An Evolutionary View of the Arms Race between Protein Kinase R and Large DNA Viruses

Carpentier, Kathryn S.; Geballe, Adam P.

doi:10.1128/jvi.01996-15

Cited by 6 publications

(3 citation statements)

References 34 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In contrast, CMVs derived from rhesus macaques (Rh), African green monkeys (AGM), and squirrel monkeys (Sm) can productively infect human cells [29][30][31]. Surprisingly, in infection-based assays, only SmTRS1 inhibited human PKR, whereas all other primate CMV TRS1 orthologs derived from these viruses did not inhibit human PKR [28,32]. The differential inhibition of human PKR by these various TRS1 orthologs is mediated by a single aa residue in the PKR αG helix at position 489.…”

Section: Species-specific Pkr Inhibition In Poxviruses and Herpesvirusesmentioning

confidence: 99%

“…Interestingly, residue 489 is also a determinant of PKR susceptibility to VACV K3 [18,33]. Despite identification of this key residue, it remains an open question how non-human primate CMVs are able to replicate in human cells, because human PKR is remarkably non-polymorphic and PKR inhibition is thought to be essential for CMV replication [32,34].…”

Section: Species-specific Pkr Inhibition In Poxviruses and Herpesvirusesmentioning

confidence: 99%

See 1 more Smart Citation

Species-Specific Host–Virus Interactions: Implications for Viral Host Range and Virulence

Rothenburg

Brennan

2020

Trends in Microbiology

View full text Add to dashboard Cite

A growing number of studies indicate that host-species-specific and virus-strain-specific interactions of viral molecules with the host innate immune system play a pivotal role in determining virus host range and virulence. Because interacting proteins are likely constrained in their evolution, mutations that are selected for to improve virus replication in one species, may stochastically alter the ability of a viral antagonist to inhibit immune responses in hosts the virus has not yet encountered. Based on recent findings of host-species interactions of poxvirus, herpesvirus and influenza virus proteins, we propose a model for viral fitness and host range, which considers the full interactome between a specific host-species and a virus, resulting from the combination of all interactions, positive and negative, that influence whether a virus can productively infect a cell and cause disease in different hosts.

show abstract

Section: Species-specific Pkr Inhibition In Poxviruses and Herpesvirusesmentioning

confidence: 99%

Section: Species-specific Pkr Inhibition In Poxviruses and Herpesvirusesmentioning

confidence: 99%

Species-Specific Host–Virus Interactions: Implications for Viral Host Range and Virulence

Rothenburg

Brennan

2020

Trends in Microbiology

View full text Add to dashboard Cite

show abstract

“…To achieve this, herpesviruses express multiple accessory proteins, many of which are dedicated to the evasion of host restriction factors [ 6 ]. These viral evasion genes display the characteristic evolutionary signatures of ongoing conflict with host defence [ 7 , 8 ].…”

Section: Introductionmentioning

confidence: 99%

Does the Zinc Finger Antiviral Protein (ZAP) Shape the Evolution of Herpesvirus Genomes?

Lin

Chau

Coutts

et al. 2021

Viruses

View full text Add to dashboard Cite

An evolutionary arms race occurs between viruses and hosts. Hosts have developed an array of antiviral mechanisms aimed at inhibiting replication and spread of viruses, reducing their fitness, and ultimately minimising pathogenic effects. In turn, viruses have evolved sophisticated counter-measures that mediate evasion of host defence mechanisms. A key aspect of host defences is the ability to differentiate between self and non-self. Previous studies have demonstrated significant suppression of CpG and UpA dinucleotide frequencies in the coding regions of RNA and small DNA viruses. Artificially increasing these dinucleotide frequencies results in a substantial attenuation of virus replication, suggesting dinucleotide bias could facilitate recognition of non-self RNA. The interferon-inducible gene, zinc finger antiviral protein (ZAP) is the host factor responsible for sensing CpG dinucleotides in viral RNA and restricting RNA viruses through direct binding and degradation of the target RNA. Herpesviruses are large DNA viruses that comprise three subfamilies, alpha, beta and gamma, which display divergent CpG dinucleotide patterns within their genomes. ZAP has recently been shown to act as a host restriction factor against human cytomegalovirus (HCMV), a beta-herpesvirus, which in turn evades ZAP detection by suppressing CpG levels in the major immediate-early transcript IE1, one of the first genes expressed by the virus. While suppression of CpG dinucleotides allows evasion of ZAP targeting, synonymous changes in nucleotide composition that cause genome biases, such as low GC content, can cause inefficient gene expression, especially in unspliced transcripts. To maintain compact genomes, the majority of herpesvirus transcripts are unspliced. Here we discuss how the conflicting pressures of ZAP evasion, the need to maintain compact genomes through the use of unspliced transcripts and maintaining efficient gene expression may have shaped the evolution of herpesvirus genomes, leading to characteristic CpG dinucleotide patterns.

show abstract

Virome: The Prodigious Little Cousin of the Family

Manoussopoulos¹,

Anastassopoulou

2020

Microbiomics

View full text Add to dashboard Cite

An Evolutionary View of the Arms Race between Protein Kinase R and Large DNA Viruses

Cited by 6 publications

References 34 publications

Species-Specific Host–Virus Interactions: Implications for Viral Host Range and Virulence

Species-Specific Host–Virus Interactions: Implications for Viral Host Range and Virulence

Does the Zinc Finger Antiviral Protein (ZAP) Shape the Evolution of Herpesvirus Genomes?

Virome: The Prodigious Little Cousin of the Family

Contact Info

Product

Resources

About