Growth Experiment of Hantaan Virus in A549 Cells: An Attempt to Improve the Immunofluorescent Antibody Technique for Hemorrhagic Fever with Renal Syndrome

Hamada, Chuya; Sato, Norikazu; Niimura, Sueo; Kato, Akira; Fujisawa, Naoki; Maeda, Yoshitaka; Kumanishi, Toshio; Lee, Ho Wang

doi:10.1538/expanim1978.35.1_1

Cited by 3 publications

(2 citation statements)

References 14 publications

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“…Since it has been proposed that macrophages may contribute to the spread of Hantaan virus, possibly through an antibody-dependent enhancement (ADE) (Yao et al, 1992), it is of interest that macrophages also support Puumala virus replication. Susceptibility of the lung-, submaxillary gland-and pharynx-derived cells (CCD-I 1 Lu, A-427, WI-38, A-253, Detroit 562) is in line with the reported sensitivity of A-549 cells (human lung carcinoma) to Hantaan virus (Hamada et al, 1986) and the proposed entry of hantaviruses through the respiratory tract. Susceptibility of the Hep G2 hepatoblastoma line suggests that the involvement of liver with elevated transaminases in NE (Lfihdevirta et al, 1984;Settergren et al, 1989) could be a consequence of virus propagation in this organ.…”

supporting

confidence: 64%

Susceptibility of human cells to Puumala virus infection

Temonen¹,

Vapalahti²,

Holthöfer

et al. 1993

Journal of General Virology

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supporting

confidence: 64%

Susceptibility of human cells to Puumala virus infection

Temonen¹,

Vapalahti²,

Holthöfer

et al. 1993

Journal of General Virology

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“…EVC-304 cells are also endovascular cells, whereas EVC-304 TLR4 − cells are TLR4-deleted cells, both of which have been used for HTNV infection related studies (15, 33). A549 cells were once used to isolate HTNV, and they were confirmed to be a mature model of infection (34–37). Additionally, Huh 7.0 and Huh 7.5 (RIG-I − ) cells used in our study have been reported to be infected by HTNV by Lee et al (5) and can be used as a cell model to study immune responses against HTNV replication (38, 39).…”

Section: Discussionmentioning

confidence: 99%

The Long Noncoding RNA NEAT1 Exerts Antihantaviral Effects by Acting as Positive Feedback for RIG-I Signaling

Han

et al. 2017

J Virol

157

167

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Hantavirus infection, which causes zoonotic diseases with a high mortality rate in humans, has long been a global public health concern. Over the past decades, accumulating evidence suggests that long noncoding RNAs (lncRNAs) play key regulatory roles in innate immunity. However, the involvement of host lncRNAs in hantaviral control remains uncharacterized. In this study, we identified the lncRNA NEAT1 as a vital antiviral modulator. NEAT1 was dramatically upregulated after Hantaan virus (HTNV) infection, whereas its downregulation in vitro or in vivo delayed host innate immune responses and aggravated HTNV replication. Ectopic expression of NEAT1 enhanced beta interferon (IFN-β) production and suppressed HTNV infection. Further investigation suggested that NEAT1 served as positive feedback for RIG-I signaling. HTNV infection activated NEAT1 transcription through the RIG-I–IRF7 pathway, whereas NEAT1 removed the transcriptional inhibitory effects of the splicing factor proline- and glutamine-rich protein (SFPQ) by relocating SFPQ to paraspeckles, thus promoting the expression of RIG-I and DDX60. RIG-I and DDX60 had synergic effects on IFN production. Taken together, our findings demonstrate that NEAT1 modulates the innate immune response against HTNV infection, providing another layer of information about the role of lncRNAs in controlling viral infections.IMPORTANCE Hantaviruses have attracted worldwide attention as archetypal emerging pathogens. Recently, increasing evidence has highlighted long noncoding RNAs (lncRNAs) as key regulators of innate immunity; however, their roles in hantavirus infection remain unknown. In the present work, a new unexplored function of lncRNA NEAT1 in controlling HTNV replication was found. NEAT1 promoted interferon (IFN) responses by acting as positive feedback for RIG-I signaling. This lncRNA was induced by HTNV through the RIG-I–IRF7 pathway in a time- and dose-dependent manner and promoted HTNV-induced IFN production by facilitating RIG-I and DDX60 expression. Intriguingly, NEAT1 relocated SFPQ and formed paraspeckles after HTNV infection, which might reverse inhibitive effects of SFPQ on the transcription of RIG-I and DDX60. To the best of our knowledge, this is the first study to address the regulatory role of the lncRNA NEAT1 in host innate immunity after HTNV infection. In summary, our findings provide additional insights regarding the role of lncRNAs in controlling viral infections.

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Strand‐Specific Detection of Hantaan Virus RNA Sequences by In Vitro DNA Amplification

Isegawa

Ohshima

Sokawa

et al. 1994

Microbiology and Immunology

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Hantaan virus often causes a fatal human disease, hemorrhagic fever with renal syndrome (HFRS). An assay for strand-specific detection and quantitation of Hantaan virus RNA was developed based on the polymerase chain reaction (PCR). A protocol for the efficient detection of both genomic RNA and its transcript is presented, in which a reverse transcriptase reaction (RTR) followed by PCR with two common primers was used to distinguish between positive-and negative-stranded RNA. Using this method, the growth characteristics of Hantaan virus, strain 76-118, were studied in Vero E6 cells. Positive-stranded RNA was detected on the next day after infection, and the amount increased remarkably beginning from 3 days after infection. The negative-stranded RNA (genomic), was detected at 2 days after infection which predominated over the transcript RNA. Three days after infection, the amount of viral RNA attained 80% of the maximum amount which was detected by 6 days after infection, while, 4 days after infection the amount of the positive-stranded RNA became over 80% of the maximum amount of 6 days after infection and reached the amount of viral RNA. Both RNAs reached plateaus at 6 days after infection and after that the amounts of synthesized viral RNA and its transcripts were constant.

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Growth Experiment of Hantaan Virus in A549 Cells: An Attempt to Improve the Immunofluorescent Antibody Technique for Hemorrhagic Fever with Renal Syndrome

Cited by 3 publications

References 14 publications

Susceptibility of human cells to Puumala virus infection

Susceptibility of human cells to Puumala virus infection

The Long Noncoding RNA NEAT1 Exerts Antihantaviral Effects by Acting as Positive Feedback for RIG-I Signaling

Strand‐Specific Detection of Hantaan Virus RNA Sequences by In Vitro DNA Amplification

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