What is the pathophysiology of herpes simplex virus (HSV) infection?

Updated: Feb 27, 2019
  • Author: J Michael Klatte, MD; Chief Editor: Russell W Steele, MD  more...
  • Print

Infection occurs in a susceptible host following exposure of abraded skin or mucosal surfaces to the virus. After inoculation, the virus travels to the sensory ganglion, where it replicates and establishes latency. Recurrence occurs when the virus subsequently migrates along the peripheral sensory nerve, replicates, and produces a typical local lesion. [20, 21] Lifelong latency and periodic recurrences are hallmarks of herpes simplex virus infection. These reactivations can follow exposure to ultraviolet light, stress, hormonal changes, immunosuppression, and other infection. [22, 23] Histology of skin lesions shows cellular balloon degeneration, condensation of nuclear chromatin, and formation of multinucleated giant cells. [21]

Disseminated infection occurs when the host is unable to control viral replication leading to viremia and multiorgan involvement. It is usually seen in neonates and immunocompromised individuals (and very rarely in immunocompetent hosts). Specific immunologic factors responsible for immunity to herpes simplex virus are not completely understood. Both antibody and cell-mediated immunity influence the severity and frequency of recurrences. Herpes simplex virus is also believed to suppress innate immunity by suppressing the production of interferon-alfa and interferon-beta. [24] Additionally, titers of antibodies that mediate antibody-dependent cellular cytotoxicity inversely correlate with severity of neonatal infection. [25]

Did this answer your question?
Additional feedback? (Optional)
Thank you for your feedback!