Pathogenesis and Pathology of Varicella-Zoster virus
المؤلف:
Stefan Riedel, Jeffery A. Hobden, Steve Miller, Stephen A. Morse, Timothy A. Mietzner, Barbara Detrick, Thomas G. Mitchell, Judy A. Sakanari, Peter Hotez, Rojelio Mejia
المصدر:
Jawetz, Melnick, & Adelberg’s Medical Microbiology
الجزء والصفحة:
28e , p482
2025-11-11
158
A. Varicella
The route of infection is the mucosa of the upper respiratory tract or the conjunctiva. After initial replication in regional lymph nodes, primary viremia spreads virus and leads to replication in the liver and spleen. Secondary viremia involving infected mononuclear cells transports virus to the skin, where the typical rash develops. Swelling of epithelial cells, ballooning degeneration, and the accumulation of tis sue fluids result in vesicle formation (Figure 1).
Fig1. Characteristic histologic changes of varicella zoster virus infection. Punch biopsies of varicella-zoster virus vesicles were fixed and stained with hematoxylin and eosin. A: Early infection showing “balloon degeneration” of cells with basophilic nuclei and marginated chromatin (reduced from 480×). B: Later infection showing eosinophilic intranuclear inclusions surrounded by wide clear zones (reduced from 480×). C: Multinucleated giant cell in the roof of a varicella vesicle (reduced from 480×). D: Low power view of an early vesicle showing separation of the epidermis (acantholysis), dermal edema, and mononuclear cell infiltration (reduced from 40×). (Reproduced with permission from Gelb LD: Varicella-zoster virus. In Fields BN, Knipe DM [editors-in-chief]. Virology, 2nd ed. Raven Press, 1990.)
Varicella-zoster virus replication and spread are limited by host humoral and cellular immune responses. Interferon is likely involved also. It has been shown that a varicella-zoster virus-encoded protein, ORF61, antagonizes the β-interferon pathway. This presumably contributes to the pathogenesis of viral infection.
B. Herpes Zoster
The skin lesions of herpes zoster are histopathologically identical to those of varicella. There is also an acute inflammation of the sensory nerves and ganglia. Often only a single ganglion may be involved. As a rule, the distribution of lesions in the skin corresponds closely to the areas of innervation from an individual dorsal root ganglion.
It is not clear what triggers reactivation of latent VZV infections in ganglia. It is believed that waning immunity allows viral replication to occur in a ganglion, causing intense inflammation and pain. Virus travels down the nerve to the skin and induces vesicle formation. Cell-mediated immunity is probably the most important host defense in containment of VZV. Reactivations are sporadic and recur infrequently.
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