Bovine ISG15: an antiviral and inducible protein in BIV infected fetal bovine lung cells

Liu, Chang; Li, Xin; Yao, Xuemei; Kong, Xiaohong; Qiao, Wentao; Geng, Yi

doi:10.1186/1743-422x-7-134

Cited by 6 publications

(9 citation statements)

References 21 publications

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“…The human and bovine ubiquitin sequences are 100% identical 12 and are 100% and 96% identical to those of zebrafish and yeast, respectively. By contrast, the human and bovine ISG15 amino-acid sequences are only 67% identical 13 and human ISG15 sequence is only 37% identical to that of the more distantly related zebrafish 5 (Figure 1). Thus, although ISG15 is indeed a ubiquitin-like molecule, it evolved much more recently and is much less well conserved than ubiquitin.…”

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confidence: 97%

ISG15: leading a double life as a secreted molecule

2013

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ISG15 is a well-known intracellular ubiquitin-like molecule involved in ISGylation. However, a recent study has revived the notion first put forward two decades ago that ISG15 is also a secreted molecule. Human neutrophils, monocytes and lymphocytes can release ISG15, even though this protein has no detectable signal peptide sequence. ISG15 has also been found in the secretory granules of granulocytes. The mechanism underlying ISG15 secretion is unknown. Secreted ISG15 acts on at least T and natural killer (NK) lymphocytes, in which it induces interferon (IFN)-γ production. However, the mechanism by which ISG15 stimulates these cells also remains unclear. ISG15 and IFN-γ seem to define an innate circuit that operates preferentially, but not exclusively, between granulocytes and NK cells. Inherited ISG15 deficiency is associated with severe mycobacterial disease in both mice and humans. This infectious phenotype probably results from the lack of secreted ISG15, because patients and mice with other inborn errors of IFN-γ immunity also display mycobacterial diseases. In addition to raising mechanistic issues, the studies described here pave the way for clinical studies of various aspects, ranging from the use of recombinant ISG15 in patients with infectious diseases to the use of ISG15-blocking agents in patients with inflammatory diseases.

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confidence: 97%

ISG15: leading a double life as a secreted molecule

2013

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“…BIV is pathologically more related to lentiviruses associated with chronic inflammatory diseases (SRLV and EIAV) than those associated with severe immunodeficiency (HIV, FIV, and SIV) [ 50 ]. Like EIAV, transmission is probably via hematophagous arthropods, such as tabanid flies, during the acute phase of disease, with high levels of viremia, although other routes of transmission are also possible [ 45 ].…”

Section: Prevention and Controlmentioning

confidence: 99%

Prospects in Innate Immune Responses as Potential Control Strategies against Non-Primate Lentiviruses

Pablo-Maiso

Doménech

Echeverría

et al. 2018

Viruses

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Lentiviruses are infectious agents of a number of animal species, including sheep, goats, horses, monkeys, cows, and cats, in addition to humans. As in the human case, the host immune response fails to control the establishment of chronic persistent infection that finally leads to a specific disease development. Despite intensive research on the development of lentivirus vaccines, it is still not clear which immune responses can protect against infection. Viral mutations resulting in escape from T-cell or antibody-mediated responses are the basis of the immune failure to control the infection. The innate immune response provides the first line of defense against viral infections in an antigen-independent manner. Antiviral innate responses are conducted by dendritic cells, macrophages, and natural killer cells, often targeted by lentiviruses, and intrinsic antiviral mechanisms exerted by all cells. Intrinsic responses depend on the recognition of the viral pathogen-associated molecular patterns (PAMPs) by pathogen recognition receptors (PRRs), and the signaling cascades leading to an antiviral state by inducing the expression of antiviral proteins, including restriction factors. This review describes the latest advances on innate immunity related to the infection by animal lentiviruses, centered on small ruminant lentiviruses (SRLV), equine infectious anemia virus (EIAV), and feline (FIV) and bovine immunodeficiency viruses (BIV), specifically focusing on the antiviral role of the major restriction factors described thus far.

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“…FBL cells infected with BIV were taken as a positive control, as we knew that BIV infection could induce the expression of bISG15 in FBL cells [15] . Uninfected FBL cells were taken as a negative control and normalized as 1.…”

Section: Bhv-1 Infection Repressed the Basal Transcription Of Bisg15 mentioning

confidence: 99%

“…We found the expression of bISG15 in fetal bovine lung (FBL) cells could be induced after treatment with poly I : C or lipopolysaccaride (LPS) [14] . Furthermore, bISG15 expression can also be induced in bovine immunodeficiency virus (BIV) infected FBL cells, and the over-expression of bISG15 can repress the replication of BIV in FBL cells [15] . Therefore, bISG15 can be regarded as an antiviral and inducible protein in FBL cells infected with BIV.…”

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confidence: 99%

Bovine Herpesvirus 1 protein bICP0 represses the transcription of bISG15 in fetal bovine lung cells

et al. 2011

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The ubiquitin-like modifier bISG15 is an antiviral protein found in fetal bovine lung (FBL) cells. Bovine Herpesvirus 1(BHV-1), which is a viral pathogen of cattle, can infect FBL cells and induce cytopathic effects. Real-time PCR assays showed that BHV-1's infection could repress the basal or inducible transcription of bISG15 in FBL cells. It demonstrates that this repression effect depends on BHV-1 viral infection and new protein synthesis. Our previous work showed that bIRF-3 was the key factor in the stimulation of bISG15 in FBL cells, so the effect of BHV-1 viral protein on bIRF-3 activating the promoter of bISG15 was confirmed. The luciferase assay showed the BHV-1 viral protein bICP0 inhibited the activation of bISG15 promoter stimulated by bIRF-3. Taken together, our work suggested that BHV-1 had some molecular mechanism to resist the cellular bISG15's antiviral functions.

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Bovine ISG15: an antiviral and inducible protein in BIV infected fetal bovine lung cells

Cited by 6 publications

References 21 publications

ISG15: leading a double life as a secreted molecule

ISG15: leading a double life as a secreted molecule

Prospects in Innate Immune Responses as Potential Control Strategies against Non-Primate Lentiviruses

Bovine Herpesvirus 1 protein bICP0 represses the transcription of bISG15 in fetal bovine lung cells

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