Native HSV type 2 (Strain G) Antigen

Herpes simplex virus 1 (HSV-1) hijacks ubiquitination machinery to modify the cellular proteome to create an environment permissive for virus replication. HSV-1 encodes its own RING-finger E3 ubiquitin (Ub) ligase, Infected Cell Protein 0 (ICP0), that directly interfaces with component proteins of the Ub pathway to inactivate host immune defences and cellular processes that restrict the progression of HSV-1 infection. Consequently, ICP0 plays a critical role in the infectious cycle of HSV-1 that is required to promote the efficient onset of lytic infection and productive reactivation of viral genomes from latency. This review will describe the current knowledge regarding the biochemical properties and known substrates of ICP0 during HSV-1 infection. We will highlight the gaps in the characterization of ICP0 function and propose future areas of research required to understand fully the biological properties of this important HSV-1 regulatory protein.

Aim There are many causes of facial nerve palsy. The most common causes are neuroborreliosis (NB), idiopathic paralysis or Herpes simplex virus (HSV) reactivation. The aim of this study was to characterize patients with facial palsy in the course of NB and to determine whether HSV-1 reactivation takes place during the acute phase of NB. Methods A retrospective analysis of 66 patients with facial nerve palsy was performed. In 38 patients, facial palsy was caused by Borrelia burgdorferi sl infection. Immunological tests for HSV-1, tick-borne encephalitis virus and B burgdorferi sl in serum and cerebrospinal fluid (CSF) were performed. Results In this analysis, 55.2% of NB patients had right nerve palsy and 21% bilateral palsy; 15.8% of patients had erythema migrans (EM). Lymphocytic meningitis was diagnosed in 92% of patients and Bannwarth's syndrome was diagnosed in 47% of patients. IgM anti-HSV-1 antibodies were detected in four patients with NB and two patients with facial nerve palsy of other origin. IgM anti-HSV-1 antibodies were detected in the CSF of three patients (7.9%) with NB, and one of them had bilateral VII paresis and EM simultaneously. Treatment with ceftriaxone or doxycycline led to complete recovery. Conclusions Neuroborreliosis should always be considered as a cause of peripheral facial nerve palsy. Peripheral facial nerve palsy is a significant symptom in the course of NB, especially in patients accompanied by meningitis. Pathomechanism of facial nerve paresis has not been well explained so far and may depend on two independent mechanisms in NB, including HSV-1 reactivation.