Induction of interferon-gamma and downstream pathways during establishment of fetal persistent infection with bovine viral diarrhea virus

Смирнова, Н. П.; Webb, Brett T.; McGill, Jodi L.; Schaut, Robert G.; Bielefeldt‐Ohmann, Helle; Campen, Hana Van; Sacco, Randy E.; Hansen, Thomas

doi:10.1016/j.virusres.2014.02.002

Cited by 24 publications

(38 citation statements)

References 51 publications

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“…Our interpretation (hypothesis) of the establishment of fetal persistent infection with ncpBVDV and development of innate (ISGs) and partial adaptive (IFN-γ) immune response in PI fetuses (Fig. 8), is different from established opinion and based on preliminary data presented herein (Smirnova et al, 2014) and previous publications from our group (Smirnova et al, 2008;Shoemaker et al, 2009;Hansen et al, 2010;Webb et al, 2012). Infection of the pregnant heifer with ncpBVDV induces rapid innate immune responses (Type I IFN and ISGs), which leads to maternal adaptive immune responses and clearance of the virus.…”

Section: Discussioncontrasting

confidence: 71%

“…A, a **P < 0.01 between groups. migration), and IFI16 (viral restriction factor) (Smirnova et al, 2014). qRTPCR confirmed upregulation of STAT1, IFI16, CXCL10, CXCL16, and chemokine (C-X-C motif) receptor 6 (CXCR6), mRNA in day 97 fetal spleen and blood.…”

Section: Fetal Spleen Transcriptomementioning

confidence: 85%

“…IRF7, but not IRF3 mRNA is upregulated in response to fetal persistent infection IRF3 and IRF7 are major transcriptional inducers of Type I IFN after RIG-I and MDA5-mediated activation through phosphorylation, heterodimerization and translocation to the nucleus to induce ISREs on Type I IFN genes. Microarray analysis comparing day 97 fetal spleen from control and PI fetuses (see Smirnova et al, 2014) revealed upregulation of IRF7, but not IRF3 mRNA in PI fetuses. IRF3 and IRF7 mRNAs were examined with qRTPCR in fetal spleen, liver and thymus to determine if downstream effectors of RIG-I and MDA5 were upregulated in fetal hematopoietic tissues in response to BVDV persistent infection (Fig.…”

Section: Upregulation Of Rna Helicases and Isgs In Response To Fetal mentioning

confidence: 99%

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Innate and adaptive immune responses toin uteroinfection with bovine viral diarrhea virus

Hansen

Смирнова

Webb

et al. 2015

Anim. Health. Res. Rev.

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Infection of pregnant cows with noncytopathic (ncp) bovine viral diarrhea virus (BVDV) induces rapid innate and adaptive immune responses, resulting in clearance of the virus in less than 3 weeks. Seven to 14 days after inoculation of the cow, ncpBVDV crosses the placenta and induces a fetal viremia. Establishment of persistent infection with ncpBVDV in the fetus has been attributed to the inability to mount an immune response before 90-150 days of gestational age. The result is 'immune tolerance', persistent viral replication and shedding of ncpBVDV. In contrast, we describe the chronic upregulation of fetal Type I interferon (IFN) pathway genes and the induction of IFN-γ pathways in fetuses of cows infected on day 75 of gestation. Persistently infected (PI) fetal IFN-γ concentrations also increased at day 97 at the peak of fetal viremia and IFN-γ mRNA was significantly elevated in fetal thymus, liver and spleen 14-22 days post maternal inoculation. PI fetuses respond to ncpBVDV infection through induction of Type I IFN and IFN-γ activated genes leading to a reduction in ncpBVDV titer. We hypothesize that fetal infection with BVDV persists because of impaired induction of IFN-γ in the face of activated Type I IFN responses. Clarification of the mechanisms involved in the IFN-associated pathways during BVDV fetal infection may lead to better detection methods, antiviral compounds and selection of genetically resistant breeding animals.

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Section: Discussioncontrasting

confidence: 71%

Section: Fetal Spleen Transcriptomementioning

confidence: 85%

Section: Upregulation Of Rna Helicases and Isgs In Response To Fetal mentioning

confidence: 99%

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Innate and adaptive immune responses toin uteroinfection with bovine viral diarrhea virus

Hansen

Смирнова

Webb

et al. 2015

Anim. Health. Res. Rev.

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“…Notably, the capacity of the PdR strain for high and prolonged IFN-α activation in piglets has been associated with an uninterrupted 36-uridine sequence found in the 3 untranslated region of the CSFV genome [23]. Activation of IFN-α response in ruminant and human foetuses, following infection with bovine viral diarrhoea and Zika virus, respectively, has been described, and it may support the results obtained in this study [37,38]. Thus, the immunotolerance mechanism that was previously associated with the development of CSF congenital persistent form [1,5] is a complex immunologic phenomenon, and further studies may explain this mechanism and its relation with the establishment of viral persistence.…”

Section: Discussionsupporting

confidence: 87%

Foetal Immune Response Activation and High Replication Rate during Generation of Classical Swine Fever Congenital Infection

Bohórquez¹,

Muñoz-González²,

Pérez‐Simó³

et al. 2020

Pathogens

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Classical swine fever virus (CSFV) induces trans-placental transmission and congenital viral persistence; however, the available information is not updated. Three groups of sows were infected at mid-gestation with either a high, moderate or low virulence CSFV strains. Foetuses from sows infected with high or low virulence strain were obtained before delivery and piglets from sows infected with the moderate virulence strain were studied for 32 days after birth. The low virulence strain generated lower CSFV RNA load and the lowest proportion of trans-placental transmission. Severe lesions and mummifications were observed in foetuses infected with the high virulence strain. Sows infected with the moderately virulence strain showed stillbirths and mummifications, one of them delivered live piglets, all CSFV persistently infected. Efficient trans-placental transmission was detected in sows infected with the high and moderate virulence strain. The trans-placental transmission occurred before the onset of antibody response, which started at 14 days after infection in these sows and was influenced by replication efficacy of the infecting strain. Fast and solid immunity after sow vaccination is required for prevention of congenital viral persistence. An increase in the CD8+ T-cell subset and IFN-alpha response was found in viremic foetuses, or in those that showed higher viral replication in tissue, showing the CSFV recognition capacity by the foetal immune system after trans-placental infection.

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“…In fact, published data indicate that low-level responses can be observed at least transiently (Hansen et al, 2010;Shoemaker et al, 2009;Smirnova et al, 2012Smirnova et al, , 2014. However, the innate immune reactions in noncp BVDVinfected fetuses are obviously reduced to a tolerable level in order to establish and maintain persistence.…”

Section: Interference With the Innate Immune Responsementioning

confidence: 99%

The Molecular Biology of Pestiviruses

Tautz

Tews

Meyers

2015

Advances in Virus Research

194

189

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Induction of interferon-gamma and downstream pathways during establishment of fetal persistent infection with bovine viral diarrhea virus

Cited by 24 publications

References 51 publications

Innate and adaptive immune responses toin uteroinfection with bovine viral diarrhea virus

Innate and adaptive immune responses toin uteroinfection with bovine viral diarrhea virus

Foetal Immune Response Activation and High Replication Rate during Generation of Classical Swine Fever Congenital Infection

The Molecular Biology of Pestiviruses

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