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A database of human genes and a gene network involved in response to tick-borne encephalitis virus infection.

ABSTRACT: BACKGROUND:Tick-borne encephalitis is caused by the neurotropic, positive-sense RNA virus, tick-borne encephalitis virus (TBEV). TBEV infection can lead to a variety of clinical manifestations ranging from slight fever to severe neurological illness. Very little is known about genetic factors predisposing to severe forms of disease caused by TBEV. The aims of the study were to compile a catalog of human genes involved in response to TBEV infection and to rank genes from the catalog based on the number of neighbors in the network of pairwise interactions involving these genes and TBEV RNA or proteins. RESULTS:Based on manual review and curation of scientific publications a catalog comprising 140 human genes involved in response to TBEV infection was developed. To provide access to data on all genes, the TBEVhostDB web resource ( http://icg.nsc.ru/TBEVHostDB/ ) was created. We reconstructed a network formed by pairwise interactions between TBEV virion itself, viral RNA and viral proteins and 140 genes/proteins from TBEVHostDB. Genes were ranked according to the number of interactions in the network. Two genes/proteins (CCR5 and IFNAR1) that had maximal number of interactions were revealed. It was found that the subnetworks formed by CCR5 and IFNAR1 and their neighbors were a fragments of two key pathways functioning during the course of tick-borne encephalitis: (1) the attenuation of interferon-I signaling pathway by the TBEV NS5 protein that targeted peptidase D; (2) proinflammation and tissue damage pathway triggered by chemokine receptor CCR5 interacting with CD4, CCL3, CCL4, CCL2. Among nine genes associated with severe forms of TBEV infection, three genes/proteins (CCR5, IL10, ARID1B) were found to have protein-protein interactions within the network, and two genes/proteins (IFNL3 and the IL10, that was just mentioned) were up- or down-regulated in response to TBEV infection. Based on this finding, potential mechanisms for participation of CCR5, IL10, ARID1B, and IFNL3 in the host response to TBEV infection were suggested. CONCLUSIONS:A database comprising 140 human genes involved in response to TBEV infection was compiled and the TBEVHostDB web resource, providing access to all genes was created. This is the first effort of integrating and unifying data on genetic factors that may predispose to severe forms of diseases caused by TBEV. The TBEVHostDB could potentially be used for assessment of risk factors for severe forms of tick-borne encephalitis and for the design of personalized pharmacological strategies for the treatment of TBEV infection.

SUBMITTER: Ignatieva EV

PROVIDER: S-EPMC5751789 | biostudies-literature | 2017 Dec

REPOSITORIES: biostudies-literature

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A database of human genes and a gene network involved in response to tick-borne encephalitis virus infection.

Ignatieva Elena V EV Igoshin Alexander V AV Yudin Nikolay S NS

BMC evolutionary biology 20171228 Suppl 2

<h4>Background</h4>Tick-borne encephalitis is caused by the neurotropic, positive-sense RNA virus, tick-borne encephalitis virus (TBEV). TBEV infection can lead to a variety of clinical manifestations ranging from slight fever to severe neurological illness. Very little is known about genetic factors predisposing to severe forms of disease caused by TBEV. The aims of the study were to compile a catalog of human genes involved in response to TBEV infection and to rank genes from the catalog based ...[more]

PMID: 29297316

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Project description:PurposeTick-Borne Encephalitis (TBE), a disease caused by Tick-Borne Encephalitis Virus (TBEV), is emerging in Italy. This study aimed to characterize the epidemiological, clinical, laboratory, imaging and electroencephalogram characteristics in Belluno, North-East Italy.Results76% were males, mean age 53 years; 50% did not report tick bite. 72% had a biphasic course, 42% a monophasic one, 8 cases of abortive TBE. Mostly no specific symptoms were observed, together with neurological signs and symptoms. None died, but 35% had sequelae at the one-month follow-up. Men had a higher risk of having neurological/neurocognitive sequelae; paresthesia or tremors were associated independently with sequelae. In terms of laboratory data, thrombocytopenia, neutropenia and lymphocytosis were associated with the first phase (p < .01), while monocytosis, lymphocytopenia, high levels of ESR and CRP with the second (p < .05). Other abnormal laboratory data were observed: high levels of transaminases, bilirubin, GGT, fibrinogen, amylase, LDH, CPK and electrolyte disorders. Most of the liquor showed pleocytosis and increased protein levels. No specific findings characterized imaging; electroencephalogram mainly reported general and focal anomalies in the temporal lobe.ConclusionsAlthough patients have not reported a tick bite, TBEV infection should be considered for diagnosis. Usually no specific symptoms are reported along with neurological signs and symptoms. The biphasic course is more often described than the monophasic course; abortive TBE is sometimes present. Paresthesia and tremors are independently associated with neurological/neurocognitive sequelae; men have a higher risk of having sequelae. The first phase is probably associated with thrombocytopenia, neutropenia and lymphocytosis; the second with monocytosis, lymphocytopenia, high levels of CRP and ESR. Electrolyte disorders, high levels of transaminases, GGT, bilirubin, CPK, LDH, fibrinogen and amylase may characterize TBEV infection.

Dataset Information

A database of human genes and a gene network involved in response to tick-borne encephalitis virus infection.

Publications

A database of human genes and a gene network involved in response to tick-borne encephalitis virus infection.

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