LOFAR 144-MHz follow-up observations of GW170817

This article has been accepted for publication in Monthly Notices of the Royal Astronomical Society, Volume 494, Issue 4, June 2020, Pages 5110–5117, ©: 2020 The Author(s). Published by Oxford University Press on behalf of the Royal Astronomical Society. All rights reserved.We present low-radio-frequency follow-up observations of AT 2017gfo, the electromagnetic counterpart of GW170817, which was the first binary neutron star merger to be detected by Advanced LIGO-Virgo. These data, with a central frequency of 144 MHz, were obtained with LOFAR, the Low-Frequency Array. The maximum elevation of the target is just 13.7 degrees when observed with LOFAR, making our observations particularly challenging to calibrate and significantly limiting the achievable sensitivity. On time-scales of 130-138 and 371-374 days after the merger event, we obtain 3$\sigma$ upper limits for the afterglow component of 6.6 and 19.5 mJy beam$^{-1}$, respectively. Using our best upper limit and previously published, contemporaneous higher-frequency radio data, we place a limit on any potential steepening of the radio spectrum between 610 and 144 MHz: the two-point spectral index $\alpha^{610}_{144} \gtrsim -2.5$. We also show that LOFAR can detect the afterglows of future binary neutron star merger events occurring at more favourable elevations.Peer reviewe

Rapid NK-cell activation in chicken after infection with infectious bronchitis virus M41

Natural killer (NK) cells are cytotoxic lymphocytes and play an important role in the early defence against viruses. In this study we focussed on NK cell and interferon (IFN) responses after infection with infectious bronchitis virus (IBV). Based on surface expression of CD107+, enhanced activation of lung NK cells was observed at 1. dpi, whereas in blood prolonged NK-cell activation was found. IFN-α and IFN-β mRNA and proteins were not rapidly induced whereas IFN-γ production in lung, measured by Elispot assay, increased over time at 2 and 4. dpi. In contrast, IFN-γ production in blood was highest at 1. dpi and decreased over time down to levels comparable to uninfected birds at 4. dpi. Collectively, infection with IBV-M41 resulted in activation of NK cells in the lung and blood and rapid production of IFN-γ and not IFN-α and IFN-β compared to uninfected birds

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Natural killer (NK) cells are cytotoxic lymphocytes and play an important role in the early defence against viruses. In this study we focussed on NK cell and interferon (IFN) responses after infection with infectious bronchitis virus (IBV). Based on surface expression of CD107+, enhanced activation of lung NK cells was observed at 1 dpi, whereas in blood prolonged NKcell activation was found. IFN- and IFN- mRNA and proteins were not rapidly induced whereas IFN- production in lung, measured by Elispot assay, increased over time at 2 and 4 dpi. In contrast, IFN- production in blood was highest at 1 dpi and decreased over time down to levels comparable to uninfected birds at 4 dpi. Collectively, infection with IBV-M41 resulted in activation of NK cells in the lung and blood and rapid production of IFN- and not IFN- and IFN- compared to uninfected birds

Transcriptional expression levels of chicken collectins are effected by avian influenza A virus inoculation.

Mammalian collectins have been found to play an important role in the defense against influenza A virus H9N2 inoculation, but for chicken collectins this has not yet been clarified. The aim of this study was to determine the effect of avian influenza A virus (AIV) inoculation on collectin gene expression in the respiratory tract of chickens and whether this was affected by age. For this purpose 1- and 4-week-old chickens were inoculated intratracheally with PBS or H9N2 AIV. Chickens were killed at 0, 8, 16 and 24 h postinoculation and trachea and lung were harvested for analysis. Viral RNA expression and mRNA expression of chicken collectins 1 and 2 (cCL-1 and cCL-2), chicken lung lectin (cLL) and chicken surfactant protein A (cSP-A) were determined using real-time quantitative RT-PCR. In lung, a decrease in mRNA expression of cCL-2, cLL and cSP-A after inoculation with H9N2 was seen in both 1- and 4-week-old birds, although at different time points, while in trachea changes were only seen in 4-week-old birds and expression was increased. Moreover, collectin expression correlated with viral RNA expression in lung of 1-week-old birds. These results suggest that both age and location in the respiratory tract affect changes in collectin mRNA expression after inoculation with H9N2 and indicate a possible role for collectins in the host response to AIV in the respiratory tract of chickens

Chicken dendritic cells are susceptible to highly pathogenic avian influenza viruses which induce strong cytokine responses

Infection with highly pathogenic avian influenza (HPAI) in birds and mammals is associated with severe pathology and increased mortality. We hypothesize that in contrast to low pathogenicity avian influenza (LPAI) infection, HPAI infection of chicken dendritic cells (DC) induces a cytokine deregulation which may contribute to their highly pathogenic nature. Infection of DC with LPAI H7N1 and H5N2 resulted in viral RNA and NP expression without increase in time, in contrast to HPAI H7N1 and H5N2 mRNA expression. No increase in IFN mRNA was detected after infection with LPAI, but after LPAI H5N2, and not LPAI H7N1, infection the level of bioactive IFNa/ß significantly increased. After HPAI H7N1 and H5N2 infection, significant increases in IL-8, IFN-a, IFN-¿ mRNA expression and in TLR1, 3, and 21 mRNA were observed. This enhanced activation of DC after HPAI infection may trigger deregulation of the immune response as seen during HPAI infection in chickens

Chicken dendritic cells are susceptible to highly pathogenic avian influenza viruses which induce strong cytokine responses

Infection with highly pathogenic avian influenza (HPAI) in birds and mammals is associated with severe pathology and increased mortality. We hypothesize that in contrast to low pathogenicity avian influenza (LPAI) infection, HPAI infection of chicken dendritic cells (DC) induces a cytokine deregulation which may contribute to their highly pathogenic nature. Infection of DC with LPAI H7N1 and H5N2 resulted in viral RNA and NP expression without increase in time, in contrast to HPAI H7N1 and H5N2 mRNA expression. No increase in IFN mRNA was detected after infection with LPAI, but after LPAI H5N2, and not LPAI H7N1, infection the level of bioactive IFNa/ß significantly increased. After HPAI H7N1 and H5N2 infection, significant increases in IL-8, IFN-a, IFN-¿ mRNA expression and in TLR1, 3, and 21 mRNA were observed. This enhanced activation of DC after HPAI infection may trigger deregulation of the immune response as seen during HPAI infection in chickens