Chickenpox

Chickenpox is an acute, highly contagious disease caused by the varicella-zoster virus (VZV), a double-stranded DNA virus belonging to the Herpesviridae family. Its transmission occurs primarily through the inhalation of respiratory droplets or direct contact with vesicular fluid from skin lesions. The incubation period typically ranges from 10 to 21 days, during which the virus replicates and disseminates through sequential phases within the host. Although generally self-limiting in children, chickenpox can lead to severe complications in neonates, adults, and immunocompromised individuals. Widespread immunization with the live-attenuated varicella vaccine has markedly reduced the incidence and severity of the disease in many populations.

Pathogenesis and Viral Dissemination

The infection begins when inhaled virions enter the upper respiratory tract and infect the mucosal epithelium. Following local replication, the virus spreads to regional lymph nodes, resulting in a primary viremia. This facilitates viral dissemination to organs such as the liver and spleen, where extensive replication occurs. A subsequent secondary viremia enables the virus to reach the skin, producing the hallmark exanthematous rash. The rash follows a centripetal distribution and evolves from macules to papules, vesicles, and eventually crusted lesions, often appearing in successive waves.

Immune Response and Viral Latency

The host immune response is critical in controlling viral spread. Humoral immunity, mediated by neutralizing antibodies, limits further dissemination, while cellular immunity—particularly CD8+ cytotoxic T lymphocytes—clears infected cells. Despite this, VZV exhibits neurotropism and establishes latency in the sensory dorsal root ganglia following the resolution of the primary infection. During this latent phase, the viral genome persists in a non-replicative state with minimal transcriptional activity, allowing it to evade immune detection.

Reactivation and Herpes Zoster

In certain individuals—often due to immunosuppression or an age-related decline in cell-mediated immunity—latent VZV may reactivate. This reactivation manifests as herpes zoster (shingles), characterized by painful, unilateral dermatomal eruptions. Unlike chickenpox, herpes zoster is frequently associated with complications such as postherpetic neuralgia, making it clinically distinct yet etiologically linked to the primary infection. Herpes zoster can be prevented in many cases through the administration of zoster vaccines, especially in older adults.