Neurologic complications of the reactivation of varicella-zoster virus.
- D. Gilden, B. Kleinschmidt-DeMasters, J. Laguardia, R. Mahalingam, R. Cohrs
- Medicine, BiologyNew England Journal of Medicine
- 2 March 2000
The detection of varicella–zoster virus in blood vessels and other tissues by methods based on the polymerase chain reaction (PCR) has widened the recognized patterns of infection.
Varicella zoster virus vasculopathies: diverse clinical manifestations, laboratory features, pathogenesis, and treatment
- D. Gilden, R. Cohrs, R. Mahalingam, M. Nagel
- Medicine, BiologyLancet Neurology
- 1 August 2009
The varicella zoster virus vasculopathies
Rash or CSF pleocytosis is not required to diagnose varicella zoster virus (VZV) vasculopathy, whereas MRI/CT abnormalities are seen in almost all patients, and determination of optimal antiviral treatment and benefit of concurrent steroid therapy awaits studies with larger case numbers.
Herpesvirus infections of the nervous system
- D. Gilden, R. Mahalingam, R. Cohrs, K. Tyler
- MedicineNature Clinical Practice Neurology
- 1 February 2007
Optimal virological studies of blood, cerebrospinal fluid and affected tissue for confirmation of diagnosis are discussed; this is particularly important because some HHV infections of the nervous system can be treated successfully with antiviral agents.
The value of detecting anti-VZV IgG antibody in CSF to diagnose VZV vasculopathy
- M. Nagel, B. Forghani, D. Gilden
- Medicine, BiologyNeurology
- 27 March 2007
In varicella zoster virus (VzV) vasculopathy, the diagnostic value of detecting anti-VZV IgG antibody in CSF is greater than that of detecting VZV DNA.
Nucleotide sequence of the mitochondrial genome of Paramecium
- A. Pritchard, J. Seilhamer, R. Mahalingam, C. Sable, S. Venuti, D. Cummings
- BiologyNucleic Acids Res.
- 11 January 1990
Based on sequence comparisons with known tRNAs, only those for phe, trp, and tyr are encoded in Paramecium mt DNA, and all of the identified genes are transcribed.
Varicella zoster virus infection: clinical features, molecular pathogenesis of disease, and latency.
- N. Mueller, D. Gilden, R. Cohrs, R. Mahalingam, M. Nagel
- Biology, MedicineNeurologic clinics
- 1 August 2008
Neurological disease produced by varicella zoster virus reactivation without rash.
- D. Gilden, R. Cohrs, R. Mahalingam, M. Nagel
- Medicine, BiologyCurrent Topics in Microbiology and Immunology
- 2010
VZV reactivation can produce chronic radicular pain without rash (zoster sine herpete), as well as all the neurological disorders listed above without rash, which are a challenge to the practicing clinician.
Prevalence and distribution of VZV in temporal arteries of patients with giant cell arteritis
Most GCA-positive TAs contained VZV in skip areas that correlated with adjacent GCA pathology, supporting the hypothesis that VZv triggers GCA immunopathology.
Simian Varicella Virus Infection of Rhesus Macaques Recapitulates Essential Features of Varicella Zoster Virus Infection in Humans
- I. Messaoudi, A. Barron, R. Mahalingam
- BiologyPLoS Pathogens
- 1 November 2009
Intrabronchial inoculation of rhesus macaques with SVV provides a novel model to analyze viral and immunological mechanisms of VZV latency and reactivation and presents the first in depth analysis of the immune response to SVV.
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