Morphology and genome
Members of the family Arenaviridae are complex enveloped viruses. Their supercapsid is represented by a lipid membrane, on the surface of which characteristic club-shaped glycoprotein spikes (GP1 and GP2) are located. Beneath the envelope lies the matrix protein (Z protein) and a nucleocapsid with helical symmetry.
A unique distinctive feature of arenaviruses is the presence of 12–15 captured host cell ribosomes inside the virion. These give the particle a granular appearance, which inspired the taxon's name (from Lat. arenosa — sandy).
The arenavirus genome is formed by a single-stranded ambisense RNA (coding information in both directions), divided into two fragments: the L segment and the S segment. The RNA is bound to a nucleoprotein, forming a ribonucleocapsid. The viral genome encodes only 5 proteins, including its own transcriptase — RNA polymerase (L protein). The reproduction 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 factors: they are rapidly inactivated by detergents (fat solvents), ultraviolet irradiation, heat, and gamma radiation. At the same time, they demonstrate high resistance to freezing and lyophilization (vacuum drying).
Viral cultivation in laboratory settings is carried out using several methods:
- In developing chicken embryos.
- In the body of susceptible animals (laboratory rodents: suckling mice, hamsters).
- In cell cultures (green monkey kidney cells are widely used).
Epidemiology and pathogenesis
The natural reservoir of infection includes rodents (house mice, Syrian hamsters, multimammate rats, and cotton rats). Transmission factors are rodent excreta (urine, feces, saliva) contaminating the environment.
Mechanisms of human infection:
- Airborne — inhalation of dust contaminated with rodent excreta.
- Alimentary (fecal-oral) — ingestion of contaminated water and food.
- Contact-household and vertical (transplacental from mother to fetus).
Note: Unlike other arenaviruses, Lassa virus is characterized by human-to-human transmission via contact and parenteral routes.
Once in the body, the virus primarily replicates in regional lymph nodes. This is followed by dissemination of the infection via the reticuloendothelial system (RES), ultimately leading to the pathogen entering the bloodstream (viremia).
Tissue damage is complex in nature. On the one hand, cytotoxic T lymphocytes attack and destroy infected body cells. On the other hand, in hemorrhagic fevers, an immune-complex mechanism is triggered: antigen-antibody complexes deposit on basement membranes, provoking vascular disorders. In severe cases, necrotic changes develop in the liver and spleen, along with myocarditis and kidney damage resembling glomerulonephritis, leading to acute renal failure.
Clinical forms and representatives
The incubation period lasts from 1 to 2 weeks (7–10 days for Lassa fever). The course varies from catarrhal, flu-like syndromes to life-threatening forms with fever, edema, and hemorrhagic syndrome. Long-lasting immunity is established after the infection.
Key representatives:
- Lymphocytic choriomeningitis virus: causes aseptic meningitis and meningoencephalitis accompanied by leukopenia and thrombocytopenia. Prevalent in Europe and America, with a winter-spring seasonality.
- Lassa virus: the causative agent of Lassa fever, discovered in 1969 in Nigeria (endemic to West and Central Africa). The reservoir is the multimammate rat. Manifests as intoxication, CNS involvement, petechial rash, bleeding, dyspepsia, and chest pain. Untreated, it has a high case fatality rate.
- South American hemorrhagic fevers (Tacaribe complex):
- Junin virus (Junin) — Argentine hemorrhagic fever.
- Machupo virus (Machupo) — Bolivian hemorrhagic fever.
- Guanarito virus (Guanarito) — Venezuelan hemorrhagic fever (reservoir — cotton rats).
- Sabia virus (Sabia) — Brazilian hemorrhagic fever (isolated in 1993).
Microbiological diagnostics and prevention
Blood, cerebrospinal fluid, urine, throat swabs, and pleural fluid are collected for laboratory testing.
Diagnostics are based on virological methods (inoculation of cell cultures and animals) followed by pathogen identification. Molecular genetic methods (PCR) and serological assays (ELISA, IFA, CF test, neutralization test) are widely used. Serodiagnosis aims to detect specific antibodies in the patient's blood serum.
Treatment and prevention: Specific therapy is effective only in the early period of the disease and consists of administering convalescent plasma or specific immune sera. Live vaccines for specific prophylaxis are currently under development. Control measures are primarily non-specific: quarantine measures and deratization (large-scale rodent control).
Briefly: answers to topical questions
Which cells of the immune system are the primary targets for arenavirus replication?
Available sources do not specify particular immune system cells acting as primary targets. It is only stated that primary arenavirus replication occurs at the tissue level in regional lymph nodes.
This is followed by dissemination — the spread of the virus via the reticuloendothelial system (RES), with subsequent release of the pathogen into the bloodstream and the development of viremia. Subsequently, infected body cells are attacked by the immune system: cytotoxic T lymphocytes recognize and destroy them, which serves as one of the mechanisms of tissue damage during infection.
Which chemotherapy drugs are used for specific etiotropic therapy of Lassa fever?
The antiviral drug ribavirin is used for specific etiotropic therapy of Lassa fever. This drug belongs to the group of nucleoside analogues that disrupt viral nucleic acid synthesis.
During Lassa fever treatment, ribavirin is administered intravenously. Systemic administration may cause the following side effects:
- CNS involvement — development of insomnia.
- CVS involvement — development of bradycardia.
- Hematotoxicity — occurrence of anemia, neutropenia, and thrombocytopenia.
Preclinical study data also show that the drug has oncogenic potential, teratogenic, and embryotoxic effects.
The word "arena" in the family name has nothing to do with a circus. Remember the Latin arenosa (sandy) — these are host cell ribosomes captured inside the virion, which look like grains of sand under an electron microscope.
Class and exam questions
How does the epidemiology of Lassa virus differ from other arenaviruses?
Unlike most arenaviruses, which are transmitted exclusively from animals, Lassa virus is capable of human-to-human transmission via contact and parenteral routes.
What mechanism underlies bleeding in arenavirus infections?
Hemorrhagic syndrome is caused by an immune-complex mechanism: antigen-antibody complexes deposit on vascular basement membranes, causing severe damage.
Who is the reservoir of lymphocytic choriomeningitis virus?
In nature, the reservoir is house mice, and in captivity, Syrian hamsters. The infection has a winter-spring seasonality.
What else to study on this topic
- Structure and functions of viral ambisense RNA
- Mechanism of virion assembly and budding through the plasma membrane
- Immunopathogenesis of hemorrhagic fevers: the role of immune complexes
- Principles of performing and interpreting ELISA and PCR in viral infections
- Features of the cellular immune response and the role of cytotoxic T lymphocytes
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