Recombinant Poliovirus type 1 Core Protein 2C [His]

Purpose of review Focusing on the key developments since January 2019, this review aims to inform policymakers and clinical practitioners on the latest on evolving global polio epidemiology and scientific advancements to guide strategies for eradication. Recent findings An upsurge in wild poliovirus type 1 cases in Pakistan and Afghanistan and an expansion of type 2 circulating vaccine-derived poliovirus transmission in multiple countries threaten the remarkable progress made over past several decades by the global eradication program. These challenges have also spurred innovation on multiple fronts, including earlier detection, enhanced environmental surveillance and safer and more affordable vaccine options. A concerted effort to adapt program strategies to address context-specific challenges and continued focus on innovations to enhance detection and response capabilities will be the key to achieve and sustain eradication of all types of polioviruses.

Introduction The varicella zoster virus (VZV) infection causes chickenpox and herpes zoster. Primary infection occurs more frequently in the pediatric age as chickenpox. Virus can be latent in cranial nerve or dorsal root ganglia and reactivate several decades later as the form of herpes zoster generally in immunosuppressed patients. Varicella zoster virus is associated with severe neurological complications, including post herpetic neuralgia, aseptic meningitis, polyneuropathy, cranial nerve palsy, meningoencephalitis, vasculopathy, encephalitis, and transverse myelitis. The transverse myelitis caused by VZV is reported rarely. Case Report A 77-year-old immunocompetent patient presented with muscle weakness and sensation loss due to the demyelinating lesion caused by VZV on C5 dermatome. Proprioception and vibratory sensation loss were also marked. Cervical spinal magnetic resonance imaging showed expansive intramedullary high-signal intensity lesion on C5 with focal swelling on T2-weighted images and gadalinium enhancement on T1-weighted images. cerebrospinal fluid viral antibody test was positive for immunoglobulin G of VZV but negative for VZV DNA. The patient was treated with oral valacyclovir (1 g) 3 times daily for 7 days and with methylprednisolone (1.0 g) every day for 5 days. After treatment, his muscle strength increased but sensorial loss and neuropathic pain did not recover. Conclusions About 40% of transverse myelitis cases are caused by viral infections, some of them are herpes viruses and poliovirus. Varicella zoster infection is a common disease but not a common cause of transverse myelitis particularly in immuncompetent patients. The clinicians must be aware of this rare complication of VZV.