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T Laskus

Publications and source records attributed to T Laskus.

At least 55 records · Page 3Linked to original sources
PubMed1995

Nucleotide sequence analysis of precore and proximal core regions in patients with chronic hepatitis B treated with interferon.

The aim of the study was to estimate the prevalence of HBeAg defective mutants among patients with chronic hepatitis B (CHB) in the United States and to study the effect of interferon-alpha (IFN-alpha) on determining the occurrence of mutations in the HBV precore and proximal core regions. Twenty CHB patients who were treated with IFN-alpha were studied. Initially, all were HBV DNA positive by dot-blot hybridization; 17/20 were HBeAg positive, and 3/20 were anti-HBe positive. The precore (87 nt) and proximal core (81 nt) regions were sequenced after PCR amplification by the dideoxy chain termination method. In pretreatment sera, 15/20 patients harbored wild-type HBV only, while in 5/20 at least one nucleotide substitution was found. Mutations that prevent HBeAg synthesis were found in three patients, all of whom had G-to-A substitution at nt 1896 and two of them were anti-HBe positive. Follow-up sera were available in 18 patients. With respect to pretreatment specimen, 15/18 patients had no changes in the sequenced regions after therapy. Sequence changes were observed in the remaining three patients: In one an HBeAg defective strain was replaced by a wild-type strain; in the second a wild-type strain was replaced by an HBeAg defective strain; and in the third two mutations changing the deduced amino acid sequence of the core protein developed in the wild-type strain. In conclusion, most of our patients (85%) were initially infected by HBV strains having no mutations that prevented HBeAg synthesis. IFN-alpha therapy infrequently resulted in the appearance of mutations in the precore and proximal core regions.

Adult↗
PubMed1995

Development of transient autoimmune hepatitis during interferon treatment of chronic hepatitis B.

A 42-year-old man was treated with interferon-alpha for chronic hepatitis B; during the fourth week of treatment he developed an exacerbation of liver disease, and nuclear and smooth muscle autoantibodies, which were previously negative, were detected in very high titers. After discontinuation of interferon therapy, ALT values subsided promptly and autoantibodies disappeared within a few months. This sequence of events strongly suggests a direct relationship between IFN treatment and a self-limited hepatitis with autoimmune markers in this case.

Adult↗
PubMed1995

Hepatitis B virus core promoter sequence analysis in fulminant and chronic hepatitis B.

BACKGROUND & AIMS: It was recently reported that two point mutations within the hepatitis B virus (HBV) core promoter region (A to T at position 1762 and G to A at position 1764) are associated with fulminant hepatitis and lead to hepatitis B e antigen (HBeAg)-negative phenotype. The aim of this study was to correlate core promoter sequence variations with HBeAg status and clinical outcome in various forms of HBV infection. METHODS: Core promoter region of HBV was amplified by polymerase chain reaction and directly sequenced in 94 patients: 37 patients with fulminant hepatitis, 20 with acute self-limited hepatitis, 30 with chronic hepatitis, and 7 patients with end-stage cirrhosis. RESULTS: Core promoter region was found to be heterogenous and no specific changes correlated with HBeAg/anti-HBeAg status or survival in patients with fulminant hepatitis. Substitutions at positions 1762 and 1764 were found in HBV strains from 4 patients (10%) with fulminant hepatitis, 2 patients (10%) with self-limited hepatitis, 8 patients (27%) with chronic hepatitis, and in 5 of 7 patients with end-stage cirrhosis. The majority of these patients were HBeAg positive. CONCLUSIONS: Mutations at positions 1762 and 1764 are rarely observed in HBV strains from patients with fulminant hepatitis B in the United States but are common in patients with chronic hepatitis. Even when present, they seem to be insufficient to lead to the HBeAg-negative phenotype.

Base Sequence↗
PubMed1994

The stem-loop structure of the cis-encapsidation signal is highly conserved in naturally occurring hepatitis B virus variants.

The region encoding the stem-loop structure of the HBV cis-encapsidation signal was sequenced in 87 patients with various forms of hepatitis. Altogether, 20 nucleotide substitutions were found; 15/20 were predicted to increase the stability of the stem-loop structure. Substitutions likely to decrease the stability of the cis-encapsidation signal were not observed.

Base Sequence↗
PubMed1994

Lack of evidence for hepatitis B virus (HBV) infection in fulminant non-A, non-B hepatitis.

We studied eight patients who had orthotopic liver transplantation for fulminant hepatic failure in the course of acute non-A, non-B hepatitis. HBV DNA was searched for extensively in the liver tissue by PCR using several sets of primers in conventional and heminested reactions. All patients were negative for HBV DNA in liver tissue by all assays employed; furthermore, they were negative for HEV RNA, HCV RNA, and HBV DNA in serum. Although the causative role of HEV and HCV in fulminant non-A, non-B hepatitis cannot be excluded, our data do not support a causative association between this syndrome and HBV infection.

Base Sequence↗
PubMed1994

Nucleotide sequence analysis of the precore region in patients with spontaneous reactivation of chronic hepatitis B.

The role of HBV precore mutations in the spontaneous reactivation of chronic hepatitis B (CHB) is currently unknown. We studied 10 patients with CHB; five were HBeAg+ (group I) and five were anti-HBe+ (group II). All 10 had spontaneous reactivation of CHB as defined by the appearance of clinical symptoms along with an increase of serum ALT activity at least 5X above baseline values, in the absence of any other known causes of liver disease or CHB reactivation. The precore (87 nt) and proximal core (81 nt) regions were sequenced after PCR amplification. From each patient three serum samples studied: one 3-12 months before, one during, and one six months after reactivation. Prior to reactivation, none of the group I patients harbored an HBV strain having a mutation that prevented HBeAg synthesis; however, 2/5 developed such a mutation during reactivation (G to A transition at nt 1896). Among the group II patients, three harbored an HBeAg defective mutant both before and during reactivation; after six months, two of these three patients were HBV DNA negative in serum by PCR. Several other sequence polymorphisms, some of which changed the predicted amino acid sequence, were either present initially or developed during reactivation. In conclusion, in this small group of CHB patients who were HBeAg+ spontaneous reactivation was accompanied in some cases by a shift to an HBeAg defective mutant, while in patients who were anti-HBe+, such mutations were frequently present prior to reactivation. In patients already harboring precore defective mutants, spontaneous reactivation may precede an attenuation of viral replication.

Adult↗
PubMed1994

Precore and contiguous regions of hepatitis B virus in liver transplantation for end-stage hepatitis B.

BACKGROUND/AIMS: Recurrent hepatitis B virus (HBV) infection is the leading cause of mortality and morbidity after orthotopic liver transplantation (OLT) for HBV-related liver disease, but the extent of viral genetic variation in this setting remains unknown. METHODS: Eight patients who underwent OLT for HBV-related liver disease were studied; 7 had cirrhosis and 1 had fulminant hepatitis. Four patients received long-term hepatitis B immunoglobulin prophylaxis. A 240-base pair fragment (1742-1981) comprising the precore region of HBV was amplified by polymerase chain reaction from sera drawn before OLT and 6, 12, and 24 months after OLT and analyzed. RESULTS: All sera were positive by polymerase chain reaction. Nucleotide sequence variations were congruent within most patients before and after OLT; however, in one patient, substantial sequence variation was observed, suggesting infection with a new HBV strain. No sequence variation associated with a particular outcome could be identified. Two patients harbored HBV variants with a deletion or insertion upstream of the precore messenger RNA initiation site. CONCLUSIONS: Reinfection after OLT can occasionally be caused by HBV strains different from the one present before OLT. Changes within the sequenced region are not predictive of the outcome of reinfection.

Adult↗
PubMed1994

Naturally occurring hepatitis B virus mutants with deletions in the core promoter region.

A novel class of hepatitis B virus mutants in patients with chronic hepatitis B is described. The predicted effect of the mutations is to disrupt the X open reading frame. The location of the genetic alterations within the putative precore promoter also suggests that they may ameliorate precore transcription, which would provide an alternate mechanism for HBeAg(-) escape variation. Definitive conclusions regarding the effects of these mutations must await additional in vitro and in vivo studies.

Adult↗
PubMed1994

[Autoimmune phenomena in the course of chronic infections].

Probable mechanisms responsible for the development of autoimmune disorders in the course of acute and chronic infectious diseases are discussed in the paper. The most common infections ongoing with significant symptoms of immune reactions directed against self antigens are also presented.

Acute Disease↗
PubMed1994

[Occurrence of free receptor for interleukin 2 in serum and quantitative determinations of CD25+ in patients infected with HIV].

Serum soluble interleukin 2 receptor (sIL-2R) concentration and the percentage of lymphocytes presenting this receptor (CD25+) were investigated in 28 asymptomatic HIV carriers or patients with lymphadenopathy only and in 15 AIDS patients. The levels of sIL-2R were found to be higher in AIDS patients (mean 1060 U/ml) than in persons during the initial stages of infection (mean 750 U/ml) or controls (mean 470 U/ml). No significant differences in the quantity of CD25+ lymphocytes between these groups were observed, with the means of 1.0; 1.3 and 1.1, respectively. However, a decrease in percentage of these cells were found in patients with advanced HIV infection. Since sIL-2R is regarded as a marker of immune system activation its detection could be helpful in the assessment of the immune status impairment in HIV infected patients.

Acquired Immunodeficiency Syndrome↗
PubMed1993

Nucleotide sequence analysis of the precore region in patients with fulminant hepatitis B in the United States.

BACKGROUND: A precore defective hepatitis B virus (HBV) mutant unable to produce hepatitis B e antigen (HBeAg) has been associated with fulminant hepatitis B. We have studied the etiologic contribution of precore mutants among North American patients with this disorder. METHODS: We studied 39 patients with fulminant hepatitis B. The precore and proximal core regions of HBV from 37 of 39 patients were sequenced. RESULTS: Four patients (10.8%) harbored nonsense mutants likely to produce an HBeAg negative HBV infection; two such mutants had a G to A substitution at position 1896, one lost the precore initiation codon, and one harbored a stop codon immediately downstream of the precore initiation codon. Recovered sequences from seven additional patients displayed silent or missense mutations in these regions. All delta coinfected patients harbored known wild type strains of HBV. A significantly poorer survival was associated with antibody to HBe positivity and presence of nucleotide substitutions in the precore/core region. CONCLUSIONS: The prevalence of precore mutations in 37 patients from the United States was lower than reported elsewhere; only two patients were found to have the G to A transition mutation in the precore region at position 1896. We conclude that HBeAg negative HBV mutants do not play a predominant etiologic role among North American patients with fulminant hepatitis B.

Adenine↗
PubMed1993

Affinity of anti-GP41 antibody in patients infected with human immunodeficiency virus type 1.

Anti-gp41 antibody affinity was investigated prospectively in 25 patients with asymptomatic and symptomatic HIV-1 infection for a period of 9-42 months. Major differences in the processes of immune response maturation towards gp41 were observed among individual subjects, however, antibody affinity increased with time in all examined persons including patients with AIDS. Anti-gp41 affinity values were found to reflect both the duration and the clinical stage of HIV infection.

Acquired Immunodeficiency Syndrome↗
PubMed1993

[Eleven year period of asymptomatic HIV infection in a patient after open heart surgery].

A case is described of a 62 years old patient in the initial stage of clinically overt HIV infection. The infection occurred probably 11 years earlier by means of blood transfusion during open heart surgery. The possible reasons for the long-term asymptomatic carriage of the virus and factors influencing the development of symptomatic HIV infection (AIDS) are discussed.

Acquired Immunodeficiency Syndrome↗
PubMed1993

[Evaluation of humoral immune response in patients with asymptomatic and symptomatic HIV infection. Analysis of titers of anti-Hbs, antibodies against cytomegalovirus, herpes simplex virus type I, rubella virus and toxoplasma gondii].

40 asymptomatic HIV carriers and 45 AIDS patients were tested for anti-HBs (Hepatitis B Virus surface antigen), anti-RV (Rubella virus), anti-Toxo (Toxoplasma gondii), anti-CMV (Cytomegalovirus) and anti-HSV-1 (Herpes simplex virus type 1) antibody titers and compared with 83 persons characterized by risk behaviours but seronegative for HIV. The prevalence of these antibodies was very high and similar in all three groups studied, however, patients with AIDS had generally lower antibody titers when compared with asymptomatic carriers. The only exception being anti-HSV-1 which was present in high titre even in gravely ill patients. It seems that subjects with clinically overt HIV infection develop a serious disturbance in the humoral immune response with depressed specific antibody synthesis.

Acquired Immunodeficiency Syndrome↗
PubMed1993

[Concomitant symptom syndrome of primary HIV infection].

A primary HIV infection presenting as an acute viral syndrome in 31-years-old male drug addict is described. Two weeks after the probable infection the patient presented with fever, sweats, anorexia, vomiting, diarrhoea, myalgia, arthralgia, headaches, macular eruption, generalized lymphadenopathy, paresthesia and thrombocytopenia. These symptoms lasted 7 weeks. The immune abnormalities included an increase of CD8+ lymphocyte percentage resulting in decrease od CD4/CD8 ratio. HIV antigenemia was found 4 weeks after the presumed exposure whereas anti-HIV became detectable 2 weeks later.

Acute Disease↗
PubMed1993

[Efficacy of hepatitis B vaccine after intramuscular or intradermal administration].

We compared the efficacy of intramuscular (im) and intradermal (id) administration of vaccine against HBV. Only one out of 25 im vaccinated subjects did not respond whereas all 25 id immunized persons developed anti-HBs above 10 IU/l. The mean serum level of anti-HBs in im and id vaccinated group was 2351 +/- 2358 IU/l and 1823 +/- 1502 IU/l, respectively (p = 0, 382; NS). It seems that the efficacy of both vaccine administration is very similar.

Adult↗
PubMed1992

Prevalence of markers of hepatotropic viruses among drug addicts in Warsaw, Poland.

We studied 100 unselected parenteral drug abusers for infection with hepatitis C, B, A and D virus (HCV, HBV, HAV and HDV). Seventy-six percent had serological evidence of HCV infection. 12% were positive for HBsAg and at least one marker of HBV infection was present in 69%. These results were significantly higher than in a matched control population. Compared to controls, the prevalence of anti-HAV (65%) was not significantly increased in drug addicts. Of the anti-HCV-positive drug addicts, 80.3% had at least one marker of HBV infection compared to 33.3% of anti-HCV-negative cases (p less than 0.001). No such correlation was found between the prevalence of HCV or HBV infection markers and the presence of anti-HAV. Antibodies against HDV were detected in 16 (16%) of the samples from drug addicts. No significant association was found between antibodies to HCV and gender, age and duration of drug abuse. The risk of HBV infection increased significantly with years of drug abuse but was not associated with age and sex. The presence of anti-HAV was related to age only. Sixteen (16%) of the subjects were definitely positive for anti-HIV-1, but at the time of the study they were asymptomatic. No significant association was found between the presence of anti-HIV and the prevalence of serological markers of HBV, HCV, HAV and HDV infection.

Adolescent↗