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Microbes & Immunity Genetic therapy with HSV-1 vectors

Patients in the HSV-1 latent state are often activated and 2.5.5. Systemic disseminated infection
transported to terminals along synapses when exposed to Systemic disseminated infection often presents with
sun exposure, stress, trauma, UV, or other infections, where herpetic lesions such as brain, liver, lung, eye, adrenal gland,
they enter the innervated skin and mucous membranes and systemic mucocutaneous lesions, and affected patients
to reproduce and cause pathological changes again, will experience high fever, cough, dyspnea, cyanosis,
resulting in the recurrence of local herpes. 12,13 Only in rare jaundice, convulsions, coma, and systemic mucocutaneous
cases do viral particles enter the central nervous system herpes, with a mortality rate of 60% –o70%.
(CNS) and initiate latent or lytic infections, which cause
symptoms such as encephalitis. 14,15 The newly replicated Once HSV-1 infects immunocompromised individuals,
virus continues to progress, usually at a local site of neural its lesions can spread to the respiratory tract, digestive
control, to form stable herpes, with a remission period tract, intestinal mucosa, etc., and the symptoms are more
of 2 – 10 days until recovery. In this process, the patient’s serious. Sporadic fatal encephalitis caused by HSV-1
immune system acts to invade the virus. 16 infection progresses rapidly and has a high mortality rate. 3

2.5. Clinical disease 2.6. Immunity
2.5.1. Acute herpetic gingivitis The clinical symptoms of acute HSV-1 infection tend
It is the most common primary infection. Acute onset, fever, to be more severe than those of reactivation infection,
oral and tongue mucosa and gingiva redness, congestion, which is associated with stimulating the body to produce
and groups of herpes, rupture after the formation of corresponding antibodies and specific T cells after HSV-1
small ulcers, ulcers can extend to the throat, palate, etc., infection. Neutralizing antibodies directed against HSV
occasionally affect the esophagus and trachea, patients envelope glycoproteins are important for host protection,
with mouth and tongue pain, cervical lymphadenopathy and such antibodies can also mediate antibody-dependent
and tenderness and other symptoms. In general, it resolves cell-mediated cytotoxicity and limit the spread of early
spontaneously after 1 – 2 weeks. HSV-1 infection. Neutralizing antibodies appear in the
serum approximately 1 week after infection, peak at 3 –
2.5.2. Acute herpetic nervous system infection 4 weeks, and persist for many years.
Acute herpetic nervous system infection is rare and presents Specific cytotoxic lymphocytes (TCs) detected during
with encephalitis, meningitis, myelitis, and radiculitis. the 2 week of HSV-1 infection can destroy infected
nd
Herpetic encephalitis is dangerous, with a mortality rate of host cells before viral replication is complete. Infection
approximately 50%, and survivors mostly have permanent with HSV-1 is able to prevent reinfection with HSV-2
sequelae. or reduce the damage caused by it. In addition, severe
HSV-1 reactivation is often induced in immunodeficient
2.5.3. Keratoconjunctivitis herpeticum
individuals, especially immunocompromised individuals,
Acute and active infections occur in the eye, herpes is seen which may be associated with prolonged viral release and
locally in the bulbar conjunctiva, and secretions are scant. persistent damage.
Lesions in the cornea, visible corneal surface dendritic
ulcers, and deeper ulcer healing can cause corneal 3. Viral diagnosis
leukoplakia, seriously affect vision, and can also cause 3.1. Virus isolation and culture
hypopyon. Iridocyclitis and uveitis can cause blindness.
Viral isolation and culture are the “gold standards”
2.5.4. Skin infection and herpetic paronychia for confirming HSV-1 infection. Blister fluid, saliva,
HSV-1 skin infection occurs in skin damage, such as eczema, cerebrospinal fluid (CSF), corneal scrapings, and other
burns, or trauma, causing eczema herpeticum, herpetic samples can be inoculated into susceptible cells, such as
paronychia, and so on. HSV-1 infection, which occurs human embryonic kidney, human amniotic membrane, or
on the basis of skin eczema, is called eczema herpeticum. rabbit kidney, and can also be inoculated into the chicken
Eczema herpeticum and skin burns can cause systemic embryonic chorioallantoic membrane, and suckling mouse
infections, which are severe and cause a high mortality rate. or mouse brain, all of which can increase the isolation rate.
Herpetic paronychia is often misdiagnosed as bacterial Cytopathic effects caused by HSV-1 often appear after 2 –
infection after skin damage to the fingers, infection of the 3 days, and the cells may show pathological features such as
fingers or nails, painful herpes, and formation of pustules. swelling, rounding, increased refraction, and the formation
17
Herpes occurs mostly in the local skin, herpes around the of confluent cells. Viruses can be identified and typed by
skin congestion, herpes dry scab and recovery. immunofluorescence or nucleic acid hybridization via

Volume 2 Issue 2 (2025) 20 doi: 10.36922/mi.7947