepatitis c virus eradication associated with hepatitis b virus superinfection and development of a hepatitis b virus specific T cell response.

    BACKGROUND/AIMS: Specific T cell responses during acute hepatitis B and during chronic hepatitis c have been described in detail. However, the T cell responses during the rare setting of acute hepatitis b virus (HBV) infection in the course of chronic hepatitis c that eventually lead to clearance of both viruses are completely unknown. methods: We analyzed the virus specific CD4 and CD8 T cell response during an acute HBV superinfection in a patient with chronic hepatitis c. RESULTS: The patient eliminated hepatitis c virus (HCV)-rna and HBV-dna from serum soon after the clinical onset of acute hepatitis B. The HBV specific T cell response found in this patient corresponds to the typical response that has been described in acute hepatitis B without chronic HCV infection. In contrast the hepatitis c specific immune response was similar to that generally found in chronic hepatitis c despite the fact that the patient also eliminated HCV-rna. CONCLUSIONS: We hypothesize that the acute HBV infection induced a HBV specific T cell response which was associated with elimination HBV dna and HCV-rna, the latter possibly by bystander mechanisms, e.g. via secretion of cytokines. If such a non-specific bystander mechanism which has proven to be effective in the experimental setting and which is formally described here for a single patient can be shown to be a more general phenomenon, it may support the approach with new antiviral strategies, e.g. the induction of non-specific defense mechanisms against HCV.
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5/10. Prospective study of amikacin versus netilmicin in the treatment of severe infection in hospitalized patients.

    PURPOSE: Four previous studies comparing netilmicin and amikacin have yielded inconclusive results concerning efficacy and rates of nephrotoxicity and ototoxicity. For this reason, we conducted a prospective, randomized, controlled trial of the two drugs in the treatment of hospitalized patients with severe infection. patients AND methods: A total of 202 patients were enrolled in the study; 100 received netilmicin and 102 received amikacin. Concomitant antimicrobials were restricted to metronidazole and benzylpenicillin. Peak and trough aminoglycoside levels were assayed within the first 36 hours and at least every 72 hours thereafter. A full blood cell count, serum electrolytes, creatinine, bilirubin, and liver enzymes were measured before therapy, weekly thereafter, and within 48 hours after the discontinuation of therapy. Nephrotoxicity and ototoxicity were assessed in patients. A standard agar dilution procedure was used to determine minimal inhibitory concentrations. RESULTS: No significant pretreatment differences were found between the two groups. patients in the amikacin group responded significantly better to treatment than did patients in the netilmicin group (90% versus 79%; p less than 0.05). A notable finding was the markedly inferior response rate of pseudomonas aeruginosa infections to netilmicin as compared with amikacin (13 of 24 with a favorable response compared with 25 of 26). No significant difference in ototoxicity was found, whereas nephrotoxicity appeared to be significantly less with amikacin (4% versus 12%, p less than 0.05). Although amikacin seemed less nephrotoxic than netilmicin, this may have been related to the significantly greater number of patients with initial renal dysfunction who received netilmicin. CONCLUSIONS: amikacin appears to be significantly more efficacious than netilmicin for the treatment of P. aeruginosa infections, especially those in non-urinary tract sites. There is no apparent difference between the two drugs in terms of ototoxicity.
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6/10. hepatitis a virus and non-A, non-B virus superinfections in HBsAg chronic carriers.

    Clinical course, morphologic changes, immunohistochemical localization of HBV-associated markers (HBsAg, HBcAg), and serum HBV-dna production are described in 2 chronic HBsAg carriers superinfected with HAV and hepatitis non-A, non-B virus. Our data suggest that the superinfections do not cause more severe disease and do not influence the clinical course of the HBsAg chronic carriers. Our observations indicate that a careful diagnosis of hepatocytolysis is necessary in HBV chronic infection, in order to discriminate causes that are able to induce severe damage in underlying disease.
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7/10. A possible misdiagnosis in patients presenting with acute HBsAg-negative hepatitis: the role of hepatitis delta virus.

    We describe here two cases of delta hepatitis (a coinfection and a superinfection) presenting as acute HBsAg-negative hepatitis. The first patient, a parenteral drug abuser, had a biphasic course of the disease, with HBsAg detectable transiently only during the relapse. Testing for delta markers on stored sera gave evidence of HBV/HDV coinfection. The other patient, a hospital nurse, chronic asymptomatic carrier of HBsAg, developed fulminant hepatitis with the transient appearance of antibody to HBsAg. She survived massive liver necrosis, and serological analysis of HDV markers documented a hepatitis delta virus superinfection. These cases demonstrate the possible substantial repression of HBV gene products exerted by the replication of delta virus, with a likely misdiagnosis if delta markers are not determined in serial serum samples.
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8/10. hepatitis b virus superinfection in a patient with chronic hepatitis c receiving alpha-interferon treatment.

    We report on a patient with chronic hepatitis c who developed acute hepatitis B during interferon alpha treatment. However, our patient promptly eliminated HBsAg and had a sustained complete response to interferon, even 6 months after the end of treatment. Acute hepatitis B superinfection in patients with chronic hepatitis c is a rarely observed event. The natural course of these patients is unknown. In our case it may be speculated that alpha-interferon treatment contributed to the prompt elimination of HBsAg from the serum.
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9/10. superinfection of heterologous hepatitis c virus in a patient with chronic type C hepatitis.

    A Taiwanese woman who had chronic infection of type II hepatitis c virus was superinfected by type III hepatitis c virus after blood transfusion. The subtypes of the hepatitis c virus were determined by direct sequencing of the envelope region of the viral genome in serial serum samples before and after transfusion. The original virus in the patient had a 95.6% homology to the Taiwanese isolate (a type II virus) by comparing nucleotide sequences of the envelope region. After transfusion, markedly elevated serum aminotransferase activities were noted and the virus sequenced showed only a 55.2% homology to the Taiwanese isolate but had a 88.9% homology to a Japanese isolate (a type III virus). After recovery from the acute episode, the newly introduced type III virus became undetectable and type II virus predominated again but with significant genetic variation in the follow-up samples as compared with the original type II virus. It was concluded that superinfection of hepatitis c virus indeed occurs in humans, and this should be taken into consideration in the pathogenesis of reactivation of chronic type C hepatitis.
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10/10. Prompt hepatitis c virus suppression following hepatitis b virus superinfection in chronic untreated hepatitis c.

    The natural course of chronic hepatitis c virus infection after hepatitis b virus superinfection is not clear since it is difficult to determine the chronology of the double infections. We report on a case of de novo hepatitis b virus infection in the course of chronic untreated hepatitis c, in which the time of hepatitis B virus infection is actually known. The patient eliminated HCV-rna, both from serum and from liver tissue, soon after the clinical onset of the acute hepatitis B. Liver histology featured hepatitis with severe portal inflammation and high-grade periportal and intralobular necro-inflammatory lesions. This observation demonstrates that hepatitis c virus replication can be promptly and spontaneously suppressed by acute hepatitis b virus superinfection.
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