A qualitative description of the peptide sharing between poliovirus and<i>Homo sapiens</i>

Capone, Giovanni; Novello, Giuseppe; Bavaro, Simona L.; Fasano, Candida; Delfino, Antonella Pesce; Polito, Anna Nunzia; Kanduc, Darja

doi:10.3109/08923973.2012.654610

Cited by 6 publications

(8 citation statements)

References 74 publications

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“…In conclusion, the present study confirmed and extended previous reports from this laboratory and others presenting evidence for a massive peptide overlap between viral and human proteomes. Having as a reference frame such a corpus of data, here we detailed the peptide commonality between WNV and the human proteome.…”

Section: Discussionsupporting

confidence: 92%

Evidence for a vast peptide overlap between West Nile virus and human proteomes

Capone

Pagoni

Delfino

et al. 2012

J. Basic Microbiol.

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The primary amino acid sequence of West Nile virus (WNV) polyprotein, GenBank accession number M12294, was analyzed by computional biology. WNV is a mosquito-borne neurotropic flavivirus that has emerged globally as a significant cause of viral encephalitis in humans. Using pentapeptides as scanning units and the perfect peptide match program from PIR International Protein Sequence Database, we compared the WNV polyprotein and the human proteome. WNV polyprotein showed significant sequence similarities to a number of human proteins. Several of these proteins are involved in embryogenesis, neurite outgrowth, cortical neuron branching, formation of mature synapses, semaphorin interactions, and voltage dependent L-type calcium channel subunits. The biocomputional study suggest that common amino acid segments might represent a potential platform for further studies on the neurological pathophysiology of WNV infections.

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Section: Discussionsupporting

confidence: 92%

Evidence for a vast peptide overlap between West Nile virus and human proteomes

Capone

Pagoni

Delfino

et al. 2012

J. Basic Microbiol.

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“…This phenomenon concerns all human proteins. For example, there are 18 000 pentapeptide overlaps between the poliovirus and the human proteome (Capone et al ., ), while a single immunogenic pentapeptide (VGGVV) within beta‐amyloid is shared by HSV‐1 and 68 other viruses (Carter, ). Host/pathogen interactomes likely result from this homology, which enables pathogen proteins to mimic their human counterparts and compete with their usual binding partners.…”

Section: Resultsmentioning

confidence: 99%

“…This phenomenon concerns all human proteins. For example, there are 18 000 pentapeptide overlaps between the poliovirus and the human proteome (Capone et al, 2012), while a single immunogenic pentapeptide (VGGVV) within beta-amyloid is shared by HSV-1 and 68 other viruses (Carter, 2010b).…”

Section: Pathogen-derived Autoimmunitymentioning

confidence: 99%

Susceptibility genes are enriched in those of the herpes simplex virus 1/host interactome in psychiatric and neurological disorders

Carter

2013

Pathogens Disease

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Herpes simplex virus 1 (HSV-1) can promote beta-amyloid deposition and tau phosphorylation, demyelination or cognitive deficits relevant to Alzheimer's disease or multiple sclerosis and to many neuropsychiatric disorders with which it has been implicated. A seroprevalence much higher than disease incidence has called into question any primary causal role. However, as also the case with risk-promoting polymorphisms (also present in control populations), any causal effects are likely to be conditional. During its life cycle, the virus binds to many proteins and modifies the expression of multiple genes creating a host/pathogen interactome involving 1347 host genes. This data set is heavily enriched in the susceptibility genes for multiple sclerosis (P = 1.3E-99) > Alzheimer's disease > schizophrenia > Parkinsonism > depression > bipolar disorder > childhood obesity > chronic fatigue > autism > and anorexia (P = 0.047) but not attention deficit hyperactivity disorder, a relationship maintained for genome-wide association study data sets in multiple sclerosis and Alzheimer's disease. Overlapping susceptibility gene/interactome data sets disrupt signalling networks relevant to each disease, suggesting that disease susceptibility genes may filter the attentions of the pathogen towards particular pathways and pathologies. In this way, the same pathogen could contribute to multiple diseases in a gene-dependent manner and condition the risk-promoting effects of the genes whose function it disrupts.

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“…This problem is extensive and concerns all human proteins, along their entire length. For example, there are 18,000 pentapeptide overlaps between the poliovirus and the human proteome [181] while a single immunogenic pentapeptide (VGGVV) within the beta-amyloid peptide is identical to that within proteins from the herpes simplex virus and from 68 other viral species [19]. The extensive host/pathogen interactomes of numerous viruses, bacteria, and parasites no doubt result from this homology which enables pathogen proteins to mimic particular motifs within their human counterparts and to compete for their usual binding partners.…”

Section: Discussionmentioning

confidence: 99%

Toxoplasmosis and Polygenic Disease Susceptibility Genes: ExtensiveToxoplasma gondiiHost/Pathogen Interactome Enrichment in Nine Psychiatric or Neurological Disorders

Carter

2013

Journal of Pathogens

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Toxoplasma gondii is not only implicated in schizophrenia and related disorders, but also in Alzheimer's or Parkinson's disease, cancer, cardiac myopathies, and autoimmune disorders. During its life cycle, the pathogen interacts with ~3000 host genes or proteins. Susceptibility genes for multiple sclerosis, Alzheimer's disease, schizophrenia, bipolar disorder, depression, childhood obesity, Parkinson's disease, attention deficit hyperactivity disorder (P from 8.01E − 05 (ADHD) to 1.22E − 71) (multiple sclerosis), and autism (P = 0.013), but not anorexia or chronic fatigue are highly enriched in the human arm of this interactome and 18 (ADHD) to 33% (MS) of the susceptibility genes relate to it. The signalling pathways involved in the susceptibility gene/interactome overlaps are relatively specific and relevant to each disease suggesting a means whereby susceptibility genes could orient the attentions of a single pathogen towards disruption of the specific pathways that together contribute (positively or negatively) to the endophenotypes of different diseases. Conditional protein knockdown, orchestrated by T. gondii proteins or antibodies binding to those of the host (pathogen derived autoimmunity) and metabolite exchange, may contribute to this disruption. Susceptibility genes may thus be related to the causes and influencers of disease, rather than (and as well as) to the disease itself.

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A qualitative description of the peptide sharing between poliovirus andHomo sapiens

Cited by 6 publications

References 74 publications

Evidence for a vast peptide overlap between West Nile virus and human proteomes

Evidence for a vast peptide overlap between West Nile virus and human proteomes

Susceptibility genes are enriched in those of the herpes simplex virus 1/host interactome in psychiatric and neurological disorders

Toxoplasmosis and Polygenic Disease Susceptibility Genes: ExtensiveToxoplasma gondiiHost/Pathogen Interactome Enrichment in Nine Psychiatric or Neurological Disorders

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