PubMed · 10879302
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A J Papadopoulos, R A Schwartz, C K Janniger. 2000. Chickenpox.. https://pubmed.ncbi.nlm.nih.gov/10879302/
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A 32 bp deletion in the chemokine receptor CCR5 gene modulates HIV-1 infection. However, whether this CCR5 gene variation modifies immunity to common herpesvirus infections is unknown. We investigated whole blood IgG concentrations of 157 normal adult blood donors. Also we assessed whether the 32 bp deletion of CCR5 (delta32CCR5) was associated with circulating IgG to four herpesviruses: varicella zoster virus, Epstein-Barr virus, cytomegalovirus, and herpes simplex virus type 1 and type 2. Individuals who carried delta32CCR5 were 9.2 times more likely to be seronegative for varicella zoster virus than non-carriers (95% CI 2.9-29.1), but no differences were seen for the other herpesviruses studied. Variation in CCR5 may modulate humoral immunity to varicella zoster virus.
A patient with acute necrotizing encephalophathy (ANE) following varicella infection with a good prognosis is reported. A somatosensory evoked magnetic field (SEF) study using a 37-channel-magnetoencephalography system demonstrated normal latency and strength of the first component (N20m) elicited by median nerve stimulation, despite bilateral symmetrical thalamic lesions on MRI. The normal SEF findings and the good prognosis suggested a reversible breakdown of the blood-brain barrier, and an edematous process as the brain pathology. Furthermore, our results support the idea of distinct generators for the three earliest cortical SEF components (N20m, P30m, N45m).