Varicella zoster virus

The varicella zoster virus, or VZV, is a human-specific pathogen. It belongs to the herpesvirus family. Specifically, it is known as human herpesvirus 3 (HHV-3). This virus is unique because it causes two distinct clinical diseases. It causes chickenpox, or varicella, in children and young adults. Later in life, the same virus can reactivate to cause shingles, or herpes zoster. Understanding VZV is vital for public health. It helps scientists develop vaccines to prevent these two different stages of illness.

The infection process begins when the virus enters the respiratory system. After entry, there is an incubation period. This is the time before symptoms appear. The average incubation period is 14 days, but it can range from 10 to 21 days. The virus then multiplies in the tonsils. It eventually targets the skin and peripheral nerves. During the primary infection, the illness typically lasts about 3 to 4 days. Infected people are most contagious 1 to 2 days before their skin lesions appear.

VZV has a complex way of staying in the body. This is called virus latency. After a person recovers from chickenpox, the virus does not leave. Instead, it lies dormant in neurons. It hides in the cranial nerve ganglia, the dorsal root ganglia, and the autonomic ganglia. These are clusters of nerve cells. Many years later, the virus can reactivate. When it wakes up, it travels along the nerves to cause shingles. Shingles lesions often cause neuropathic pain. This pain is frequently described as a burning sensation. It usually occurs on only one side of the body.

Scientists have studied the structure of VZV for decades. The virus is a spherical particle. It is between 180 and 200 nm in diameter. It has a lipid envelope that covers a 100 nm nucleocapsid. This nucleocapsid is made of 162 capsomeres in an icosahedral form. The genome is a single, linear, double-stranded DNA molecule. It is 125,000 nucleotides long. The genome has at least 70 open reading frames. VZV is closely related to herpes simplex viruses (HSV). However, it lacks the HSV gD protein. It also does not produce latency-associated transcripts (LAT) like HSV does.

History shows how our understanding of VZV has grown. Ancient civilizations recognized chickenpox-like rashes. However, the link between shingles and chickenpox was not discovered until 1888. In 1943, researchers noted that the virus particles looked similar in both diseases. Later, Evelyn Nicol and Thomas Huckle Weller isolated the virus. This allowed for better medical responses. In the 1970s, Michiaki Takahashi and colleagues developed an attenuated Oka strain. This led to the development of the Varivax vaccine in the 1980s. The vaccine was approved by the FDA in 1995.

Epidemiological data show the significant impact of VZV. In a 2015 Swedish study, the annual incidence of shingles was 315 cases per 100,000 inhabitants. For people aged 50 or older, this rose to 577 cases per 100,000. The lifetime risk of developing shingles is between 20% and 30%. For people aged 85 and older, the risk increases to 1 in 2. Shingles can lead to serious complications. These include postherpetic neuralgia, which is chronic pain lasting over three months. It can also cause encephalitis or pneumonia. In rare cases, Ramsay Hunt syndrome type 2 can occur.

VZV also shows significant genetic diversity through various clades and genotypes. Clade 1 and 3 include strains from Europe and North America. Clade 2 consists of Asian strains, especially from Japan. Clade 5 is based in India. Clade 4 includes some European strains. Scientists use phylogenetic analysis to sort these into genotypes. There are nine known genotypes, such as E1 and E2. In a study of 342 specimens from 18 European countries, the E1 genotype was the most common at 65%. This diversity helps researchers track how the virus moves across the globe.