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Biomedical subjects

R Esteban

Publications and source records attributed to R Esteban.

At least 73 records · Page 4Linked to original sources
PubMed1989

Chronic delta hepatitis: detection of hepatitis delta virus antigen in serum by immunoblot and correlation with other markers of delta viral replication.

To investigate the presence of serum hepatitis delta virus antigen by immunoblot and its correlation with other markers of active viral replication (intrahepatic hepatitis D antigen, IgM antibody to hepatitis D and serum hepatitis D virus RNA), we studied serum samples from 50 patients with chronic hepatitis D virus infection (38 with and 12 without intrahepatic hepatitis D antigen). Of the 38 patients with intrahepatic hepatitis D antigen, 27 (71%) had antigen detectable in serum by immunoblot, whereas only two were reactive by conventional enzyme-linked immunosorbent assay. Thirty-one (82%) patients were also positive for serum hepatitis D virus RNA by spot hybridization and 33 (87%) were positive for IgM anti-hepatitis D virus. All markers were simultaneously present in 24 patients. Circulating hepatitis D antigen was detected in one (8%), IgM anti-hepatitis D in seven (58%) and hepatitis D virus RNA in two (17%) of the 12 patients who had anti-hepatitis D in serum but not detectable hepatitis D antigen in liver. Hepatitis D antigen was not detected in serum of any of the 15 control patients. The results suggest that serum hepatitis D antigen as detected by immunoblot and serum hepatitis D virus RNA are similar in sensitivity for detection of active hepatitis D virus replication during chronic infection and constitute useful, sensitive and noninvasive tests for the diagnosis and monitoring of chronic hepatitis D virus infection.

Adolescent↗
PubMed1989

Internal and terminal cis-acting sites are necessary for in vitro replication of the L-A double-stranded RNA virus of yeast.

Empty particles of the L-A dsRNA virus of Saccharomyces cerevisiae bind to added viral (+) strands and convert them to dsRNA (RNA replication) in an in vitro reaction that is dependent on host factors. X dsRNA (530 bp long) is a deletion derivative of L-A dsRNA (4.5 kb). By modifying our cDNA clone of X and testing template activity of T7 RNA polymerase transcripts, we have found that both the 3' end 30 bases and an internal site on the (+) strand are necessary for optimal replication [in vitro (-) strand synthesis]. Changing any one of the 3' terminal three bases eliminates template activity, but the 3' terminal five bases of M1 (a satellite virus of L-A) can replace the 3' terminal four bases of X. A subterminal stem-loop structure is also important for template activity. The internal site that enhances replication is approximately 400 bp from the 3' end and is distinct from the site necessary for binding of (+) strands to the empty viral particles.

Base Sequence↗
PubMed1989

Serological profile of tissue autoantibodies during acute and chronic delta hepatitis.

In order to assess the serological profile in relation to other serological and histological markers of hepatitis delta virus (HDV) infection we have investigated the presence of autoantibodies during acute and chronic delta infection in 353 serum samples from different patients with acute and chronic hepatitis and autoimmune diseases. Basal cell layer antibodies (BCLA) were found in 58% acute hepatitis B, in 73% chronic hepatitis D and in 4% primary biliary cirrhosis. Stellate thymic epithelial cell antibodies (SECA) were detected in 40% acute D hepatitis and in 49% chronic D hepatitis. No tissue autoantibodies were detected in 50 acute B hepatitis, 35 autoimmune chronic liver diseases, 24 connective tissue diseases or 25 controls. In addition, two previously unreported specificities of anti-thymic antibodies reacting with reticular (TRA) and perithymocytic cells (PTA) were identified in 33% and 9% acute D hepatitis, respectively, and in 13% and 6% chronic D hepatitis cases. Among patients with acute HBV-HDV coinfection these antibodies were detected transiently (less than 4 weeks) and at low titer, whereas in those with chronic infection autoantibodies levels tend to be high and persistent throughout the follow-up. Among patients with chronic HDV infection no correlation was found between the presence of tissue autoantibodies and hepatic delta antigen expression and serum HDV-RNA which suggest that autoimmune phenomena observed during chronic delta infection are not related to the level of viral replication.

Acute Disease↗
PubMed1989

[Clinical characteristics of chronic autoimmune hepatitis. Study of 51 cases].

The clinical and histological features of the 51 patients affected with chronic autoimmuno hepatitis are analyzed. 65% of them were over 50 years old. 41% were without symptoms. The incidence of systemic symptoms was of 25.5%. 84.3% had antinuclear antibodies superior of 1/40 and 53% had positive LMA. The incidence of HCA and CH was similar. 26.7% of the patients had complications.

Adolescent↗
PubMed1988

Epidemiology of delta infection in Spain.

The prevalence of hepatitis D virus infection was studied in 954 sera samples collected in Spain between 1974 and 1986 from 838 patients in a variety of epidemiological categories with HBsAg-positive liver disease, and from 116 haemophiliacs and drug addicts with hepatitis B antibodies. Hepatitis D markers were detected in 64% of drug addicts and 33% of HBsAg-positive haemophiliacs but were absent in asymptomatic chronic carriers, homosexual males, mentally retarded patients and haemodialysis patients. Hepatitis D markers were found in 6% of patients with acute hepatitis, in 5.6% of those with chronic hepatitis B from general population, and in 65% of those with acute hepatitis B and 67% of those with chronic hepatitis B among drug addicts. During the 12-year study, no changes were observed in the frequency of Delta infection. The prevalence was less than 10% in chronic HBsAg-positive hepatitis. These findings indicate that in Spain Delta infection is restricted mainly to HBsAg-positive drug addicts and multitransfused haemophiliacs, while in the general population only 6.7% of those with chronic hepatitis B show D superinfection. Anti-HD sera detection is correlated with more severe forms of chronic hepatitis such as chronic active hepatitis and cirrhosis.

Epidemiologic Methods↗
PubMed1988

Chronic hepatitis D in intravenous drug addicts and non-addicts. A comparative clinico-pathological study.

In recent years chronic infection by the hepatitis delta virus (HDV) has become an important cause of chronic liver disease among drug addicts. To evaluate the influence of addiction to i.v. drugs on the course of this disease we have analyzed the clinical, histopathological, virological and evolutive features in 18 addicts and 11 non-addicts with chronic delta infection. Recent acute hepatitis D, documented as HDV superinfection, was observed in 14 addicts (77%) and in 2 non-addicts (18%) (P less than 0.02). At the time of evaluation for chronic liver disease, the frequency of symptoms, the degree of biochemical disturbances and the histopathological severity were similar in the two groups but the duration of HDV infection was probably shorter in drug addicts. HBV replication, as indicated by the presence of HBeAg and HBV-DNA in serum and HBcAg in liver, was more frequent in addicts. The amount of HDAg in liver tissue was also greater in addicts (P less than 0.005). Antibodies against the human immunodeficiency virus were detected in all of the addicts (P less than 0.001). Although most patients remained asymptomatic, significant histological worsening occurred in one half of the cases after a relatively short period of follow-up (25.1 +/- 16.3 months). The tendency to deteriorate in addicts (61% of cases) was greater than in non-addicts (36%). These observations suggest that the prognosis of chronic HDV infection is particularly poor in drug addicts in whom rapid deterioration may be related to simultaneous and inadequately controlled replication of hepatotropic viruses.

Chronic Disease↗
PubMed1988

Site-specific binding of viral plus single-stranded RNA to replicase-containing open virus-like particles of yeast.

X double-stranded RNA is a deletion mutant of L-A double-stranded RNA and is encapsidated in viral particles by the L-A-encoded major coat protein. X double-stranded RNA has all the cis sites necessary to be transcribed, encapsidated, and replicated. We have cloned X double-stranded RNA and sequenced it. The complete X double-stranded RNA sequence deduced indicates that the first 25 bases of the X plus-strand 5' end originated from the 5' end of the L-A plus strand and that most, if not all, of the rest comes from the 3' end of the L-A plus strand. The X plus strand made by X double-stranded RNA-containing virus-like particles binds specifically to empty open virus-like particles and is converted by these particles to X double-stranded RNA. RNA transcripts of the X complementary DNA clones and deletion derivatives thereof were made in vitro by T7 and T3 RNA polymerases and tested for specific binding to the virus-like particles. The results suggest that the binding is due to the sequence UUUGGCCAGG, 370 bases upstream from the X plus-strand 3' end. This sequence is also present in the M1 plus strand 140 bases from its 3' end.

Amino Acid Sequence↗
PubMed1988

A deletion mutant of L-A double-stranded RNA replicates like M1 double-stranded RNA.

X double-stranded RNA (dsRNA) is a 0.52-kilobase dsRNA molecule that arose spontaneously in a nonkiller strain of Saccharomyces cerevisiae originally containing L-A and L-BC dsRNAs (L-BC is the same size as L-A but shares no homology with it). X hybridized with L-A, and direct RNA sequencing of X showed that the first 5' 25 base pairs (of the X positive strand) and at least the last 110 base pairs of the 3' end were identical to the ends of L-A dsRNA. X showed cytoplasmic inheritance and, like M1, was dependent on L-A for its maintenance. X was encapsidated in viruslike particles whose major coat protein was provided by L-A (as is true for M1), and X was found in viruslike particles with one to eight X molecules per particle. This finding confirms our "head-full replication" model originally proposed for M1 and M2. Like M1 or M2, X lowers the copy number of L-A, especially in a ski host. Surprisingly, X requires many chromosomal MAK genes that are necessary for M1 but not for L-A.

Base Sequence↗