Varicella-zoster virus (VZV) refers to the virus that causes chickenpox in children when they are first infected. The main source of infection is the patient. The virus is contained in the contents of the acute chickenpox and respiratory secretions of the patient. The virus can become active again and lead to herpes zoster when individuals get older or experience weakened immune system function. Children primarily transmit VZV through direct contact and droplet transmission methods. People can prevent chickenpox and herpes zoster effectively with a VZV vaccination.
VZV is an enveloped virus measuring approximately 180-200 nm in diameter which features a triple lipid host-derived envelope. All VZV genes are positioned across two DNA strands but some genes overlap between these strands. The genome structure of VZV shows such close resemblance to that of herpes simplex virus type 1 (HSV-1) that it indicates a shared common ancestor.
1. Herpes zoster
The reactivation of VZV leads to herpes zoster and this process commonly takes place in later life under conditions of stress or immunosuppression. Herpes zoster presents as a neuralgic rash on one side of the body which spreads only over skin supplied by a single sensory ganglion. The rash appears as distinct segments and most often develops on the chest area. Herpes zoster neuralgia persists as chronic burning pain or itching which doctors term postherpetic neuralgia. Herpes zoster can develop into severe complications like encephalitis and meningitis in people with weakened immune systems. In addition to the above-mentioned atypical herpes zoster, some special parts or special types of herpes zoster can be seen clinically, as follows:
Herpes zoster ophthalmicus: Herpes zoster ophthalmicus is mostly sporadic, and the disease is more common in September-November. Clinically, herpes zoster oculi is accompanied by involvement of the first branch of the ipsilateral trigeminal nerve, with red and swollen pupils, conjunctival congestion, blisters and crusts. The cornea may be affected to form ulcerative keratitis, and then blindness may occur due to scarring. In severe cases, panophthalmitis, encephalitis, and even death may occur.
H erpes zoster meningitis: It is caused by the virus directly invading the central nervous system from the front and back of the spinal nerves. It is mostly seen in patients with invasion of cranial nerves, cervical or upper thoracic spinal nerve segments. Manifestations include headache, vomiting, convulsions or other progressive sensory disorders, and there may also be ataxia and other cerebellar symptoms.
Visceral herpes zoster: The virus invades the visceral nerve fibers of the sympathetic and parasympathetic nerves from the back of the spinal cord, causing gastrointestinal or urinary tract symptoms. When it invades the pleura and peritoneum, irritation symptoms or even effusion occur. When the virus invades the visceral nerve fibers of the sympathetic and parasympathetic nerves from the dorsal root of the spinal cord
2. Varicella
Varicella represents a highly contagious childhood illness which presents as a systemic diffuse bilateral vesicular rash. The varicella disease commonly affects young children between the ages of 2 and 6. Varicella develops after an incubation time of 10-21 days during which the rash spreads centripetally and presents the highest density of lesions on the trunk while the distal limbs show the fewest lesions. The rash develops in successive stages where multiple lesion types including maculopapular rash, vesicles and crusts appear together in one location. Fever occurs alongside every new outbreak of rash.
VZV is morphologically identical to HSV. There is only one serotype. The genome has 71 genes, encoding 67 different proteins, including 6 glycoproteins (gpⅠ～gpⅥ), which are now uniformly named gE, gB, gH, gI, gC and gL. In infected cells, glycoproteins gE, gB and gH are extremely abundant, and these glycoproteins are also present in the cell membrane of the virus body. Human fibroblasts and various monkey cells are commonly used to culture VZV. Typical cytopathic changes occur in about 3 days to 2 weeks, such as nuclear inclusions and the formation of multinucleated giant cells. The virus spreads between cells and then infects neighboring cells.
VZV spreads through droplet transmission and direct contact transmission as its primary transmission modes. Patients infected with varicella transmit the virus through their respiratory secretions and remain contagious from 1-2 days before the rash develops until the rash forms scabs. . Patients with varicella transmit VZV through skin lesion contact as well as through exposure to respiratory secretions. Herpes zoster spreads mainly through ganglia which leads to a unilateral neuralgic rash. The transmission efficiency of VZV exhibits higher rates in temperate regions compared to tropical regions.
The antibodies induced by the three main glycoproteins of VZV can neutralize the virus. Among them, the glycoprotein gB has 49% of the same amino acids as HSV gB, but the immune relationship is unclear. Specific humoral immunity and cellular immunity as well as cytokines such as interferon play a major role in limiting the spread of VZV and the recovery of varicella and herpes zoster. Among them, specific cellular immunity is more important, but it cannot prevent the occurrence of herpes zoster. Lifelong immunity can be obtained after varicella disease.
Laboratory testing of either vesicular rash samples or blood tests allows for the confirmation of VZV diagnosis. Commonly used diagnostic methods include:
| Diagnostic Methods | Details |
| Viral culture | Collect the virus present in the vesicular rash and then perform tests with cell culture technology. |
| Cytopathology | Apply Giemsa staining to the ulcer base scraping to examine cytopathological transformations. |
| Antigen detection | Direct immunofluorescence staining serves as a method to identify specific viral antigens. |
| Serological testing | Detection of IgM and IgG antibodies confirms VZV infection. |
1. Antiviral treatment Acyclovir, valacyclovir and famciclovir stand as the primary antiviral treatments for VZV infections at present. These antiviral drugs work by reducing the length of illness and minimizing symptoms and complications. Antiviral therapy decreases postherpetic neuralgia risk in herpes zoster patients. People with weakened immune systems require antiviral treatment because they face a higher risk of severe complications during the initial infection or reactivation phase.
2. Preventive measures Vaccination stands as the most effective method to prevent VZV infection. There are currently two vaccines available: The available vaccines include a monovalent varicella vaccine and a recombinant vaccine for herpes zoster which prevents shingles. Healthcare providers administer the varicella vaccine to children to prevent the development of varicella effectively. People who are older than 50 years old can benefit from the recombinant herpes zoster vaccine which reduces both the frequency and seriousness of herpes zoster cases. High-risk populations with weakened immune systems should consider passive immunoglobulin for preventive measures.
The worldwide occurrence of VZV demonstrates regional differences. The incidence of varicella is higher in temperate regions but lower in tropical regions. The World Health Organization reports that every year there are approximately 4 million varicella cases globally and herpes zoster affects 100,000 of these patients. Varicella shows a higher incidence rate in places that do not implement vaccination strategies whereas regions with high vaccination coverage experience a significant reduction in varicella cases.
The Varicella-Zoster Virus (VZV) represents a contagious herpes virus responsible for both chickenpox and herpes zoster as its primary diseases. A range of laboratory methods can detect VZV while antiviral therapy and vaccination remain the primary prevention and treatment strategies for VZV infections. Through advancing research on VZV we expect to create better vaccines and treatments that will reduce both the incidence and severity of VZV infections.
| Cat. No. | Product Name | Host | Isotype | Application | |
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| DMAB-CBXY25238 | Human Anti-VZV gB Monoclonal antibody, clone 29G | Human | IgG | Control, ELISA | Inquiry |
| DMAB-CBXY25239 | Human Anti-VZV gB Monoclonal antibody, clone 29M | Human | IgM | Control, ELISA | Inquiry |
| DMAB-CS25168 | Mouse Anti-VZV Monoclonal antibody, clone 1226 [HRP] | Mouse | IgG | ELISA | Inquiry |
| Cat. No. | Product Name | Size | Species Reactivity | Application | Detection Method | |
| DEIA4425 | Varicella zoster virus IgG ELISA Kit | 96T | Human | Qualitative | Indirect ELISA | Inquiry |
| DEIA472 | VZV IgG ELISA Kit | 96T | Human | Qualitative and semiquantitative | iELISA | Inquiry |
| DEIA473 | VZV IgG and IgG avidity ELISA Kit | 96T | Human | Qualitative, Semiquantitative | iELISA | Inquiry |
| DEIA387 | Varicella-Zoster Virus IgG ELISA Kit | 96T | Human | Quantitative and qualitative | iELISA | Inquiry |
| DEIA388 | Varicella-Zoster Virus IgA ELISA Kit | 96T | Human | Quantitative and qualitative | iELISA | Inquiry |
| DEIA389 | Varicella-Zoster Virus IgM ELISA Kit | 96T | Human | Quantitative and qualitative | iELISA | Inquiry |
| DEIA500 | VZV IgM ELISA Kit | 96T | Human | Qualitative | / | Inquiry |
| DEIA501 | VZV IgG ELISA Kit | 96T | Human | Qualitative | / | Inquiry |
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| DAG1215 | Lidocaine [HRP] | 0.5 ml | Lidocaine | N/A | Inquiry |
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| DAG2631 | Recombinant Cytomegalovirus UL146 Protein(a.a. 23-117) | / | / | CMV | Inquiry |
