Varicella zoster virus and shingles – what is the connection?

The causative agent of shingles is the varicella zoster virus (VZV). It belongs to the herpes virus family. It can be transmitted via the air (droplet infection), but also via contact with the contents of the vesicles containing the virus or crusts (smear infection).

When first infected with the varicella zoster virus, the disease manifests itself as chickenpox. Chickenpox often occurs in childhood. It causes small, usually raised, round-oval, red spots and blisters on the trunk, face, arms and legs, accompanied by headache, aching limbs and fever.

Once healed, the virus may reappear many years later (reactivation) and cause shingles. This reactivation is favored by a weakened immune system (e.g. in cases of stress, infections, tumor diseases, immunosuppressive therapy). The viruses spread along the nerve fibers into the skin. There, a stripe-shaped skin rash with the formation of blisters containing secretions occurs. At the same time, the patient reports severe pain in the affected area.

Diagnosis

In addition to the clinical appearance with the groundbreaking skin changes, a lumbar puncture with examination of the nerve fluid is also performed to confirm the diagnosis, although this is often not necessary. One finds 20 – 70 cells (lymphocytes = white blood cells) and normal protein values. Both levels increase when an extensive inflammation of the meninges (zoster meningitis) develops with high fever, clouding of consciousness and neck stiffness.

The PCR test detects the VZV genetic material. PCR can detect DNA substance of varicella zoster virus in the cerebrospinal fluid (CSF -> CSF diagnostics), which is evidence of infection. Immunoglobulins G (IgG) are part of the specific immune defence and are released by plasma cells (B-lymphocytes).

They are used to fight viruses and bacteria. In an initial infection, IgG antibodies are formed and released with a delay. Therefore, they often already show that an infection has subsided.In case of reinfection, however, they are released after 24 to 48 hours.

For this reason, IgG antibodies play an important role in the diagnosis of shingles. Immunoglobulins M (IgM) are also part of the specific immune defense and are released by plasma cells (B lymphocytes). They serve to fight viruses and bacteria.

They are formed and released directly upon initial infection and represent the first defence reaction to invading pathogens. After the acute phase of an infection has subsided, the concentration of IgM antibodies in the blood decreases rapidly. For this reason, IgM antibodies are primarily used to identify acute infections.

If the varicella zoster virus is reactivated in the course of shingles, an increase in IgM levels can be completely absent. In the case of an infection with varicella zoster virus, the clinical picture of chickenpox appears during initial infection. After healing, however, the viruses remain in the human body and can be reactivated when the immune system is weakened.

The spread along the nerves results in the image of shingles. The analysis of immunoglobulins (= antibodies) plays a major role, especially for the diagnosis of shingles. The immunoglobulins G in particular are assessed.

An increase in IgG antibodies indicates a renewed infection with the varicella zoster virus and thus the presence of shingles. An eight to fortnightly follow-up of the IgG level is recommended to assess the disease activity. IgM antibodies play only a minor role in the diagnosis of shingles.

Immunoglobulins M can be measured for the diagnosis of chickenpox. These are elevated especially in the acute phase of the infection. In the further course of the disease, increased IgG levels in the blood may also occur as the symptoms subside. However, the analysis of immunoglobulins plays only a minor role in chickenpox. General information can be found under: Antibodies