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A K Banerjee

Publications and source records attributed to A K Banerjee.

At least 55 records · Page 3Linked to original sources
PubMed2000

Specific phosphorylated forms of glyceraldehyde 3-phosphate dehydrogenase associate with human parainfluenza virus type 3 and inhibit viral transcription in vitro.

We previously reported specific interaction of cellular glyceraldehyde 3-phosphate dehydrogenase (GAPDH), the key glycolytic enzyme, and La protein, the RNA polymerase III transcription factor, with the cis-acting RNAs of human parainfluenza virus type 3 (HPIV3) and packaging of these proteins within purified virions (B. P. De, S. Gupta, H. Zhao, J. Z. Drazba, and A. K. Banerjee, J. Biol. Chem. 271:24728-24735, 1996). To gain further insight into these molecular interactions, we analyzed the virion-associated GAPDH and La protein using two-dimensional gel electrophoresis and immunoblotting. The GAPDH was resolved into two major and one minor molecular species migrating in the pI range of 7.6 to 8.3, while the La protein was resolved into five molecular species in the pI range of 6.8 to 7.5. The GAPDH isoforms present in the virions were also detected in the cytoplasmic fraction of CV-1 cell extract, albeit as minor species. On the other hand, the multiple molecular forms of La protein as seen within the virions were readily detected in the total CV-1 cell extract. Further analysis of virion-associated GAPDH by in vivo labeling with [(32)P]orthophosphate revealed the presence of multiple phosphorylated species. The phosphorylated species were able to bind specifically to the viral cis-acting 3' genome sense RNA but failed to bind to the leader sense RNA, as determined by gel mobility shift assay. In contrast, the La protein isoforms present within the virions were not phosphorylated and bound to the viral cis-acting RNAs in a phosphorylation-independent manner. The GAPDH isoforms purified from the CV-1 cell cytoplasmic fraction inhibited viral transcription in vitro. Consistent with this, flag-tagged recombinant GAPDH synthesized by using the vaccinia virus expression system also inhibited viral transcription. Together, these data indicate that specific phosphorylated forms of GAPDH associate with HPIV3 and are involved in the regulation of virus gene expression.

Autoantigens↗
PubMed2000

Human parainfluenza virus type 3 upregulates ICAM-1 (CD54) expression in a cytokine-independent manner.

Human parainfluenza virus type 3 (HPIV3) causes bronchiolitis, pneumonia, and croup in newborns and infants. Several studies have implicated intercellular adhesion molecule-1 (ICAM-1) in inflammation during infection by viruses. In this study, we investigated the potential for HPIV3 to induce ICAM-1 in HT1080 cells. FACS analysis showed that HPIV3 strongly induced ICAM-1 expression in these cells. The ICAM-1 induction was significantly reduced when the virions were UV inactivated prior to infection, indicating that ICAM-1 induction was mostly viral replication dependent. Culture supernatant of HPIV3-infected cells induced ICAM-1 at an extremely low level, indicating that virus-induced cytokines played only a minor role in the induction process. Consistent with this, potent inducers of ICAM-1 such as IFN-gamma, TGF-beta, and TNF-alpha were absent in the culture supernatant, but a significant amount of IFN type 1 was present. By using U2A cells, which are defective in IFN type I signaling, we confirmed that ICAM-1 induction by HPIV3 occurred in a JAK/STAT signaling-independent manner. These data strongly indicate that HPIV3 induces ICAM-1 directly by viral antigens in a cytokine-independent manner; this induction may play a role in the inflammation during HPIV3 infection.

Animals↗
PubMed2000

Fatal complications of systemic lupus erythematosus--an autopsy study from north India.

Systemic lupus erythematosus (SLE) is a multisystem, autoimmune disease with varied clinical manifestations and outcome. It may prove fatal due to disease activity or intercurrent infections. In recent years, earlier diagnosis and better treatment modalities have resulted in a change in the pattern of organ involvement and mode of death in the west. This aspect of the disease is unknown in India. Hence, in this autopsy series of SLE, the organ involvement and cause of death have been studied. Twenty five cases of clinically diagnosed SLE have been analysed retrospectively. Renal involvement was invariably present (96%) with class IV being the commonest lesion in 60% cases. Disease activity was noted in 60% cases. Pleuro pulmonary lesions were seen in 92% cases with infection being the commonest. Pulmonary infections included bacterial pneumonias (13), disseminated tuberculosis (3), pulmonary mucormycosis (1) and aspergillosis (1). Massive pulmonary haemorrhage in 5 cases and acute lupus pneumonitis in one, contributed to the demise of the patient. Vasculitis was evident in single organ in 9 cases, in two or more organs in 3 cases with systemic vasculitis significantly attributing to morbidity in 1 case. Active disease was the cause of death in 60% cases and infection in 40%.

Autopsy↗
PubMed1999

Involvement of actin microfilaments in the transcription/replication of human parainfluenza virus type 3: possible role of actin in other viruses.

Multifunctional involvement of actin microfilaments during viral infection has been documented in many studies. The molecular mechanism underlying this important host-virus interaction, however, remains poorly understood. We have investigated the role of actin microfilaments in the life cycle of human parainfluenza virus type 3 (HPIV3), a paramyxovirus that causes severe respiratory illness in children. In vitro transcription with purified viral ribonucleoprotein (RNP) complex showed a requirement of cellular actin, in the polymeric form, for mRNA synthesis in vitro. This was further confirmed by using recombinant actin, which interacted with the viral RNP and also activated mRNA synthesis in vitro. Consistent with the role of the polymeric form of actin, the actin microfilaments of the cytoskeletal framework participate in the virus replication in vivo. Biochemical and immunological analyses revealed the association of viral RNPs with cytoskeletal framework during early stages of infection, and involvement of these RNPs in the synthesis of mRNAs and genome-length RNA. Immunofluorescent labeling and confocal microscopy showed that the viral nucleocapsids colocalize with the actin microfilaments. Treatment of cells with cytochalasin D, which depolymerizes actin microfilaments, inhibited viral RNA synthesis and RNP accumulation. These data indicate that actin microfilaments play a critical role in HPIV3 life cycle, specifically at the level of viral transcription and replication. Involvement of the cytoskeletal framework in the life cycle of several viruses containing RNA and DNA genomes is reviewed.

Actin Cytoskeleton↗
PubMed1999

Carboxy-terminal five amino acids of the nucleocapsid protein of vesicular stomatitis virus are required for encapsidation and replication of genome RNA.

The encapsidation of vesicular stomatitis virus (VSV) genome RNA, a prerequisite step to the replication process by the nucleocapsid protein (N) was studied by its ability to package VSV leader RNA in vitro in a RNase-resistant form. The VSV leader RNA was derived from the SP6 transcription vector while the N protein was made in rabbit reticulocyte lysate. The in vitro encapsidation was carried out by translating N mRNA in the presence of 32P-labeled presynthesized leader RNA. The RNA encapsidation property of the N protein was completely abrogated when the C-terminal five amino acids (VEFDK-COOH) were deleted. Systematic mutational analyses within the C-terminal five amino acid regions reveal that the RNA encapsidation activity was lost in all mutants except K --> A and K --> R, indicating that C-terminal five amino acids, in particular the lysine residue play critical role in genome RNA encapsidation. To correlate the in vitro encapsidation abilities of these mutant N proteins with genome RNA replication, we have used a full-length cDNA clone of VSV genome RNA to rescue infectious virions from cells expressing L, P, and wt or mutant N proteins and measured the recovery of plaque forming units. The results indicate that the N mutants that are defective in in vitro encapsidation of leader RNA do not support replication, establishing the requirement of C-terminal five amino acids of the N protein in viral replication.

Amino Acids↗
PubMed1999

Spermatocytic seminoma: a cytology and histology case report with review of the literature.

Fine-needle aspiration cytology (FNAC) findings are described in a case of spermatocytic seminoma occurring in a 52-yr-old male, involving the left testis. The smears showed three populations of cells (small, medium, and large), with a preponderance of medium-sized cells showing visible nucleoli. The background was clean, in contrast to the "tigroid" substance seen in classical seminoma. Low mitotic rate and absence of lymphocytes were the other features helpful in diagnosis. Because of these distinct morphological features, a preoperative diagnosis of spermatocytic seminoma was possible, with subsequent confirmation on histopathology. The case is being reported because of the rarity of this tumor, and because there have been only a few reported cases of FNAC diagnosis.

Humans↗
PubMed1999

MRI of the brain in HIV-positive patients: what is the value of routine intravenous contrast medium?

Our purpose was to assess the value of routine administration of intravenous gadolinium-DTPA (Gd-DTPA) for cranial MR in a series of human immunodeficiency virus (HIV)-positive patients. Two radiologists retrospectively reviewed 150 consecutive examinations of 104 patients. All patients underwent unenhanced and contrast-enhanced images. Each radiologist independently assessed first the unenhanced images alone and then the pre- and postinjection images together. Then both reviewed the complete study and produced a consensus report. The history, investigations and management were collated separately and were unknown to the radiologists. Contrast-enhanced T1-weighted images showed new focal abnormalities, not seen on the T2-weighted or unenhanced images in 15 (14 %) patients, but almost always in the context of abnormal unenhanced images. In only 2 patients (2 %) did contrast medium reveal abnormalities when the unenhanced study had been considered normal. In only 1 of these (1 %) was the new finding, cytomegalovirus diffuse ependymal enhancement, of clinical importance, although the diagnosis of encephalitis was made on routine examination of cerebrospinal-fluid. The other revealed a toxoplasma lesion in a patient known to have resolving disease. Meningeal disease not suspected on the unenhanced images was shown in 2 patients (2 %). In these case the unenhanced images were abnormal in other respects. Intravenous Gd-DTPA was helpful to the radiologist in making a radiological diagnosis in 11 patients (11 %), usually by improving characterisation of a lesion seen on the unenhanced images. The contribution of intravenous Gd-DTPA in this series does not warrant recommending its use in every case.

AIDS Dementia Complex↗
PubMed1999

Human parainfluenza virus type 3 up-regulates major histocompatibility complex class I and II expression on respiratory epithelial cells: involvement of a STAT1- and CIITA-independent pathway.

Human parainfluenza virus type 3 (HPIV3) infection causes severe damage to the lung epithelium, leading to bronchiolitis, pneumonia, and croup in newborns and infants. Cellular immunity that plays a vital role in normal antiviral action appears to be involved, possibly because of inappropriate activation, in the infection-related damage to the lung epithelium. In this study, we investigated the expression of major histocompatibility complex (MHC) class I and II molecules on human lung epithelial (A549) and epithelium-like (HT1080) cells following HPIV3 infection. MHC class I was induced by HPIV3 in these cells at levels similar to those observed with natural inducers such as beta and gamma interferon (IFN-beta and -gamma). MHC class II was also efficiently induced by HPIV3 in these cells. UV-irradiated culture supernatants from infected cells were able to induce MHC class I but not MHC class II, suggesting involvement of released factors for the induction of MHC class I. Quantitation of IFN types I and II in the culture supernatant showed the presence of IFN-beta as the major cytokine, while IFN-gamma was undetectable. Anti-IFN-beta, however, blocked the HPIV3-mediated induction of MHC class I only partially, indicating that viral antigens, besides IFN-beta, are directly involved in the induction process. The induction of MHC class I and class II directed by the viral antigens was confirmed by using cells lacking STAT1, an essential intermediate of the IFN signaling pathways. HPIV3 induced both MHC class I and class II molecules in STAT1-null cells. Furthermore, MHC class II was also induced by HPIV3 in cells defective in class II transactivator, an important intermediate of the IFN-gamma-mediated MHC class II induction pathway. Together, these data indicate that the HPIV3 gene product(s) is directly involved in the induction of MHC class I and II molecules. The induction of MHC class I and II expression by HPIV3 suggests that it plays a role in the infection-related immunity and pathogenesis.

Animals↗
PubMed1999

Optimal replication activity of vesicular stomatitis virus RNA polymerase requires phosphorylation of a residue(s) at carboxy-terminal domain II of its accessory subunit, phosphoprotein P.

The phosphoprotein, P, of vesicular stomatitis virus (VSV) is a key subunit of the viral RNA-dependent RNA polymerase complex. The protein is phosphorylated at multiple sites in two different domains. We recently showed that specific serine and threonine residues within the amino-terminal acidic domain I of P protein must be phosphorylated for in vivo transcription activity, but not for replication activity, of the polymerase complex. To examine the role of phosphorylation of the carboxy-terminal domain II residues of the P protein in transcription and replication, we have used a panel of mutant P proteins in which the phosphate acceptor sites (Ser-226, Ser-227, and Ser-233) were altered to alanines either individually or in various combinations. Analyses of the mutant proteins for their ability to support replication of a VSV minigenomic RNA suggest that phosphorylation of either Ser-226 or Ser-227 is necessary for optimal replication activity of the protein. The mutant protein (P226/227) in which both of these residues were altered to alanines was only about 8% active in replication compared to the wild-type (wt) protein. Substitution of alanine for Ser-233 did not have any adverse effect on replication activity of the protein. In contrast, all the mutant proteins showed activities similar to that of the wt protein in transcription. These results indicate that phosphorylation of the carboxy-terminal domain II residues of P protein are required for optimal replication activity but not for transcription activity. Furthermore, substitution of glutamic acid residues for Ser-226 and Ser-227 resulted in a protein that was only 14% active in replication but almost fully active in transcription. Taken together, these results, along with our earlier studies, suggest that phosphorylation of residues at two different domains in the P protein regulates its activity in transcription and replication of the VSV genome.

Amino Acid Substitution↗
PubMed1999

Hyponatraemia and seizures after ecstasy use.

A patient presented to our unit with seizures and profound hyponatraemia after ingestion of a single tablet of ecstasy. The seizures proved resistant to therapy and ventilation on the intensive care unit was required. Resolution of the seizures occurred on correction of the metabolic abnormalities. The pathogenesis of seizures and hyponatraemia after ecstasy use is discussed. Ecstasy use should be considered in any young patient presenting with unexplained seizures and attention should be directed towards electrolyte levels, particularly sodium.

Adult↗
PubMed1999

Phlegmonous inflammation of gastrointestinal tract autopsy study of three cases.

Three cases of Phlegmonous inflammation of gastrointestinal tract detected at necropsy are described. Predisposing factors were seen in all three cases. These were chronic alcoholism with submissive hepatic necrosis (HbsAg and HbcAg positive) in Case 1, Indian Childhood cirrhosis in Case 2 and acute on chronic Budd Chiari syndrome in Case 3. In case 1 and 3 the inflammation was limited to the large intestine where as in Case 2 it was seen both in the stomach and large intestine. In two of the three cases blood culture grew Staphylococcus aureus (Case 1) and gram negative organisms (Case 2).

Adult↗