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S Jameel

Publications and source records attributed to S Jameel.

At least 37 records · Page 2Linked to original sources
PubMed1995

Protracted viremia during acute sporadic hepatitis E virus infection.

BACKGROUND/AIMS: Hepatitis E virus (HEV) is associated with epidemic and sporadic hepatitis in developing countries. The disease is largely self-limited with no long-term sequelae. The source of HEV for maintenance of the disease in an endemic area is unknown. This study investigated the occurrence and duration of viremia in patients with acute sporadic HEV infection. METHODS: In 26 of 37 patients with sporadic acute non-A, non-B viral hepatitis, HEV infection was diagnosed based on positivity for immunoglobulin M anti-HEV and/or presence of viremia as shown by reverse-transcription polymerase chain reaction. In 4 patients, fecal samples were analyzed for presence of virus using polymerase chain reaction. Multiple samples were studied at varying times in 20 patients. RESULTS: Viremia was detected in 19 of 26 patients. Two patients had viremia in the absence of immunoglobulin M anti-HEV. Four patients had protracted viremia of 45-112 days' duration. One patient showed fecal virus shedding up to the 52nd day of illness. CONCLUSIONS: Protracted viremia and prolonged fecal shedding of HEV were shown in a small group of patients. These patients may serve as temporary virus carriers responsible for continuous contamination of the sewage water.

Acute Disease↗
PubMed1995

A genetic analysis of HIV-1 from Punjab, India reveals the presence of multiple variants.

OBJECTIVE: To determine the extent of HIV-1 genetic variation in Indian patients. DESIGN: To avoid any bias in selecting viral variants, HIV-1 DNA was amplified directly from the peripheral blood mononuclear cells of patients and sequenced. Genetic similarity between Indian sequences and other geographic isolates was analysed by phylogenetic analysis algorithms. METHODS: A fragment encompassing the C2/V3-V5 regions of HIV-1 gp120 was amplified from the lymphocyte DNA of 12 Indian patients. Multiple clones from each patient were sequenced. Nucleotide sequences encompassing about 650 base pairs were aligned for the Indian and other geographically distinct isolates. Inter-isolate relationships were analysed by means of distance, parsimony and neighbour-joining algorithms. RESULTS: Nucleotide sequence comparisons showed low interpatient variation. Amino-acid comparisons revealed a high degree of homology between Indian sequences in this study and those studied earlier. On distance and parsimony trees, most of the Indian sequences clustered together as subtype C. However, sequences from three patients also showed significant homologies and phylogenetic clustering outside of subtype C. CONCLUSIONS: The predominant strain of HIV-1 in India belongs to subtype C and little interpatient nucleotide sequence divergence in the majority of cases suggests recent spread of HIV-1 in this region. This study also presents the first evidence for non-C subtypes in the Indian population with two epidemiologically linked samples remaining unclassified for any existing env subtype. The presence of variant subtypes in Indian patients sheds light on the transmission routes of HIV-1 to India and emphasizes the need to include these sequences in vaccine development strategies.

Acquired Immunodeficiency Syndrome↗
PubMed1995

An Indian strain of hepatitis E virus (HEV): cloning, sequence, and expression of structural region and antibody responses in sera from individuals from an area of high-level HEV endemicity.

Hepatitis E virus (HEV) is responsible for a majority of sporadic and epidemic viral hepatitides in India and other developing countries. Even though the genomes of four geographically distinct strains of HEV have been cloned and sequenced, the Indian strain of HEV remains largely uncharacterized. We have cloned and sequenced about 2.2 kb of the HEV genome constituting the structural region from an Indian strain of HEV. The nucleotide and amino acid sequences show a high degree of conservation with sequences from other HEV strains. Open reading frames (ORF) 2 and 3 were expressed in Escherichia coli as N-terminal hexahistidine epitope fusions. The purified proteins were then used in an immunoblot assay to evaluate the antibody status in sera from individuals from an area of high-level HEV endemicity. The anti-ORF2 antibodies were found to be nonspecific and could not be correlated to clinical disease. The immunoglobulin M anti-ORF3 was found to be specific for the presence of acute disease. The implications of these findings in HEV diagnosis and vaccine development are discussed.

Amino Acid Sequence↗
PubMed1994

Etiological role of hepatitis E virus in sporadic fulminant hepatitis.

Non-A, non-B hepatitis viruses have been implicated as the etiological agent(s) in up to 60% of patients with fulminant hepatitis. These agents are reported to induce a higher mortality than other causes of fulminant hepatitis. Hepatitis E virus (HEV) and hepatitis C virus (HCV) at present constitute the major identifiable non-A, non-B hepatitis agents. Of these, HEV has been established as the sole cause of epidemic hepatitis in Afro-Asian countries, and fulminant hepatitis has been recorded during such epidemics. However, in sporadic cases, the etiological role of HEV in fulminant hepatitis has remained uncertain. The role of HCV in acute liver disease and fulminant hepatitis remains unclear. The present study was undertaken to investigate the association of HEV and HCV in patients with fulminant hepatitis by direct detection of the viral genome using reverse transcription-polymerase chain reaction (RT-PCR). Serum samples from 50 serologically identified non-A, non-B fulminant hepatitis cases negative for cryptic hepatitis B virus (HBV) infection examined via PCR were tested for HEV and HCV RNA using RT-PCR. For HEV primers from the nonstructural region (ORF-1) were used, and for HCV primers from the highly conserved 5' untranslated regions were used. The products were analysed using agarose gel electrophoresis and confirmed by hybridisation with radiolabelled internal oligonucleotide probes. HEV was detected in 31 (62%) of the 50 fulminant non-A, non-B hepatitis cases. In 18 (36%) cases, HCV RNA was detected. In 11 (22%) of the HCV cases, the HEV genome was also amplified. In 20 (40%) cases, HEV was detected alone.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1994

Detection of the negative strand of hepatitis E virus RNA in the livers of experimentally infected rhesus monkeys: evidence for viral replication.

Hepatitis E virus (HEV), the causative agent of enteric non-A, non-B hepatitis, is a positive-stranded RNA virus. Because of the virus's inability to grow in culture, several nonhuman primates have been used for the propagation of HEV. Using strand-specific reverse transcription-polymerase chain reaction (RT-PCR), we demonstrate the presence of negative-stranded HEV RNA replicative intermediates in the livers of infected animals. This constitutes the first direct evidence of HEV replication in the liver of the infected animals and reinforces the validity of such a model to study HEV infection, disease pathogenesis, and immunity.

Animals↗
PubMed1994

Mapping of the hepatitis B virus genome in hepatocellular carcinoma using PCR and demonstration of a potential trans-activator encoded by the frequently detected fragment.

The association of hepatitis B virus (HBV) infection with hepatocellular carcinoma (HCC) is well established. Insertional mutagenesis, trans-activation by truncated X or preS2/S regions and activation of growth regulatory genes or oncogenes have all been suggested as possible mechanisms for this carcinogenesis. However, no consensus regarding the mechanism or region of the HBV genome involved has been established. Of the 36 HCC tissues analysed for the presence and extent of the HBV genome, using multiple overlapping PCR, 22 (61%) were found to be positive. Twenty of these showed the presence of a fragment (nucleotides 636 to 746) that covered part of the surface antigen gene. The recognized trans-activators, X and preS2/S, were present in only seven (31.8%) and 12 (54.5%) cases, respectively. In two cases the entire viral genome was detected. The trans-activation potential of the cloned S fragment (nucleotides 426 to 851) covering the frequently detected fragment (nucleotides 636 to 746) was investigated in cotransfection experiments. This fragment was able to trans-activate the HBV enhancer-X promoter target. To define the specificity of the trans-activation and the sequences involved, frameshift and deletion mutants of this fragment were constructed and analysed. The trans-activation activity was lost in the frameshift mutants. The deletion mutants that retained nucleotide sequences 436 to 679 showed trans-activation activity whereas the other ones (nucleotide sequences 436 to 611) did not show any activity. It is suggested that the frequently detected HBV genome fragment belonging to the S gene frame has a trans-activation potential. This may explain the mechanism for pathogenicity of HBV-associated HCC.

Base Sequence↗
PubMed1993

Hepatitis E virus transmission to a volunteer.

Hepatitis E virus (HEV) causes an enteric non-A, non-B hepatitis. The disease occurs in epidemic settings and sporadically, and viral transmission is thought to be faecal-oral. We present here a single volunteer study of HEV transmission followed by disease. Clinical and biochemical features of the infection correlated with HEV detection in the stools and sera by reverse transcription/polymerase chain amplification. IgG antibody has persisted for 2 years. The presence of HEV in serum before clinical signs appeared suggests that in endemic areas sporadic transmission of HEV may also occur parenterally.

Feces↗
PubMed1992

Common aetiological agent for epidemic and sporadic non-A, non-B hepatitis.

Enterovirus-like particles have been reported in the acute phase of both epidemic and sporadic non-A, non-B (NANB) hepatitis. To examine whether these particles were the causative agent in the two types of disease, 29 patients with acute viral hepatitis in a north Indian epidemic outbreak and 9 with sporadic acute disease were investigated. 25 (86%) of 29 patients with epidemic hepatitis and 5 (56%) of 9 with sporadic disease were diagnosed as having enterically-transmitted-NANB hepatitis by exclusion. Virus-like particles (VLP) of 30-34 nm were detected in stool of 1 patient with epidemic and 1 with sporadic hepatitis. The VLPs crossreacted serologically and a specific IgM response was seen in acute epidemic and sporadic serum samples. After inoculation with infected stool rhesus monkeys had a mild rise in liver enzymes, and bile samples contained VLPs. These results suggest that the aetiological agent in epidemic and sporadic disease is the same.

Animals↗
PubMed1992

Hepatitis B virus envelope epitopes: gene assembly and expression in Escherichia coli of an immunologically reactive novel multiple-epitope polypeptide 1 (MEP-1).

A novel synthetic 323-bp gene with the open reading frame of a multiple-epitope polypeptide has been assembled and cloned. The gene is engineered by contiguous alignment of selected epitopes and functional domains of the hepatitis B virus envelope proteins separated by pairs of glycine residues. High-level bacterial production of this 100-amino acid (approx. 10 kDa) protein has been achieved and the gene product is stable. ELISA and Western blot experiments using epitope-specific antisera confirm that the corresponding epitopes are present in the engineered protein.

Amino Acid Sequence↗
PubMed1992

Enteric non-A, non-B hepatitis: epidemics, animal transmission, and hepatitis E virus detection by the polymerase chain reaction.

We studied epidemics of viral hepatitis occurring at three different places in India. One was a combined epidemic due to hepatitis E virus (HEV) and hepatitis A virus (HAV) infections. In this epidemic, HAV affected children below 10 years of age, whereas HEV infected the young adult population. HEV was transmitted to rhesus monkeys (Macaca mulata) and confirmed by the polymerase chain reaction (PCR) on bile from the animals. Fecal material from acutely infected patients in one of the epidemics was also found positive for HEV RNA by PCR. This may help in confirming the nature of future epidemics. The bile and liver from experimental animals can be used as a source of material for further virological and molecular biological studies of HEV.

Adolescent↗
PubMed1992

Indian hepatitis E virus shows a major deletion in the small open reading frame.

Enterically transmitted non-A, non-B hepatitis virus (HEV), the causative agent for sporadic and large epidemic outbreaks in developing countries, contains a positive-sense single-stranded RNA genome. The genome of the virus encodes three open reading frames (ORF1, ORF2, and ORF3). The gene segment corresponding to the small open reading frame (ORF3), overlapping between ORF1 and ORF2, was synthesized by reverse transcription-polymerase chain reaction (RT-PCR) from a number of previously identified HEV-positive clinical specimens. A DNA fragment of 166 bp was consistently obtained from all the clinical specimens. This small fragment was cloned, sequenced, and found to contain an open reading frame encoding only 41 amino acid residues. Comparison of our results with that of geographically related Burma HEV suggests a major inframe deletion of 246 bp in the ORF3 of Indian strain. The protein encoded by ORF3 does not appear to be useful for early serodiagnosis as a synthetic peptide deduced from the truncated ORF3 failed to show any demonstrable immunoreactivity against HEV-infected acute phase sera in an enzyme-linked immunosorbent assay.

Antibody Formation↗
PubMed1992

Direct detection of hepatitis B virus from dried blood spots by polymerase chain reaction amplification.

The presence of hepatitis B virus DNA in the sera of individuals is the most definitive marker of an active viral infection. We have used polymerase chain reaction detection of hepatitis B virus DNA directly on whole blood dried as a spot on filter paper. The method is rapid, specific, and sensitive and has the ability to detect as little as 10 virus particles by ethidium bromide staining of the polymerase chain reaction-amplified products. The method is cost-effective, and the stability of the spots makes the collection and transportation of potentially infectious blood safe.

Base Sequence↗
PubMed1990

Hepatitis B virus X protein produced in Escherichia coli is biologically functional.

The hepatitis B virus X gene product trans activates transcription from a variety of viral and cellular regulatory elements. We expressed the complete, nonfused X protein in Escherichia coli and showed it to be active in trans activating a human immunodeficiency virus long terminal repeat-linked chloramphenicol acetyltransferase reporter gene.

Chloramphenicol O-Acetyltransferase↗
PubMed1989

IL-1 beta production in cultured human monocytes is regulated at multiple levels.

Cultured human monocytes and tissue macrophages exhibit a marked decrease in LPS-stimulated IL-1 production. Preincubation of monocytes in 100 U/ml IFN-gamma or in 0.25 microgram/ml cycloheximide (Cx) leads to a partial maintenance of the ability to produce IL-1 in response to subsequent stimulation with LPS, whereas preincubation in both reagents leads to a near complete maintenance of this response. These studies were performed to determine the mechanisms of these alterations in regulation of IL-1 production in cultured monocytes. In comparison to LPS-induced fresh monocytes, cells preincubated in medium for 1 day, then stimulated for 24 h with 100 ng/ml LPS, exhibited a 50% or more decrease in steady-state IL-1 beta mRNA levels. This reduction was accompanied by a four- to fivefold decrease in relative transcriptional rate, as determined by the nuclear run-on technique. The medium-aged cells also displayed greatly decreased IL-1 beta production with deficient secretion. Monocytes preincubated in IFN-gamma for 1 day before LPS stimulation exhibited a variable maintenance in IL-1 beta production, secondary both to prolonged duration of transcription and to increased IL-1 beta mRNA stability. Monocytes were preincubated for 1 day in Cx alone or in both IFN-gamma and cycloheximide, then these substances were washed out before a subsequent 24-h culture in LPS. Cx preincubation led to increases in both the peak and duration of transcription as well as to enhanced secretion of IL-1 beta protein. Monocytes preincubated in both IFN-gamma and Cx exhibited increased IL-1 beta mRNA levels due to both enhanced transcription and mRNA stability; more IL-1 beta protein secretion also was present in these cells. In summary, IFN-gamma and Cx may maintain LPS-induced IL-1 beta production in cultured human monocytes through multiple mechanisms. These alterations in regulation of IL-1 beta production during monocyte differentiation may be relevant to tissue macrophages where impaired IL-1 production may be present.

Blood Proteins↗
PubMed1989

Interactions between nuclear factors and the hepatitis B virus enhancer.

We have previously established that the tissue-specific activity of the hepatitis B virus (HBV) enhancer is mediated by trans-acting cellular factors. Here we have studied in vitro the interactions between the HBV enhancer DNA and cellular factors present in nuclear extracts from both liver and nonliver cell types. The results presented in this study imply the involvement of several distinct, ubiquitous, and liver-specific cellular factors with the HBV enhancer. Sequence analysis of the binding sites for these proteins on HBV DNA showed homologies to sequence motifs known to bind other previously characterized and purified transcription factors including CAAT/enhancer-binding protein. Thus, all of these binding sites may function in concert to activate liver-specific transcription of HBV genes from their respective promoters.

Base Sequence↗
PubMed1987

Expression of the hepatitis B virus X gene in mammalian cells.

The hepatitis B virus (HBV) DNA contains an open reading frame (ORF) designated X, which has the capacity to encode a protein of 16,560 Da (subtype adw). Such a protein has not been identified in either HBV particles or infected human livers, and therefore its role in the viral life cycle remains unknown. We report here the expression of the HBV X ORF in cultured cells using recombinant vectors. A protein of 16 kDa was identified by means of an antiserum prepared against a synthetic peptide and with human antisera from hepatitis B patients as well as those with hepatocellular carcinoma. Cell fractionation and immunofluorescence studies suggest a probable association with cytoskeletal components. Our studies further located a promoter sequence upstream of the X ORF, which directs the transcription of a 0.7- to 0.8-kilobase X-specific RNA in transfected human hepatoma cells.

Acetyltransferases↗