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Send Home Our method Usage examples Index Contact StatisticsWe do not evaluate or guarantee the accuracy of any content in this site. Slideshare uses cookies to improve functionality and performance, and to provide you with relevant advertising. A characteristic feature of all herpesviruses is their ability to become latent, primarily in ganglia of the nervous system and lymphoid tissue. Virologic analysis of endoneurial fluid obtained during decompression surgery revealed HSV-1 DNA in 11 out of 14 patients with Bell's palsy. Primary HSV-1 infection often results in painful skin or mucosal lesions, but can also be asymptomatic.
HSV-1 from postmortem explants of human trigeminal,[7,8] nodose, vagal[9] and ciliary[10] ganglia.


Neurons are the exclusive site of HSV-1 latency in human ganglia, and also in mouse and rabbit models.
DNA is endless—that is, circular or concatameric[16]—and does not integrate into the host genome.
In ganglia latently infected with HSV-1, only one region of the viral genome is abundantly transcribed.
HSV-1 reactivates after ultraviolet (UV) light stimulation, epinephrine iontophoresis, hyperthermia, or even social stress. The majority of infections are caused by human herpesvirus 1 (herpesvirus 1, human) and less often by human herpesvirus 2 (herpesvirus 2, human). Increased CSF antibody to HSV-1, and a reduced serum:CSF antibody ratio, might help to diagnose HSV-1 encephalitis.


Right, Coronal section showing mesial temporal lobe, insular necrosis in a case of herpes simplex virus (HSV) encephalitis.
A precontrast CT scan showing a case of herpes encephalitis, notice the left medial temporal hemorrhagic zone surrounded by edema. Pathologically, the condition is marked by a hemorrhagic necrosis involving the medial and inferior temporal lobe and orbital regions of the frontal lobe.



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