ABSTRACT
Infection is a well-known cause of cerebral vasculopathy and vasculitis. We report a 36-year-old woman with cerebral vasculitis and ischemic stroke secondary to herpes simplex virus (HSV). MRI studies revealed a pontine stroke with basilar artery stenosis and vessel wall gadolinium enhancement. This case demonstrates the ability of HSV to cause a focal brainstem vasculitis and the utility of enhanced MRI in the diagnosis of stroke related to HSV central nervous system vasculitis.
Subject(s)
Basilar Artery/pathology , Herpes Simplex/diagnosis , Simplexvirus/pathogenicity , Vasculitis, Central Nervous System/diagnosis , Adult , Basilar Artery/virology , Female , Herpes Simplex/complications , Humans , Vasculitis, Central Nervous System/complications , Vasculitis, Central Nervous System/virologyABSTRACT
BACKGROUND AND PURPOSE: There are major differences in susceptibility of intracranial and extracranial arteries to atherosclerosis. The goal of this study was to examine adenovirus-mediated gene transfer to basilar and carotid arteries of Watanabe heritable hyperlipidemic (WHHL) rabbits, which have spontaneous hypercholesterolemia and atherosclerosis, and normal New Zealand White (NZW) rabbits. We used 2 different adenoviral vectors, driven by either cytomegalovirus (CMV) or Rous sarcoma virus (RSV) promoters. METHODS: Basilar and carotid arteries were removed from WHHL and NZW rabbits and cut into rings. The arteries were incubated with an adenoviral vector that expresses beta-galactosidase and is driven by either a cytomegalovirus (CMV) or Rous sarcoma virus (RSV) promoter (AdCMVbetagal or AdRSVbetagal). Arteries were incubated with virus for 2 hours, and then incubated in medium for 24 hours to allow expression of transgene. Transgene expression was assessed by enzyme activity (Galacto-Light assay) and by a histochemical method after X-Gal staining. RESULTS: After gene transfer, beta-galactosidase was expressed in endothelium and adventitia but not media. There were moderately severe atherosclerotic lesions in carotid arteries and early lesions in basilar arteries. Enzyme activity after gene transfer with AdCMVbetagal (3x10(11) particles/mL) was greater in the basilar artery of WHHL than NZW (137+/-40 versus 25+/-10 mU/mg protein, P<0.05) (mean+/-SE) and in the carotid artery (133+/-27 versus 34+/-11 mU/mg protein, P<0.05). After gene transfer with AdRSVbetagal, transgene expression was similar in arteries from WHHL and normal NZW rabbits. CONCLUSIONS: This is the first study to examine gene transfer to intracranial and extracranial arteries from atherosclerotic animals. The findings suggest that an adenoviral vector with a CMV, but not RSV, promoter provides greater transgene expression in the basilar and carotid arteries from spontaneously atherosclerotic rabbits than from normal rabbits.
Subject(s)
Adenoviridae , Basilar Artery/physiology , Carotid Arteries/physiology , Gene Transfer Techniques , Hypercholesterolemia/physiopathology , Animals , Arteriosclerosis/genetics , Arteriosclerosis/physiopathology , Basilar Artery/virology , Carotid Arteries/virology , Enzyme Activation , Female , Gene Expression Regulation, Viral , Genes, Reporter , Hypercholesterolemia/genetics , Male , Promoter Regions, Genetic/physiology , Rabbits , Transgenes/physiology , beta-Galactosidase/genetics , beta-Galactosidase/metabolismABSTRACT
This article reports a man who had herpes varicella zoster cervicalis with delayed stroke in the posterior circulation. Empiric treatment was acyclovir, methylprednisolone, and aspirin. Pontine infarction involving migration of the virus via cervicovascular innervation from C2 dorsal root ganglia to the vertebrobasilar circulation with attendant angiitis/angiopathy and thrombosis is proposed.
