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HSV shows three unique biological properties: neurovirulence, latency, and reactivation
Neurovirulence: The viruses have capacity to invade andmultiply in the nervous system.
Latency: Establishment and maintenance of latent infec-tion in the nerve cell ganglion is the unique property of the virus. HSV-1 affects most commonly the trigeminal ganglion, whereas HSV-2 affects the sacral nerve root ganglion (S2–S5).
Reactivation: Reactivation and replication of latent HSVcan lead to overt or covert recurrent infections and excretion of HSV. Reactivation can be caused by a variety of stimuli, including fever, trauma, emotional stress, sunlight, etc. In immunocompetent patients, HSV-1 reactivates more frequently in the oral cavity rather than on the genital parts, but HSV-2 reactivates eight to ten times more frequently in the genital parts as compared to orolabial infection. In immunocompromised patients, reactivation by either HSV-1 or HSV-2 is more frequent and more severe. The viruses cause disseminated infection in individuals with HIV-related disease and in people with impaired T-cell immunity, such as organ transplant recipients.
Herpes simplex virus causes disease by direct cytopathologic effects. The infection is initiated by direct contact and depends on the infected tissues whether oral, genital, or brain, etc. The infection occurs by inoculation of virus into susceptible muco-sal surfaces, such as the oropharynx, conjunctiva, or cervix or through small abrasions on the skin.
The viruses infect cells of ectodermal origin, the cells com-ing in contact with infected material, such as saliva or genital secretion. Viruses replicate at the site of entry in the skin or mucous membrane. The neuroinvasiveness (the ability of virus to invade the brain), neurotoxicity (ability to multiply in the brain and destroy the brain), and its latency (ability to remain in a nonreplicating stage in the dorsal root ganglia of the cen-tral nervous system, or CNS) are the properties of HSV that influence the course of infection in an infected host.
The virus multiplies locally with cell-to-cell spread. The virus replicates in the infected cells at the base of the lesion and infects the innervating neuron. Subsequently, the viruses travel by retrograde transport to the ganglion, such as the trigemi-nal ganglion for HSV-1 and the sacral ganglion for HSV-2. The virus then returns back to the initial site of infection and may cause inapparent infection or produce vesicular lesions. Thin-walled umbilicated vesicles—the roof of which breaks down, leaving tiny superficial ulcers—are the typical lesions caused by HSV. These vesicles heal without forming any scars. The vesicle fluid contains infectious virions.
After this retrograde axonal flow from neurons, the viral genomes become latent in the ganglia, particularly those of the trigeminal (HSV-1) and sacral (HSV-2) nerves. No viral par-ticles are produced during this phase of latency. Also, latent infection in neurons does not cause any demonstrable damage in neurons. This latency phase may be reactivated periodically in some individuals, causing recurrent oral and genital lesions.
Various stimuli, such as physical or emotional stress, trauma, fever, and sunlight can induce a recurrence in which the virus travels back down the nerve, leaving lesions to develop at the skin, at the same spot each time. These stimuli trigger reactivation:
· by facilitating viral replication in the nerve,
· by inhibiting cell-mediated immunity (CMI) transiently, or
· by inducing both the mechanisms.
Thus, recurrences or reactivation of infection can occur in the pres-ence of specific antibodies. However, the recurrent infections are more localized, less severe, and of short duration than the primary infection, due to presence of past memory immune responses.
Immunity is type specific, but some cross-protection may occur. In primary HSV infection, the immunity is characterized by the appearance of specific antibody responses within a few days, followed by a cellular immune response in the second or third week of infection.
Humoral antibodies to HSV-1 increase with age, starting at childhood during which HSV-1 is usually acquired. Antibodies to HSV-2 appear in sexually mature adults, correlating with their degree of sexual activity. The antibodies usually do not prevent recurrence of disease, but reduce the severity of clini-cal disease. Immunity is incomplete, and both reinfection and reactivation occur in the presence of circulating antibodies.
CMI plays an important role in conferring immunity to HSV infection and facilitates recovery from the infection. Hence, the virus tends to cause more frequent and severe infec-tions in the patients with altered CMI, such as HIV and other CMI-deficient diseases.
Tissue damage occurring in HSV infection is due to a combi-nation of viral pathology and immunopathology. These immu-nopathologic effects of CMI and inflammatory responses are the major causes of symptoms seen during the disease.
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