Morphology and Genome
Members of the family Arenaviridae are enveloped viruses. Their envelope consists of a lipid membrane studded with characteristic club-shaped glycoprotein spikes (GP1 and GP2). Beneath the envelope lie the matrix protein (Z protein) and a nucleocapsid with helical symmetry.
A unique distinguishing feature of arenaviruses is the presence of 12–15 captured host cell ribosomes inside the virion. These give the particle the granular appearance that inspired the taxon name (from Latin arenosa — sandy).
The arenavirus genome consists of single-stranded ambisense RNA (coding information in both directions), divided into two segments: the L segment and the S segment. The RNA is bound to the nucleoprotein, forming a ribonucleocapsid. The viral genome encodes only 5 proteins, including its own transcriptase, an RNA-dependent RNA polymerase (L protein). The replication cycle takes place in the cell cytoplasm, and new virions egress by budding through the plasma membrane.
Resistance and Cultivation
Arenaviruses are highly sensitive to physical and chemical agents: they are rapidly inactivated by detergents (lipid solvents), ultraviolet radiation, heat, and gamma irradiation. However, they exhibit high stability to freezing and lyophilization (vacuum drying).
Laboratory cultivation of the virus is performed using several methods:
- In developing chick embryos.
- In susceptible animal models (laboratory rodents: suckling mice, hamsters).
- In cell cultures (African green monkey kidney cells are widely used).
Epidemiology and Pathogenesis
Rodents serve as the natural reservoir of infection (house mice, Syrian hamsters, multimammate mice, and cotton rats). Transmission occurs via rodent excreta (urine, feces, saliva) contaminating the environment.
Routes of human transmission:
- Aerosol (inhalation) — breathing in dust contaminated with rodent excreta.
- Alimentary (fecal-oral) — ingestion of contaminated water and food.
- Contact-mediated and vertical (transplacental from mother to fetus).
Note: Unlike other arenaviruses, Lassa virus can be transmitted from person to person via contact and parenteral routes.
Upon entering the body, the virus initially replicates in regional lymph nodes. This is followed by dissemination of the infection through the reticuloendothelial system (RES), ultimately leading to the release of the pathogen into the bloodstream (viremia).
Tissue damage is complex. On one hand, cytotoxic T lymphocytes attack and destroy infected host cells. On the other hand, in hemorrhagic fevers, an immune complex mechanism is triggered: antigen-antibody complexes deposit on basement membranes, provoking vascular disturbances. In severe cases, necrotic changes develop in the liver and spleen, along with myocarditis and glomerulonephritis-type renal damage leading to acute kidney injury.
Clinical Manifestations and Key Species
The incubation period lasts from 1 to 2 weeks (7–10 days for Lassa fever). The clinical course ranges from catarrhal, flu-like syndromes to life-threatening forms with fever, edema, and hemorrhagic syndrome. Long-lasting immunity develops following recovery.
Key species:
- Lymphocytic choriomeningitis virus (LCMV): Causes aseptic meningitis and meningoencephalitis accompanied by leukopenia and thrombocytopenia. Prevalent in Europe and the Americas with a winter-spring seasonality.
- Lassa virus: The causative agent of Lassa fever, identified in 1969 in Nigeria (endemic to West and Central Africa). Reservoir: multimammate rat (Mastomys). Manifests with intoxication, CNS involvement, petechial rash, hemorrhages, dyspepsia, and chest pain. High case fatality rate without treatment.
- South American hemorrhagic fevers (Tacaribe complex):
- Junin virus — Argentine hemorrhagic fever.
- Machupo virus — Bolivian hemorrhagic fever.
- Guanarito virus — Venezuelan hemorrhagic fever (reservoir: cotton rats).
- Sabia virus — Brazilian hemorrhagic fever (isolated in 1993).
Microbiological Diagnostics and Prevention
Laboratory specimens include blood, CSF, urine, throat swabs, and pleural fluid.
Diagnosis relies on virological methods (inoculation of cell cultures and animals) followed by pathogen identification. Molecular genetic methods (RT-PCR) and serological assays (ELISA, IFA, complement fixation, neutralization tests) are widely used. Serodiagnosis aims to detect specific antibodies in the patient's serum.
Treatment and Prevention: Specific therapy is effective only in the early stages of the disease and consists of administering convalescent plasma or specific immune sera. Live vaccines for specific prophylaxis are still under development. Disease control relies primarily on non-specific measures: quarantine protocols and rodent control (deratization).