Electron micrograph of Varicella zoster virus. Approximately 150,000× magnification. The virus diameter is 150-200nm. Progression of<unk> . A cluster of small bumps (1) turns into blisters (2). The blisters fill with lymph, break open (3), crust over (4), and finally disappear. Postherpetic neuralgia can sometimes occur due to nerve damage (5).|thumb The causative agent for<unk>  is the varicella zoster virus (VZV) – a double-stranded DNA virus related to the herpes simplex virus. Most individuals are infected with this virus as children which causes an episode of chickenpox. The immune system eventually eliminates the virus from most locations, but it remains dormant (or latent) in the ganglia adjacent to the spinal cord (called the dorsal root ganglion) or the trigeminal ganglion in the base of the skull.<unk>  occurs only in people who have been previously infected with VZV; although it can occur at any age, approximately half of the cases in the United States occur in those aged 50 years or older. Repeated attacks of<unk>  are rare, and it is extremely rare for a person to have more than three recurrences. The disease results from virus particles in a single sensory ganglion switching from their latent lysogenic cycles to their active lytic cycles. In contrast to the herpes simplex virus, the latency of VZV is poorly understood. The virus has never been successfully recovered from human nerve cells by cell culture. Virus-specific proteins continue to be made by the infected cells during the latent period, so true latency, as opposed to chronic, low-level, active infection, has not been proven to occur in VZV infections. Although VZV has been detected in autopsies of nervous tissue, there are no methods to find dormant virus in the ganglia of living people. Unless the immune system is compromised, it suppresses reactivation of the virus and prevents<unk>  outbreaks. Why this suppression sometimes fails is poorly understood, but<unk>  is more likely to occur in people whose immune systems are impaired due to aging, immunosuppressive therapy, psychological stress, or other factors. Upon reactivation, the virus replicates in neuronal cell bodies, and virions are shed from the cells and carried down the axons to the area of skin innervated by that ganglion. In the skin, the virus causes local inflammation and blistering. The short- and long-term pain caused by<unk>  outbreaks originates from inflammation of affected nerves due to the widespread growth of the virus in those areas. As with chickenpox and other forms of alpha-herpesvirus infection, direct contact with an active rash can spread the virus to a person who lacks immunity to it. This newly infected individual may then develop chickenpox, but will not immediately develop<unk> . The complete sequence of the viral genome was published in 1986.
Shingles
Insect bites and stings
Sealpox
Angina
Farmyard pox
Herpes simplex
Streptococcal intertrigo
Sciatica