antviral/stroke

A sixty-nine year old man suffered a stroke fourteen weeks after the onset of right herpes zoster ophthalmicus (HZO). Hemispheric infarction was documented by a computed tomography which showed a small hypodense zone in the right internal capsula; after contrast there was enhancement of this

OBJECTIVE Inrtoduction: Post-stroke complications are one of the urgent and insufficiently resolved problems. According to different literature data 23% to 65% of patients suffer from the post-stroke development of an infectious process. Herpes simplex virus type 1 and 2 can also be etiological

Among infectious factors, varicella-zoster virus (VZV) is a leading cause of central nervous system vasculopathy and stroke in childhood. Not only have viral markers been detected in the cerebrospinal fluid of affected patients, but also direct evidence of viral particles in the wall of cerebral

A 37-year-old man with a known history of neurofibromatosis 1 (NF1) presented within 2 days of diarrhoeal illness followed by encephalopathy, facial twitching, hypoglycaemia, hypotension, tachycardia and low-grade fever. Examination showed multiple café-au-lait spots and neurofibromas over the

Varicella zoster virus (VZV) primary infection usually causes varicella and its reactivation may lead to different clinical manifestations depending on the site of viral reactivation and its subsequent tissue spread. There is a growing recognition of the association between VZV reactivation and

We report on a case of a 80-year-old man who developed progressive drowsiness with headache, fever and signs of meningeal irritation 2 days after a head trauma. Suspecting an infective meningoencephalitis, the patient was treated with wide spectrum antibiotic and antiviral therapy. Brain CT scan

BACKGROUND Herpes zoster (HZ) is caused by reactivation of the latent varicella-zoster virus (VZV). A severe complication of HZ is VZV vasculopathy which can result in ischemic or hemorrhagic stroke. The aims of our study were to assess the risk of stroke after the onset of HZ and to investigate the

Varicella zoster virus (VZV) is the only human virus known to replicate in arteries. After the acute infection, the virus persists in a noninfectious latent form in ganglia along the neuraxis, with intermittent periods of reactivation. Both primary and secondary reactivation are associated with

Routine data from electronic health records (EHRs) provide insights into links between herpes zoster (HZ) and cardiovascular complications such as stroke or myocardial infarction (MI) in different populations worldwide. Evidence from large EHR studies using both self-controlled case series and

Varicella zoster virus (VZV) infects >95 % of the world population. Typically, varicella (chickenpox) results from primary infection. The virus then becomes latent in ganglionic neurons along the entire neuraxis. In immunocompromised individuals, VZV reactivates and causes herpes zoster (shingles),

OBJECTIVE Herpes zoster (HZ) is an opportunistic infection caused by varicella-zoster virus and observed with increasing frequency in patients receiving immunosuppressive therapies. The literature has suggested that the risk of stroke may increase shortly after HZ, but little is known about this

BACKGROUND Although hepatitis C virus (HCV) is a known risk factor for cardiovascular disease, whether antiviral therapy (AVT) can reduce heart failure (HF) hospitalizations is unknown.Methods and Results:In this population-based cohort study, we used data from the Taiwan National Health Insurance