Pathogenesis and Immunity - Varicella Zoster Virus

Pathogenesis and Immunity

Chickenpox is the primary disease, whereas herpes zoster represents reactivation of a previous infection.

◗ Pathogenesis of varicella zoster virus infections

Primary VZV infection occurs in humans when the virus comes into contact with the mucosa of the respiratory tract or con-junctiva. From these sites, the virus enters the blood stream and lymphatic system to the cells of the reticuloendothelial sys-tem. After 11–13 days, a secondary viremia occurs and the virus spreads throughout the body and to the skin. In tissues, VZV spreads from cell to cell via direct contact to produce its effects.

After primary infection, the virus migrates along the sen-sory nerve fibers to the satellite cells of the dorsal root ganglia or cranial nerve ganglia, where it becomes latent. This latency may be permanent, or the virus may become reactivated in old adults or in patients with impaired cellular immunity. On reac-tivation, the virus replicates and spreads along the nerve fibers to the skin, known as herpes zoster or shingles.

◗ Host immunity

CMI is important in controlling the infection. It limits the progression of the disease and results in early resolution of the disease. The virus causes a disseminated life-threatening and more serious disease in immunocompromised patients with a deficient CMI. Depression of the CMI during life in the old age may cause recurrence of VZV and may cause herpes zoster. Humoral antibodies also play an important role by limiting the spread of the virus in the circulation. CMI also contributes to the immunopathology and symptomatology in the infected host. In some infected adults, it is responsible for more severe manifestations and more extensive cell damage than seen in children.

Immunity following varicella is lifelong; the individual does not suffer from varicella again, but can suffer from herpes zoster despite having immunity to varicella. Immunity is also lifelong in herpes zoster.