Abstract Toll‐like receptors (TLR) are important tools of innate immunity, localized mainly on cells of the immune system, but also have been shown on cells of other origin. In the current study, they have been searched in biopsy specimens of liver from children bearing chronic viral hepatitis of C type (HCV). TLR2, TLR3 and TLR4 were traced by means of polyclonal antibodies and avidin‐biotin complex (ABC) immunohistochemistry. Besides, mRNA for TLR was looked for using specific primers and polymerase chain reaction. Several controls, including neutralization of primary antibody with respective blocking peptide, confirmed the specificity of the immunohistochemical reaction. All TLR tested could be visualized in a focal distribution in single hepatocytes and some cells of inflammatory infiltrates. There was no reaction whatsoever in liver samples not infected with hepatotropic virus. In molecular studies, mRNA for TLR2 and TLR4 was detected in both noninfected and hepatitis B virus‐infected established cell lines of human hepatoma as well as in HCV + biopsy samples. These data indicate that TLR can be traced in liver cells, both at the protein and at the mRNA level. Their irregular and focal distribution in HCV + , but not in HCV – , liver suggests some role of TLR in the pathogenesis of chronic viral hepatitis, at least in children.
Background. Hepatitis A is related to significant morbidity and occasional mortality. Based on data from the Polish National Institute of Hygiene, from 2000 to 2013 a mean of 213 hepatitis A cases were reported yearly.Objectives. The aim of the study was to assess selected data in adults hospitalized for symptomatic hepatitis A during an eight-year period in a single center in the Wielkopolska Region of Poland.Material and Methods. All the hepatitis A patients hospitalized in the center from 2005 to 2013 were analyzed retrospectively. Data were extracted from the medical records of these individuals. The disease was confirmed by anti-HAV IgM testing.Results. In total, 108 patients (71 men and 37 women), aged 18–65 years, were identified. All but 1 patient recovered (99.1%) and in 6 cases (5.6%) a relapse occurred. Risk factors for hepatitis A were identified in 56 patients (52%), with travel abroad being the most common one (32 patients); 19 cases were secondary and 5 patients were men who have sex with men. One hepatitis A outbreak was noted in the region during the study period. Acalculous cholecystitis was found in 33.3% of the patients who underwent abdominal ultrasound. This tended to be more common among older individuals (47.8% in patients over 40 vs. 22.6% in patients aged 18–40, p = 0.0521). Patients with this finding had significantly higher mean peak ALT in comparison to those with no gallbladder abnormalities.Conclusion. Although hepatitis A in adults is typically a benign, self-limited disease, it can occasionally have a fatal course. In a significant proportion of patients with an evident risk factor for hepatitis A, the possibility of active prophylaxis was not used. Hepatitis A should be regarded as a sexually transmitted infection. Acalculous cholecystitis is a frequent finding among adults with symptomatic hepatitis A.
Background: Liver fibrosis largely influences the course and prognosis of chronic hepatitis C (CHC). Although percutaneous liver biopsy is a valuable tool in the evaluation of liver injury, it posses significant drawbacks that limit repeated use of this technique. The aim of this study was to assess chosen serum markers of liver fibrosis – laminin (LAM), hyaluronic acid (HA) and transforming growth factor beta 1 (TGF-beta-1) with their relation to histopathological findings as well as their alterations after antiviral treatment with recombinant interferon alpha (IFN-alpha) and ribavirin (Rib) in children with CHC. Methods: Study group included 68 children, age range 6–18 years (mean 13,34 ± 3,27 years) with diagnosed CHC. History data were analysed. Diagnosis was confirmed by the presence of HCV-RNA in serum by RT-PCR. All children underwent histopathological evaluation of liver biopsy specimen according to Ishak scoring system. Serum sample and liver biopsy specimen were collected the same day. LAM, HA and TGF-beta-1 were measured in serum by enzyme linked immunosorbent assay kits. Children were treated with IFN-alpha (3 MU/m2 3 x/week in s.c. injections) and Rib (orally, twice daily) for 48 weeks. Serum markers of fibrosis were also assessed at the end of the treatment. Results: Length of infection was 7.34 ± 4.03 years (range 2–13.5 years). Mean ALT activity was 60,82 ± 65,02 IU/l. Increasing mean serum TGF-beta-1 (p = 0.029) and decreasing mean LAM level (p = 0.039) was found in the groups of children with increasing stage of fibrosis. Level of LAM was defined a risk factor of significant fibrosis (95%CI 18.05; 67.87, p = 0.001), while level of TGF-beta -1 of significant (95%CI: -33.51;-1.73, p = 0.030) and progressed liver fibrosis (95%CI -36.09; -3.37, p = 0.019). Conducted antiviral treatment with IFN-alpha and Rib resulted in significant decrease of TGF-beta-1 (51.42 ± 30.68 vs. 35.24 ± 31.50 ng/ml, p = 0.032) and increase of LAM (60.26 ± 52.38 vs. 83.70 ± 46.25 ng/ml, p = 0.002) in serum. No significant alterations were detected in the control group of untreated children. Conclusion: Level of liver injury in children with CHC varies in severity. TGF-beta-1 and LAM are not only proportional to the stage of fibrosis but also seem to be a good risk factor for the development of significant and advanced fibrosis. Their alterations during antiviral treatment allow monitoring the progression of liver fibrosis. Abstracts for SupplementInternational Journal of Infectious DiseasesVol. 14Preview Full-Text PDF Open Archive
Infections with hepatitis C virus (HCV) are widespread in most countries. Vertical transmission of HCV has become quite frequent. This study presents the case of a female neonate infected in the womb. The mother had been exposed to infectious material, and developed asymptomatic acute hepatitis with high-maternal viral load, which was the primary cause of the infection in the neonate. At birth, the neonate developed hyperbilirubinemia, followed by an increased aminotransferase activity, resulting in liver insufficiency, and finally the neonate's death. In conclusion, it seems that maternal viral load is extremely significant when vertical transmission of the infection to the fetus is concerned.
Our aim was to evaluate the recent clinical data concerning the course of chronic hepatitis C in children and the rationale indications for therapy. There is no doubt that in adult group the pegylated interferon is better than standard interferon and results in higher response rate in combination with ribavirin. Actually complicating the issues surrounding hepatitis C in children is the lack of information on the efficacy and safety of this therapy in pediatric age group. The first preliminary data of our clinical study concerning the therapy with pegylated interferon alpha 2b and ribavirin in 10 children with chronic hepatitis C (genotype 1) suggest a good tolerance of this drug and the end of treatment virologic response in 8 children (80%).
Hepatitis C virus (HCV) was discovered in 1989. HCV is a positive single-strand RNA. We all have thought, that HCV can replicate only in liver tissue, but now we know, that HCV can replicate in extrahepatic tissue as well. In about 48-86% of HCV infected patients, chronic hepatitis C (CHC) has been noticed and eventually, after tens of years, liver insufficiency, cirrhosis or hepatocellular carcinoma. The current recommended treatment for CHC is a combination of pegylated-interferon alpha and Ribavirin. Presently it is known, that HCV infection can persist as an occult infection. RNA HCV can be detected in patients after successful treatment for CHC or spontaneous elimination. Persistent HCV replication in hepatocytes or lymphoid cells would likely lead to continuous antigenic stimulation of the immune system. This prolonged replication may contribute to the immune tolerance of HCV, impairment of immune response and even further virus persistence. This occult infection grows more important in transplantation.
Objective. Human cytomegalovirus (HCMV) is one of the most common congenital infections worldwide and a frequent opportunistic infection that aggravates the condition of human immunodeficiency virus (HIV)-infected patients. The aim of the study was to evaluate the frequency and factors influencing HCMV infection among infants of HIV-positive women.Methods. The study included 35 infants born to HIV-1-infected mothers examined for congenital infections. Children were evaluated for human immunodeficiency virus type 1 (HIV-1), HCMV, and HCV infection by serological and molecular methods.Results. HIV-1 infection was found in one child whose mother did not receive antiretroviral treatment during pregnancy, and HCV infection in another infant. HCMV-DNA in the urine was present in 13/35 infants (37.14%) on the 10th day and 24/35 infants (68.57%) in the 4th week of life. The majority of HCMV-infected infants were asymptomatic, although they manifested microcephaly and low birth weight significantly more frequently (p = 0.006 and p = 0.02, respectively). Type HIV prophylaxis did not influence HCMV transmission.Conclusions. Although often asymptomatic, HCMV infection in infants born to HIV-infected mothers is frequent and may be associated with prematurity, low birth weight, and microcephaly. Diagnostic procedures in children of HIV-infected mothers should involve HCMV.
1Department of Infectious Diseases, J. Struś Multispecialist City Hospital, Poznan Head of Department: prof. Iwona Mozer-Lisewska, MD, PhD 2Department and Clinic of Infectious Diseases, Poznan University of Medical Sciences Head of Department: prof. Iwona Mozer-Lisewska, MD, PhD 3Department of Biology and Environmental Protection, Poznan University of Medical Sciences Head of Department: prof. Krzysztof Wiktorowicz, PhD 4Department of Bioinformatics and Computational Biology, Chair of Clinical Pathomorphology, Poznan University of Medical Sciences Head of Department: prof. Elzbieta Kaczmarek, PhD
