Abstract

Animal coronaviruses, such as infectious bronchitis virus (IBV), and arteriviruses, such as porcine reproductive and respiratory syndrome virus (PRRSV), are able to manifest highly contagious infections in their specific native hosts, thereby arising in critical economic damage to animal industries. This review discusses recent progress in studies of virus-host interactions during animal and human coronavirus and arterivirus infections, with emphasis on IBV-host cell interactions. These interactions may be directly involved in viral replication or lead to the alteration of certain signaling pathways, such as cell stress response and innate immunity, to facilitate viral replication and pathogenesis.

Highlights

  • IntroductionCoronaviruses, together with arteriviruses and toroviruses, belong in the order Nidovirales, a group of large, non-segmented, positive sense and single stranded RNA animal viruses that produce an extensive 3'-nested set of subgenomic mRNAs for transcription during infection [1] (Table 1)

  • Major receptor systems that conduct immune surveillance and trigger the production and subsequent release of type I IFNs are known as pattern recognition receptors (PPRs), which detect viral infection through the identification of various pathogen-associated molecular patterns (PAMPs); PPR families include the toll-like receptor (TLR), RIG-like helicase (RLH) and Nucleotide-binding oligomerization domain (NOD)-like receptor (NLRs)

  • While the elicitation of TLRs and RLRs by PAMPs trigger their distinct signaling cascades through divergent downstream effectors at varying efficacies, they cross paths at the juncture of transcriptional activation of interferon regulatory factor 3 (IRF3) [81], IRF7 [82] and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) [83,84,85,86], all of which translocate to the nucleus and activate the transcription of both type I interferons (IFNα and IFNβ) and inflammatory cytokines that eventually culminates in the concerted induction and development of adaptive antiviral immune response

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Summary

Introduction

Coronaviruses, together with arteriviruses and toroviruses, belong in the order Nidovirales, a group of large, non-segmented, positive sense and single stranded RNA animal viruses that produce an extensive 3'-nested set of subgenomic mRNAs for transcription during infection [1] (Table 1) Nidoviruses such as avian infectious bronchitis coronavirus (IBV), human coronavirus 229E (HCoV-229E), equine arteritis virus (EAV) and the porcine reproductive and respiratory syndrome arterivirus (PRRSV) are important pathogens of both human and animals [2,3,4], and are commonly associated with mild respiratory and enteric diseases, they are known to cause more. Coronavirus (TGEV), for example, affects mainly the gastrointestinal tract [17] that may lead to the onset of fatal watery diarrhoea and severe dehydration in pigs [18], while human coronaviruses mostly cause respiratory infections [4] With respect to their significance to the economy, vaccines have been developed for many of these viruses in a bid to prevent localized infections from progressing into serious outbreaks.

Virus Infection and Host Responses
The Effect of Virus Infection on Apoptosis
Extrinsic and Intrinsic Apoptotic Pathways
Other Apoptotic Pathways
Viruses and Apoptosis
IBV-Induced Apoptosis and Its Regulation
Viral Genes Implicated in Apoptosis
The Effect of Virus Infection on Host Innate Immunity
Pathogen Detection and Host Antiviral Defense
Interferons and the Antiviral Response
Pattern Recognition Receptor Families
Type I Interferon Response
The Effect of Coronaviruses and Arteriviruses on Host Innate Immune Responses
Animal Coronavirus Infection and Unfolded Protein Response
Virus Infection and the MAPK Signaling Pathway
Induction of Other Pro-Inflammatory Cytokines
Coronaviruses and Autophagy
The Effect of Virus Infection on Cell Cycle Regulation
The Effect of Virus Infection on the Host Translation Machinery
Cellular Factors Involved in the Virus Life Cycle
Conclusions
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