Epstein-Barr virus

Structure and antigenic composition

EBV virions were first discovered using electron microscopy in Burkitt lymphoma biopsy samples. The pathogen's pathogenicity and its ability to evade the immune response are determined by a complex set of antigens and molecules:

• VCA (Viral Capsid Antigen): viral capsid antigen, which plays a key role in the early stages of infection.
• EBNAs (Epstein–Barr Nuclear Antigens): a group of nuclear antigens (types 1, 2, 3A, 3B, 3C). By nature, these are DNA-binding proteins. The EBNA-1 protein is critical for the development of the infection itself, while EBNA-2 is responsible for the immortalization (infinite division) of infected cells.
• LMPs (Latent Membrane Proteins): type 1 and type 2 latent membrane proteins. It is they that possess a pronounced oncogene-like effect by interfering with the cell cycle.
• EBERs (Epstein–Barr Encoded RNAs): small viral RNAs (EBER1 and EBER2) involved in the regulation of viral activity.

Epidemiology and pathogenesis

The infection has low contagiousness; the source of infection is a sick person or an asymptomatic virus carrier. Transmission of the pathogen occurs predominantly via airborne droplets or contact routes (through saliva). There is a high level of herd immunity in the population—specific antibodies are detected in the vast majority of people.

The portal of entry is the mucous membrane of the oropharynx. The virus finds its main target—B lymphocytes—by binding to their surface receptor CD21. Upon penetration, EBV does not simply destroy the cell, but acts as a mitogen, stimulating the active multiplication (proliferation) of B lymphocytes.

The infection is prone to latency. The virus persists for life in B cells and forms hidden foci in lymphoid tissue (primarily in the palatine tonsils), as well as in the epithelial cells of the oropharynx and salivary glands. Even after clinical recovery (at the convalescence stage), the virus continues to be actively secreted from the mucous membranes of the nasopharynx and mouth for several months.

Clinical forms: mononucleosis and chronic infection

Epstein-Barr virus is capable of causing asymptomatic carriage, as well as acute and chronic forms of the disease.

Acute form (Infectious mononucleosis) The classic manifestation of primary contact with the virus. The disease is accompanied by severe malaise and high fever. Mononucleosis is characterized by the classic clinical triad:

1. Oropharyngeal involvement (severe tonsillitis involving the palatine and pharyngeal tonsils).
2. Lymphadenopathy (generalized enlargement of lymph nodes).
3. Hepatosplenomegaly (enlargement of the liver and spleen).

Severe intoxication and specific shifts in the hemogram are also observed.

Chronic infection May occur as a cyclic recurrent disease. The main symptoms are vague: persistent low-grade fever (subfebrile temperature), sore throat, headaches, and pathological fatigue.

In AIDS patients, a specific lesion of the oral mucosa occurs—oral hairy leukoplakia, which is considered an important marker condition.

Oncogenesis and lymphoproliferative diseases

Since EBV is a potent mitogen for B lymphocytes, it has direct oncogenic potential. The risk of tumor development directly depends on the competence of the T-cell arm of the immunity.

In risk groups (patients with T-cell immunity defects, HIV infection, genetic X-linked lymphoproliferative disease, as well as individuals receiving immunosuppressive therapy in transplantation), severe pathologies may develop instead of classical mononucleosis: a polyclonal leukemia-like B-cell disease or various lymphomas.

Specific tumors associated with the virus:

• Burkitt lymphoma: an African endemic form, the development of which is closely associated with malaria.
• Hodgkin lymphoma: in a significant proportion of cases, tumor cells contain viral DNA.
• Nasopharyngeal carcinoma: endemic to Eastern countries. Unlike lymphomas, this pathology affects epithelial cells rather than lymphoid cells, and viral DNA is also detected in them.

Immunity and laboratory diagnostics

Specific antiviral drugs and vaccines against EBV have not yet been developed. The developing immunity is robust—cases of reinfection have not been described. Cytotoxic CD8+ lymphocytes play the main role in the cellular response, and the production of specific antibodies plays the main role in the humoral response.

Diagnostics is based on several methods:

1. Hematological analysis: pronounced lymphocytosis is characteristic, with the proportion of monocytes reaching 60–70% of all leukocytes. The key marker of mononucleosis is the appearance of atypical lymphocytes (mononuclear cells) in the blood in an amount of about 30%.
2. Serology (ELISA):
3. Acute (recent) infection: IgM class immunoglobulins to the capsid antigen (VCA) are detected, and a rise in the titer of antibodies to the nuclear antigen (EBNA) is observed.
4. Height or past infection: IgG to the VCA antigen appear.
5. Auxiliary methods: detection of heterophile antibodies using the sheep erythrocyte agglutination reaction.

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