Review of Varicella zoster virus : from epidemiology to prevention

The Varicella zoster virus is a human pathogen which causes Varicella after primary infection and herpes zoster after secondary reactivation. Both disease manifestations can occur at any age; however, Varicella is seen more commonly in children whilst herpes zoster is mainly observed in the elderly. Although uncommon, disease complications secondary to Varicella may be severe and life-threatening especially at the extremes of age, during pregnancy and in the immunocompromised. Attenuated Varicella vaccines have been successfully formulated to prevent Varicella and its complications and are part of the routine childhood immunisation programmes in several countries including the US, Canada, Germany and Australia. This review discusses the epidemiology of Varicella, the clinical presentation and management of Varicella zoster virus infections and the potential of preventing Varicella and herpes zoster through immunisation.peer-reviewe

A 46-year-old female presenting with worsening headache, nuchal rigidity and a skin rash in varicella zoster virus meningitis: a case report

Varicella zoster virus causes two distinct clinical diseases. Varicella is the primary infection and results from exposure of a person susceptible to the virus. The virus remains latent in cranial nerve ganglia, dorsal root ganglia, and autonomic ganglia along the entire neuraxis. Years later, in association with a decline in cell-mediated immunity in the elderly and immuno-compromised, varicella zoster virus reactivates and can cause a wide range of neurologic disease, including herpes zoster (‘shingles’), postherpetic neuralgia, vasculopathy, myelopathy, retinal necrosis, cerebellitis, and zoster sine herpete. Herpes zoster is associated with numerous neurologic complications and varied presentations. Patients who have a dermatomal distribution of varicella zoster virus and who have headaches should be considered to have VZV meningitis. Virologic confirmation requires testing the cerebrospinal fluid for varicella zoster virus deoxyribonucleic acid via polymerase chain reaction. The application of polymerase chain reaction to the cerebrospinal fluid can be used to detect varicella zoster virus deoxyribonucleic acid and, therefore, infections of the central nervous system. We present a case report of a 46-year-old female who initially presented with worsening headache, nuchal rigidity, fever, and a skin rash, who was subsequently found to have varicella zoster meningitis

Clinical features of varicella-zoster virus infection

Varicella-zoster virus (VZV) is a pathogenic human herpes virus that causes varicella (chickenpox) as a primary infection, following which it becomes latent in peripheral ganglia. Decades later, the virus may reactivate either spontaneously or after a number of triggering factors to cause herpes zoster (shingles). Varicella and its complications are more severe in the immunosuppressed. The most frequent and important complication of VZV reactivation is postherpetic neuralgia, the cause of which is unknown and for which treatment is usually ineffective. Reactivation of VZV may also cause a wide variety of neurological syndromes, the most significant of which is a vasculitis, which is treated with corticosteroids and the antiviral drug acyclovir. Other VZV reactivation complications include an encephalitis, segmental motor weakness and myelopathy, cranial neuropathies, Guillain–Barré syndrome, enteric features, and zoster sine herpete, in which the viral reactivation occurs in the absence of the characteristic dermatomally distributed vesicular rash of herpes zoster. There has also been a recent association of VZV with giant cell arteritis and this interesting finding needs further corroboration. Vaccination is now available for the prevention of both varicella in children and herpes zoster in older individuals

Theories on Varicella Zoster Virus Reactivation Based on Shingles Patterns

Herpes zoster, a disease also known as shingles or as zoster, infects the sensory nerve ganglion and the peripheral nerve and its branches, resulting in pain to the affected dermatomes. Infection results from reactivation of the varicella-zoster virus, the same virus which causes varicella, or chickenpox. The varicella-zoster virus usually causes chickenpox to its host at an early age and then withdraws to the dorsal root ganglia where it enters a latency stage. The virus may reemerge at any time and infect its host with shingles. As shingles is most common in ages 50 and above, it is assumed that cell-mediated immunity plays a role in suppressing the virus, and, therefore, a decline in this immunity allows the virus to reemerge from latency. Shingles also appears to be more common in temperate regions than in tropical regions, leading to a suggestion that certain genotypes of the varicella-zoster virus are more prone to reactivation than others. Decreased herpes zoster incidence in the African American population and the detection of increased presence of the ATA and GCC haplotypes in herpes zoster patients may point to a genetic predisposition to reactivation of varicella-zoster virus. Evidence of increased female shingles incidence has lead to numerous hypotheses, some of which may shed some light on the mechanism of varicella-zoster reactivation, a phenomenon which is still poorly understood

Herpes Zoster Ophthalmicus in Healthy 13-month Infant: An Unforeseen Scenario

Herpes zoster (HZ) as well as varicella are caused by varicella-zoster virus. It is uncommon in children. Cases have been reported in literature among all ages from neonate to old age. We report this case of HZ ophthalmicus in a healthy child born to healthy mother with a history of varicella infection in the third trimester (7th month of gestation). Early diagnosis and treatment reduce complications. Preconceptional varicella-zoster vaccine is also a matter of concern

Varicella-Zoster viruses associated with post-herpetic neuralgia induce sodium current density increases in the ND7-23 Nav-1.8 neuroblastoma cell line

Post-herpetic neuralgia (PHN) is the most significant complication of herpes zoster caused by reactivation of latent Varicella-Zoster virus (VZV). We undertook a heterologous infection in vitro study to determine whether PHN-associated VZV isolates induce changes in sodium ion channel currents known to be associated with neuropathic pain. Twenty VZV isolates were studied blind from 11 PHN and 9 non-PHN subjects. Viruses were propagated in the MeWo cell line from which cell-free virus was harvested and applied to the ND7/23-Nav1.8 rat DRG x mouse neuroblastoma hybrid cell line which showed constitutive expression of the exogenous Nav 1.8, and endogenous expression of Nav 1.6 and Nav 1.7 genes all encoding sodium ion channels the dysregulation of which is associated with a range of neuropathic pain syndromes. After 72 hrs all three classes of VZV gene transcripts were detected in the absence of infectious virus. Single cell sodium ion channel recording was performed after 72 hr by voltage-clamping. PHN-associated VZV significantly increased sodium current amplitude in the cell line when compared with non-PHN VZV, wild-type (Dumas) or vaccine VZV strains ((POka, Merck and GSK). These sodium current increases were unaffected by acyclovir pre-treatment but were abolished by exposure to Tetrodotoxin (TTX) which blocks the TTX-sensitive fast Nav 1.6 and Nav 1.7 channels but not the TTX-resistant slow Nav 1.8 channel. PHN-associated VZV sodium current increases were therefore mediated in part by the Nav 1.6 and Nav 1.7 sodium ion channels. An additional observation was a modest increase in message levels of both Nav1.6 and Nav1.7 mRNA but not Nav 1.8 in PHN virally infected cells

Epidemiology and potential preventative measures for viral infections in children with malignancy and those undergoing hematopoietic cell transplantation.

In pediatric patients with malignancy and those receiving hematopoietic stem cell transplants, bacterial and fungal infections have been the focus of fever and neutropenia episodes for decades. However, improved diagnostic capabilities have revealed viral pathogens as a significant cause of morbidity and mortality. Because of limited effective antiviral therapies, prevention of viral infections is paramount. Pre-exposure and post-exposure prophylaxis and antiviral suppressive therapeutic approaches are reviewed. Additionally, infection control practices specific to this patient population are discussed. A comprehensive approach utilizing each of these can be effective at reducing the negative impact of viral infections

Herpes Zoster: Clinical Manifestation, Treatment, and Prevention

Herpes zoster (HZ, shingles, zoster) is a disease due to reactivation and multiplication of persistent varicella zoster virus (VVZ) after suffering from previous varicella with characteristics of dermatomal rashes, pain, and unilateral. Dermatoms most often involved in HZ lesions are thoracal, trigeminal, lumbal, and cervical. The first lesion is usually erythematous macule or papule, which then turns into vesicle, then to pustule and to become crust, and persists for 2-3 weeks. The main goal of antiviral therapy in HZ patients is to reduce the expansion, duration, and severity of rashes and pain in primary dermatomes; prevent the spread of HZ to other places; and prevent post-herpes neuralgia. One of the prevention strategies for HZ in the elderly and high-risk individuals is vaccination using the varicella zoster virus vaccine that is live zoster vaccine or recombinant zoster vaccine