Characterization of an in vitro system for the synthesis of mRNA from human parainfluenza virus type 3

De, Bishnu P.; Galinski, Mark S.; Banerjee, Amiya K.

doi:10.1128/jvi.64.3.1135-1142.1990

Cited by 42 publications

(22 citation statements)

References 50 publications

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“…The role of host cell factors in optimal HPIVS transcription has recently been described (De et al, 1990(De et al, , 1991. Extension of these observations to address the question of whether host cell factors participate in RNA editing, or if this process is dependent solely upon viral components was pursued.…”

Section: Resultsmentioning

confidence: 99%

“…In vitro synthesized mRNA, a generous gift from Bishnu De (Cleveland Clinic Foundation), was prepared as previously described (De et al, 1990(De et al, , 1991 using purified nucleocapsid complexes in the presence or absence of cell lysates. Transcribed mRNA was removed from the genomic vRNA following oligo dT-cellulose chromatography.…”

Section: Nucleocapsid-associatedmentioning

confidence: 99%

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RNA editing in the phosphoprotein gene of the human parainfluenza virus type 3

1992

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RNA editing of the human parainfluenza virus type 3 (HPIV3) phosphoprotein (P) gene was found to occur for the accession of an alternate discontinuous cistron. Editing occurred within a purine-rich sequence (AAUUAAAAAAGGGGG) found at the mRNA nucleotides 791-805. This sequence resembles an HPIV3 consensus transcription termination sequence and is located at the 5'-end of the putative D protein coding sequences. Editing at an alternate site (AAUUGGAAAGGAAAGG), mRNA nucleotides 1121-1136, for accession of a conserved V cistron, which is present in a number of paramyxovirus P genes, was not found to occur in HPIV3. In contrast with many other paramyxoviruses, editing was indiscriminate with the insertion of 1-12 additional G residues not present in the gene template. RNA editing was found to occur in both in vivo (HPIV3 infected cells) and in vitro (purified nucleocapsid complexes) synthesized mRNAs. Further, the in vitro prepared mRNA was edited regardless of whether the nucleocapsid complexes were transcribed in the presence or absence of uninfected human lung carcinoma (HLC) cell lysates. These results support the notion that RNA editing appears to be exclusively a function of viral proteins.

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Section: Resultsmentioning

confidence: 99%

Section: Nucleocapsid-associatedmentioning

confidence: 99%

RNA editing in the phosphoprotein gene of the human parainfluenza virus type 3

1992

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“…We previously reported the development of an in vitro transcription system for HPIV3 using partially purified RNP from infected cells that contained the viral N, L, and P proteins and, in addition, some cellular proteins (De et al, 1990). Under the same conditions, when we used RNP from highly purified progeny virions, it was inactive in mRNA synthesis despite containing all necessary viral proteins.…”

Section: Activation Of Hpiv3 Transcription In Vitro By Cellular Actinmentioning

confidence: 99%

“…Requirement of host proteins for mRNA synthesis in vitro by purified viral RNP. HPIV3 (HA-1; NIH 47885) was grown in CV-1 cells and purified as reported previously (De et al, 1990. The RNP was extracted from purified virions and further purified (De et al, 1990.…”

Section: Activation Of Hpiv3 Transcription In Vitro By Cellular Actinmentioning

confidence: 99%

“…The N protein enwraps the genome RNA while L and P proteins together constitute the RNA-dependent RNA polymerase complex that transcribes the N-bound genome RNA both in vitro and in vivo Durbin et al, 1997;Hoffman and Banerjee, 1998). Previous studies indicated that, in addition to the RNP-associated viral proteins, cellular factor(s) is necessary for the activation of HPIV3 tran-scription in vitro (De et al, 1990). Further analyses of cellular proteins demonstrated for the first time that an enveloped RNA virus, the HPIV3, requires cellular actin for its transcription .…”

Section: Introductionmentioning

confidence: 99%

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

Banerjee

1999

Microsc. Res. Tech.

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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.

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Virologic, immunologic, and clinical follow-up of a couple infected by the human immunodeficiency virus type one, group O

et al. 1997

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The pathogenic course (virologic, immunologic, and clinical changes) of infection due to human immunodeficiency virus type one (HIV-1) group O viruses is unknown at present. To address this issue, serial HIV-1 isolates from a married couple (patients A and B) infected with a group O virus were analyzed to determine the temporal association between disease status and alterations in several parameters including plasma viral burden as measured by semiquantitative polymerase chain reaction, changes in CD4+ T cells, presence of neutralizing antibodies, and the ability to induce syncytia on the MT2 cells. For patient A who has been asymptomatic for at least 8 years, both the absence of syncytium-inducing (SI) variants and the presence of autologous and heterologous neutralizing antibodies correlated with a clinically healthier status. In contrast, a switch from NSI to SI variants was observed in patient B in 1990, followed by an expanded in vitro host range, increased viral burden, and a sharp decrease in CD4+ T cells 4 years later. Moreover, plasma obtained from this patient uniformly failed to neutralize both autologous and heterologous viruses. These observations in patient B correlated with a slightly unfavorable clinical status. Based on our preliminary results, it appears that the pathogenic course of infections due to group O viruses is similar to that reported previously for infections due to group M viruses.

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Characterization of an in vitro system for the synthesis of mRNA from human parainfluenza virus type 3

Cited by 42 publications

References 50 publications

RNA editing in the phosphoprotein gene of the human parainfluenza virus type 3

RNA editing in the phosphoprotein gene of the human parainfluenza virus type 3

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

Virologic, immunologic, and clinical follow-up of a couple infected by the human immunodeficiency virus type one, group O

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