In vivo detection of porcine reproductive and respiratory syndrome virus RNA by in situ hybridization at different times postinfection

Sur, Jung Hyang; Cooper, Vickie L.; Galeota, J. A.; Hesse, Richard; Doster, Alan R.; Osorio, Fernando A.

doi:10.1128/jcm.34.9.2280-2286.1996

Cited by 71 publications

(56 citation statements)

References 26 publications

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“…Upon coinfection of PCLS, we did not detect any co-infected cells, confirming the importance of bronchial epithelial cells and alveolar macrophages as the main target of SIV and PRRSV in lung, respectively (Crisci et al, 2013;Meulenberg, 2000;Sang et al, 2011;Taubenberger and Morens, 2008). However, our study also confirms that some alveolar epithelial cells such as pneumocyte type 1 can be infected by PRRSV virus as previously reported (Sur et al, 1996). Many different cell types are present in the PCLS, e.g.…”

Section: Discussionsupporting

confidence: 90%

In vitro and ex vivo analyses of co-infections with swine influenza and porcine reproductive and respiratory syndrome viruses

Dobrescu

Levast

Lai

et al. 2014

Veterinary Microbiology

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Viral respiratory diseases remain problematic in swine. Among viruses, porcine reproductive and respiratory syndrome virus (PRRSV) and swine influenza virus (SIV), alone or in combination, are the two main known contributors to lung infectious diseases. Previous studies demonstrated that experimental dual infections of pigs with PRRSV followed by SIV can cause more severe disease than the single viral infections. However, our understanding of the impact of one virus on the other at the molecular level is still extremely limited. Thus, the aim of the current study was to determine the influence of dual infections, compared to single infections, in porcine alveolar macrophages (PAMs) and precision cut lung slices (PCLS). PAMs were isolated and PCLS were acquired from the lungs of healthy 8-week-old pigs. Then, PRRSV (ATCC VR-2385) and a local SIV strain of H1N1 subtype (A/Sw/Saskatchewan/18789/02) were applied simultaneously or with 3h apart on PAMs and PCLS for a total of 18 h. Immuno-staining for both viruses and beta-tubulin, real-time quantitative PCR and ELISA assays targeting various genes (pathogen recognition receptors, interferons (IFN) type I, cytokines, and IFN-inducible genes) and proteins were performed to analyze the cell and the tissue responses. Interference caused by the first virus on replication of the second virus was observed, though limited. On the host side, a synergistic effect between PRRSV and SIV co-infections was observed for some transcripts such as TLR3, RIG-I, and IFNβ in PCLS. The PRRSV infection 3h prior to SIV infection reduced the response to SIV while the SIV infection prior to PRRSV infection had limited impact on the second infection. This study is the first to show an impact of PRRSV/SIV co-infection and superinfections in the cellular and tissue immune response at the molecular level. It opens the door to further research in this exciting and intriguing field.

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Section: Discussionsupporting

confidence: 90%

In vitro and ex vivo analyses of co-infections with swine influenza and porcine reproductive and respiratory syndrome viruses

Dobrescu

Levast

Lai

et al. 2014

Veterinary Microbiology

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“…The most consistent pathological lesions caused by PRRSV during acute infection are interstitial pneumonia and mild lymphocytic encephalitis (Halbur et al, 1995;Plagemann, 1996;Rossow et al, 1995Rossow et al, , 1996. Tissue macrophages and monocytes are the major target cells during both acute and persistent infection (Molitor et al, 1997), although pneumocytes and epithelial germ cells of the testis have also been shown to be infected (Sur et al, 1996(Sur et al, , 1997.…”

Section: Introductionmentioning

confidence: 99%

Porcine arterivirus activates the NF-κB pathway through IκB degradation

2005

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Nuclear factor-kappaB (NF-kappaB) is a critical regulator of innate and adaptive immune function as well as cell proliferation and survival. The present study demonstrated for the first time that a virus belonging to the Arteriviridae family activates NF-kappaB in MARC-145 cells and alveolar macrophages. In porcine reproductive and respiratory syndrome virus (PRRSV)-infected cells, NF-kappaB activation was characterized by translocation of NF-kappaB from the cytoplasm to the nucleus, increased DNA binding activity, and NF-kappaB-regulated gene expression. NF-kappaB activation was increased as PRRSV infection progressed and in a viral dose-dependent manner. UV-inactivation of PRRSV significantly reduced the level of NF-kappaB activation. Degradation of IkappaB protein was detected late in PRRSV infection, and overexpression of the dominant negative form of IkappaBalpha (IkappaBalphaDN) significantly suppressed NF-kappaB activation induced by PRRSV. However, IkappaBalphaDN did not affect viral replication and viral cytopathic effect. PRRSV infection induced oxidative stress in cells by generating reactive oxygen species (ROS), and antioxidants inhibited NF-kappaB DNA binding activity in PRRSV-infected cells, suggesting ROS as a mechanism by which NF-kappaB was activated by PRRSV infection. Moreover, NF-kappaB-dependent expression of matrix metalloproteinase (MMP)-2 and MMP-9 was observed in PRRSV-infected cells, an observation which implies that NF-kappaB activation is a biologically significant aspect of PRRSV pathogenesis. The results presented here provide a basis for understanding molecular pathways of pathology and immune evasion associated with disease caused by PRRSV.

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“…The most consistent pathological lesions caused by PRRSV during acute infection are interstitial pneumonia and mild lymphocytic encephalitis Plagemann, 1996;Rossow et al, 1995Rossow et al, , 1996. Tissue macrophages and monocytes are the major target cells during both acute and persistent infection (Molitor et al, 1997), although pneumocytes and epithelial germ cells of the testes have also been shown to be infected (Sur et al, 1996(Sur et al, , 1997. It is important to note that clinical disease caused by PRRSV is highly variable, ranging from mild, subclinical infections to acute deaths of adult animals .…”

Section: Introductionmentioning

confidence: 99%

“…After the acute phase of PRRSV infection, which is typically characterized by viremia and clinical disease, many pigs fully recover yet carry a low-level viral infection for an extended period of time. Under experimental conditions, persistent infection with PRRSV has been well documented (Albina et al, 1994;Allende et al, 2000;Christopher-Hennings et al, 1995;Horter et al, 2002;Sur et al, 1996;Yoon et al, 1993;Wills et al, 2003). These ''carrier'' pigs are persistently infected with PRRSV and shed the virus, either intermittently or continuously, and may infect naïve pigs following direct or indirect contact.…”

Section: Introductionmentioning

confidence: 99%

Porcine reproductive and respiratory syndrome virus field isolates differ in in vitro interferon phenotypes

Lee

Schommer

Kleiboeker

2004

Veterinary Immunology and Immunopathology

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Type I interferons (IFN-alpha and -beta) play an important role in the innate host defense against viral infection by inducing antiviral responses. In addition to direct antiviral activities, type I IFN serves as an important link between the innate and adaptive immune response through multiple mechanisms. Therefore, the outcome of a viral infection can be affected by IFN induction and the IFN sensitivity of a virus. North American porcine reproductive and respiratory syndrome virus (PRRSV) field isolates were studied with regard to IFN-alpha sensitivity and induction in order to understand the role of type I IFN in PRRSV pathogenesis. PRRSV isolates were differentially sensitive to porcine recombinant IFN-alpha (rIFN-alpha) and varied in their ability to induce IFN-alpha in porcine alveolar macrophages (PAM) cultures as measured by a porcine IFN-alpha specific ELISA on cell culture supernatants. Fifty-two plaques were purified from three PRRSV isolates (numbers 3, 7, and 12) and tested for IFN sensitivity and IFN induction. Plaque-derived populations were composed of heterogeneous populations in terms of IFN-inducing capacity and sensitivity to rIFN-alpha. When macrophages infected with isolates 3, 7, or 12 were treated with polycytidylic acid (polyI:C), IFN-alpha production was enhanced. Cells infected with isolate 3 and treated with polyI:C showed the most consistent and strongest enhancement of IFN-alpha production. It was demonstrated that the relatively low concentrations of IFN-alpha produced by isolate 3 contributed to the enhanced IFN-alpha synthesis in response to polyI:C. Isolates 7 and 12 significantly suppressed the enhanced IFN-alpha production by isolate 3 in polyI:C treated cells. To determine if suppression was at the level of IFN-alpha transcription, quantitative RT-PCR was performed for IFN-alpha mRNA and compared to GAPDH and cyclophilin mRNA quantification. However, the relative number of IFN-alpha transcript copies did not correlate with IFN-alpha protein levels, suggesting a post-transcriptional mechanism of suppression. In summary, these results demonstrate that PRRSV field isolates differ both in IFN-alpha sensitivity and induction. Furthermore, a PRRSV field isolate strongly enhance polyI:C-induced IFN-alpha production in PAM cultures and this priming effect was suppressed by other PRRSV isolates.

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In vivo detection of porcine reproductive and respiratory syndrome virus RNA by in situ hybridization at different times postinfection

Cited by 71 publications

References 26 publications

In vitro and ex vivo analyses of co-infections with swine influenza and porcine reproductive and respiratory syndrome viruses

In vitro and ex vivo analyses of co-infections with swine influenza and porcine reproductive and respiratory syndrome viruses

Porcine arterivirus activates the NF-κB pathway through IκB degradation

Porcine reproductive and respiratory syndrome virus field isolates differ in in vitro interferon phenotypes

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