Classification of herpesviruses
The Herpesviridae family includes about 80 species, but only eight are pathogenic to humans. Depending on cellular tropism and the rate of cytopathic action (destruction of infected cells), they are divided into three subfamilies:
- Alphaherpesviruses (Alphaherpesvirinae). Characterized by a high rate of cell destruction. This includes herpes simplex virus type 1 (HSV-1), herpes simplex virus type 2 (HSV-2), and the causative agent of chickenpox and shingles (VZV).
- Betaherpesviruses (Betaherpesvirinae). Possess a less pronounced cytopathic effect. The group includes cytomegalovirus (CMV), as well as human herpesviruses 6 and 7 (HHV-6, HHV-7).
- Gammaherpesviruses (Gammaherpesvirinae). Exhibit a pronounced tropism for T- and B-lymphocytes, where they are capable of long-term persistence. They include Epstein-Barr virus (EBV) and human herpesvirus type 8 (HHV-8).
Pathogenesis features: persistence and relapse
After invading the epithelium, the virus not only replicates but also begins migrating along the axons of nerve cells (retrogradely). Upon reaching the neuron cell bodies in autonomic and sensory ganglia, the viral DNA integrates into the host cell genome, forming a latent focus.
Any factors that reduce immune control (hypothermia, stress, excessive sun exposure, use of cytostatics or glucocorticoids) trigger the reactivation process. Viral particles move back toward the periphery (anterogradely), infecting capillary endothelium and epithelial cells. As a result of active viral replication on the skin or mucous membranes, characteristic vesicular rashes appear again.
With normal immunity, the process remains localized. In severe immunodeficiency, viremia develops: lesions become extensive, involve new ganglia, and can generalize with involvement of internal organs.
Clinical manifestations (HSV-1 and HSV-2)
A typical localized infection is characterized by an acute onset with fever (up to 40–41 °C) and pronounced intoxication. Local manifestations appear synchronously with general symptoms.
Evolution of the rash in herpes simplex:
- Prodrome (itching, burning, local pain).
- Appearance of grouped vesicles (blisters with serous content) on a hyperemic base.
- Rapid rupture of vesicles with the formation of painful erosions (aphthae).
- Drying of the elements with crust formation and subsequent residual pigmentation.
Of particular danger are CNS lesions (herpetic encephalitis and meningitis), which are characterized by high mortality, as well as generalized forms in newborns. Infant infection most often occurs intranatally and, in the absence of treatment, rapidly leads to DIC syndrome and infectious-toxic shock.
Diagnostics and treatment principles
The diagnosis of typical forms is established clinically, but in atypical or severe courses, laboratory verification is required. Methods for direct virus detection (PCR, ELISA, DFA) are most informative. In cytological examination, multinucleated giant cells with viral inclusions serve as a specific marker.
Basics of therapy:
- All specific drugs (acyclovir, valacyclovir, famciclovir) act strictly virostatically—they stop viral DNA synthesis but do not completely eliminate the virus from the body.
- For mild localized forms, local therapy combined with oral acyclovir is sufficient.
- For generalized processes or CNS involvement, immediate intravenous administration of acyclovir is indicated.
- Patients with severe immunodeficiency are additionally prescribed interferon-series drugs for non-specific virus suppression.
To remember the stages of rash elements, use the chain "P-V-E-C": Prodrome (itching) → Vesicle → Erosion → Crust. All elements in herpes simplex follow this path.
Class and exam questions
Why can't herpes be cured permanently with antibiotics or antivirals?
Anti-herpetic drugs have only a virostatic effect. They block replication but cannot "cut out" the viral DNA that has integrated into the neuron genome for life.
What are the specific MRI and CSF signs of herpetic encephalitis?
MRI typically shows involvement of the temporal and frontal lobes. Cerebrospinal fluid reveals moderate pleocytosis, a slight increase in protein, and characteristic xanthochromia due to microhemorrhages.
How does infection of newborns most commonly occur?
In the vast majority of cases (intranatally), infection occurs during the passage of the child through the mother's infected birth canal.
What else to study on this topic
- Clinical picture and triggers for the development of Kaposi's varicelliform eruption
- Differential diagnosis of herpetic stomatitis and enteroviral herpangina
- Specifics of eye involvement (ophthalmoherpes) and risks of vision loss
- Suppressive therapy protocols for frequent recurrences of genital herpes
- Features of serological diagnostics (interpretation of IgG and IgM titers over time)
Master the entire topic in the Pediatrics course
This is a summary. The course covers everything tested in classes and exams.
- Full methodological guide on "Herpesvirus infections" and 3,738 more pages of the subject
- Assignments and quizzes after every topic — just like in a colloquium
- AI tutor answers questions on the topic anytime
- 71 video lessons on the subject
Other topics from the section «Chapter 12. Infectious and parasitic diseases»
Prepared by WhiteCoat Pro faculty in accordance with the medical school curriculum. For educational purposes only.