Publications by authors named "Igor Traktinskiy"

9 Publications

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Burning mouth syndrome due to herpes simplex virus type 1.

BMJ Case Rep 2015 Apr 1;2015. Epub 2015 Apr 1.

Department of Neurology, University of Colorado School of Medicine, Aurora, Colorado, USA Departments of Microbiology and Immunology, University of Colorado School of Medicine, Aurora, Colorado, USA.

Burning mouth syndrome is characterised by chronic orofacial burning pain. No dental or medical cause has been found. We present a case of burning mouth syndrome of 6 months duration in a healthy 65-year-old woman, which was associated with high copy numbers of herpes simplex virus type 1 (HSV-1) DNA in the saliva. Her pain resolved completely after antiviral treatment with a corresponding absence of salivary HSV-1 DNA 4 weeks and 6 months later.
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http://dx.doi.org/10.1136/bcr-2015-209488DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4401976PMC
April 2015

Inhibition of phosphorylated-STAT1 nuclear translocation and antiviral protein expression in human brain vascular adventitial fibroblasts infected with varicella-zoster virus.

J Virol 2014 Oct 23;88(19):11634-7. Epub 2014 Jul 23.

Department of Neurology, University of Colorado School of Medicine, Aurora, Colorado, USA Department of Microbiology, University of Colorado School of Medicine, Aurora, Colorado, USA.

In varicella-zoster virus (VZV)-infected primary human brain vascular adventitial fibroblasts (BRAFs), levels of beta interferon (IFN-β,) STAT1, and STAT2 transcripts as well as STAT1 and STAT2 protein were decreased. IFN-α transcript levels were increased but not secreted IFN-α protein levels. Compared to IFN-α-treated control results, in VZV-infected BRAFs, phosphorylated STAT1 did not translocate to the nucleus, resulting in impaired downstream expression of interferon-inducible antiviral Mx1. Overall, VZV interference with the type I interferon pathway may promote virus persistence in cerebral arteries.
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http://dx.doi.org/10.1128/JVI.01945-14DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4178816PMC
October 2014

Search for varicella zoster virus and herpes simplex virus-1 in normal human cerebral arteries.

J Neurovirol 2013 Apr 1;19(2):181-5. Epub 2013 Mar 1.

Department of Neurology, University of Colorado School of Medicine, 12700 E. 19th Avenue, Mail Stop B182, Aurora, CO 80045, USA.

Virological confirmation of varicella zoster virus (VZV) vasculopathy is provided by presence of virus in the cerebral arteries, frequently associated with inflammation. Yet, cerebral arteries from normal subjects have never been studied for VZV DNA or antigen. We analyzed 63 human cerebral arteries from 45 subjects for VZV DNA and antigen, control herpes simplex virus (HSV)-1 DNA and antigen, and leukocyte-specific CD45 antigen. No cerebral arteries contained VZV or HSV-1 DNA or antigen; eight arteries from seven subjects contained leukocytes expressing CD45. Thus, the presence of VZV antigen in cerebral arteries of patients with stroke is likely to be clinically significant.
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http://dx.doi.org/10.1007/s13365-013-0155-0DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3644002PMC
April 2013

Varicella-zoster virus vasculopathy: immune characteristics of virus-infected arteries.

Neurology 2013 Jan 12;80(1):62-8. Epub 2012 Dec 12.

Department of Neurology, University of Colorado School of Medicine, Aurora, CO, USA.

Objective: Pathologic changes in varicella-zoster virus (VZV)-infected arteries include inflammation, thickened intima, and paucity of smooth muscle cells. Since no criteria have been established for early vs late VZV vasculopathy, we examined inflammatory cells and their distribution in 6 normal arteries, and 2 VZV-infected arteries 3 days after onset of disease (early) and 10 months after protracted neurologic disease (late).

Methods: VZV-infected temporal artery obtained 3 days after onset of ischemic optic neuropathy from an 80-year-old man, VZV-infected middle cerebral artery (MCA) obtained 10 months after protracted disease from a 73-year-old man, and 5 MCAs and 1 temporal artery from normal subjects, age 22-60 years, were examined histologically and immunohistochemically using antibodies against VZV and inflammatory cell subsets.

Results: In both early and late VZV vasculopathy, T cells, activated macrophages, and rare B cells were found in adventitia and intima. In adventitia of early VZV vasculopathy, neutrophils and VZV antigen were abundant and a thickened intima was associated with inflammatory cells in vaso vasorum vessels. In media of late VZV vasculopathy, viral antigen, but not leukocytes, was found. VZV was not seen in inflammatory cells. Inflammatory cells were absent in control arteries.

Conclusions: Both VZV and neutrophils exclusively in adventitia in early VZV vasculopathy indicate that disease begins there. Late VZV vasculopathy is distinguished by viral antigen without inflammation in media, revealing a human virus in an immunoprivileged arterial media. Association of thickened intima and inflammation in vaso vasorum vessels in early VZV vasculopathy support the role of virus-induced inflammation in vessel wall remodeling.
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http://dx.doi.org/10.1212/WNL.0b013e31827b1ab9DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3589199PMC
January 2013

Human anti-varicella-zoster virus (VZV) recombinant monoclonal antibody produced after Zostavax immunization recognizes the gH/gL complex and neutralizes VZV infection.

J Virol 2013 Jan 17;87(1):415-21. Epub 2012 Oct 17.

Department of Neurology, University of Colorado School of Medicine, Aurora, Colorado, USA.

Varicella-zoster virus (VZV) is a ubiquitous, highly cell-associated, and exclusively human neurotropic alphaherpesvirus. VZV infection is initiated by membrane fusion, an event dependent in part on VZV glycoproteins gH and gL. Consistent with its location on the virus envelope, the gH/gL complex is a target of neutralizing antibodies produced after virus infection. One week after immunizing a 59-year-old VZV-seropositive man with Zostavax, we sorted his circulating blood plasma blasts and amplified expressed immunoglobulin variable domain sequences by single-cell PCR. Sequence analysis identified two plasma blast clones, one of which was used to construct a recombinant monoclonal antibody (rec-RC IgG). The rec-RC IgG colocalized with VZV gE on the membranes of VZV-infected cells and neutralized VZV infection in tissue culture. Mass spectrometric analysis of proteins immunoprecipitated by rec-RC IgG identified both VZV gH and gL. Transfection experiments showed that rec-RC IgG recognized a VZV gH/gL protein complex but not individual gH or gL proteins. Overall, our recombinant monoclonal anti-VZV antibody effectively neutralizes VZV and recognizes a conformational epitope within the VZV gH/L protein complex. An unlimited supply of this antibody provides the opportunity to analyze membrane fusion events that follow virus attachment and to identify multiple epitopes on VZV-specific proteins.
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http://dx.doi.org/10.1128/JVI.02561-12DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3536365PMC
January 2013

Persistence of varicella zoster virus DNA in saliva after herpes zoster.

J Infect Dis 2011 Sep;204(6):820-4

Departments of Neurology, University of Colorado School of Medicine, Aurora, CO, USA.

Analysis of saliva samples from individuals aged ≥ 60 years who had a history of zoster (group 1), zoster and postherpetic neuralgia (PHN; group 2), or no history of zoster (group 3) revealed varicella zoster virus (VZV) DNA in saliva samples from 11 of 17 individuals in group 1, 10 of 15 individuals in group 2, and 2 of 17 individuals in group 3. The frequency of VZV DNA detection was significantly higher (P = .001) in saliva of subjects with a history of zoster, with or without PHN (21 [67%] of 32 subjects in groups 1 and 2), than in saliva of age-matched subjects with no zoster history (2 [12%] of 17 subjects in group 3). Thus, persistence of VZV DNA in saliva is the outcome of zoster, independent of PHN. Because VZV infection can produce neurological and ocular disease without zoster rash, future studies are needed to establish whether VZV DNA can be detected in the saliva of such patients.
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http://dx.doi.org/10.1093/infdis/jir425DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3156921PMC
September 2011

Varicella-zoster virus transcriptome in latently infected human ganglia.

J Virol 2011 Mar 22;85(5):2276-87. Epub 2010 Dec 22.

Department of Neurology, University of Colorado School of Medicine, Aurora, CO 80045, USA.

We recently developed a novel multiplex reverse transcription (RT)-PCR assay that allows rapid and sensitive detection of transcripts corresponding to all 68 unique varicella-zoster virus (VZV) open reading frames (ORFs) in only five amplification reactions (M. A. Nagel, D. Gilden, T. Shade, B. Gao, and R. J. Cohrs, J. Virol. Methods 157:62-68, 2009). Herein, we applied multiplex RT-PCR analysis to mRNA extracted from 26 trigeminal ganglia latently infected with VZV and one control trigeminal ganglion negative for VZV DNA that were removed from 14 men and women, 16 to 84 years of age, within 24 h after death. Analysis identified VZV transcripts mapping to VZV ORFs 29, 62, and 63, previously detected and sequence verified; VZV ORFs 4 and 40, previously detected by in situ hybridization; and VZV ORFs 11, 41, 43, 57, and 68, not previously detected. VZV ORF 63 transcripts were the most prevalent. Comparison of the 10 VZV ORFs transcribed during latency to their herpes simplex virus type 1 homologues reveals that the latently transcribed VZV genes encode immediate-early, early, and late transcripts.
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http://dx.doi.org/10.1128/JVI.01862-10DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3067783PMC
March 2011