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Lymphatic choriomeningitis is a central nervous system infectious disease caused by lymphocytic choriomeningitis virus (LCMV), belonging to the sand particle virus genus of the sand particle virus family. The virus is circular or polymorphic, with rod-shaped protrusions on its surface, and is mainly transmitted through contact with food or dust contaminated with rodent excrement. Laboratory workers are a high-risk population. The natural host of this virus is rodents such as mice and hamsters, which can continuously detoxify through urine, feces, and respiratory secretions. Influenza like symptoms appear 5-10 days after human infection, manifested as high fever, muscle pain, and aseptic meningitis. About 10% of cases also develop orchitis or mumps. Animal infections are classified into three types: cerebral type (tremors, convulsions), visceral type (hepatitis, lymph node lesions), and delayed type (glomerulonephritis). The pathological features are infiltration of leptomeningeal monocytes and formation of choroidal plexus inclusions. Diagnosis needs to be confirmed through virus isolation or serological testing (ELISA, immunofluorescence).
Figure 1. Role of Lymphocytic Choriomeningitis Virus (LCMV) in Understanding Viral Immunology.( Zhou, Xin, et al.2012)
Lymphocytic choriomeningitis (LCM) is prevalent in rodents. The most common cause of human infection is inhalation of dust contaminated by rodents and ingestion of contaminated food, while mice or hamsters can carry the Lymphocytic choriomeningitis virus (LCMV) for life and excrete it through urine, feces, semen, and nasal secretions. Infected cases in humans are mainly observed in adults and are more likely to occur in winter. Key viral antigens involved in LCMV infection and detection include the viral Nucleoprotein and Glycoprotein G2, and corresponding recombinant products—Recombinant Lymphocytic choriomeningitis virus Nucleoprotein and Recombinant Lymphocytic choriomeningitis virus Glycoprotein G2—are widely used in LCMV-related research, serological detection, and diagnostic reagent development.
The immune response to LCMV has been extensively studied in mouse models, providing fundamental insights for viral immunology. The control of acute infections mainly relies on CD8+T cells (cytotoxic T lymphocytes), which recognize and eliminate virus-infected cells. CD4+T cells (helper T cells) also play a crucial role in supporting CD8+T cell responses and generating strong antibody responses from B cells. A key concept elucidated by LCMV research is T cell exhaustion. In cases of high viral load and persistent infection (e.g. using clone 13), virus specific CD8+T cells gradually become dysfunctional. They upregulate inhibitory receptors (such as PD-1), lose the ability to produce effector cytokines such as interferon gamma (IFN - γ), and undergo apoptosis, leading to failed virus clearance. On the contrary, natural killer (NK) cells can also affect the outcome of infection. Although they contribute to early antiviral defense, their activity sometimes promotes chronicity by limiting the initial CD8+T cell response.
The LCMV virus is mainly transmitted through house mice. Once infected, these mice can become chronic carriers through the sustained presence of the virus in their blood or the continuous excretion of the virus in their urine. Chronic infected female mice usually transmit the virus to their offspring (vertical transmission), and the offspring become chronic carriers as a result. Other routes of transmission among mice include nasal secretions, milk from infected mother mice, bites, and social grooming behavior within the mouse population. Airborne transmission may also occur. The virus seems to have strong resistance to dryness, so humans may be infected by inhaling particles containing infectious aerosols in rodent urine, feces, or saliva, ingesting food contaminated with the virus, contaminating mucous membranes with infected body fluids, or directly contacting infected blood in wounds. The currently recorded cases of animal to animal transmission have only occurred between humans and mice or hamsters.
Influenza like symptoms appear 5-10 days after infection. Fever usually ranges from 38.5 to 40 ℃, accompanied by chills. More than half of the patients experience discomfort, fatigue, muscle pain (especially in the lower back), headache behind the eye sockets, photophobia, lack of appetite, nausea, and dizziness. Symptoms such as sore throat and delayed sensation are relatively rare. In the first week of onset, positive signs are rare; There may be relative bradycardia, with congestion in the throat but no exudation. After 5 days to 3 weeks, patients may feel their symptoms improve for 1-2 days. But many patients subsequently experience recurrent fever, headache, rash, swelling of the metacarpophalangeal and proximal finger joints, meningeal irritation, orchitis, mumps, and baldness. Almost all patients with aseptic meningitis can recover without any sequelae. 33% of encephalitis patients have neurological sequelae.
The white blood cell count and classification count in peripheral blood are usually normal, with occasional presence of atypical lymphocytes and normal erythrocyte sedimentation rate. The appearance of cerebrospinal fluid examination is normal, with normal or slightly elevated pressure, normal or slightly low glucose levels, and normal chloride levels.
The diagnosis of a patient requires evidence of virus isolation or serum antibody testing. During the acute fever phase, lymphocytic choriomeningitis virus can be isolated from the patient's blood or cerebrospinal fluid. Double serum testing for virus antibodies during the acute and recovery phases can help identify acute infections. Immunofluorescence technology can detect antibodies in the early stages of the disease and is a rapid and sensitive diagnostic method. In the case of only a single serum sample, high titer complement binding antibodies may be an indication of recent infections. Since neutralizing antibodies can persist in the serum for many years, a positive neutralizing antibody alone is not sufficient to determine the diagnosis of this disease.
There is currently no specific treatment for this disease. The treatment should focus on symptomatic treatment, and patients should rest in bed. Severe headaches and high intracranial pressure can be treated with dehydrating agents such as mannitol.
This disease is self limiting and has a good prognosis. The vast majority of patients can fully recover. Patients with meningitis have a slower recovery, which can last for weeks or months, and generally do not have significant sequelae. Individual severe patients may have residual symptoms such as persistent headaches, dizziness, fatigue, and memory impairment. Occasionally, there are also fatalities.
Research has shown that human infection with the virus mainly occurs in autumn and winter, possibly due to indoor exercise in mice. Various measures can be taken to prevent wild rodents at home from coming into contact with LCM. The Centers for Disease Control and Prevention in the United States has provided a list of preventive measures, including tips for sealing homes to prevent rodents from entering, using traps to eliminate existing rodents, and maintaining a clean and healthy home. The new technology reflects the trend towards more humane eradication of rodents. The products include devices that emit ultrasound waves, which are said to stimulate mice and drive them away, as well as faster and more painless ways of death, such as mini electrocution or gas chambers. However, the traditional fast trap remains an economical and popular choice.
Ribavirin, a nucleoside analogue, is used in certain situations because it has inhibitory effects on sand viruses in vitro. However, there is insufficient evidence to support its efficacy in humans for routine use. Early and intravenous administration of ribavirin is necessary to achieve maximum efficacy, and it can have significant side effects. Ribavirin has not yet been evaluated in controlled clinical trials. It is generally not recommended to use ribavirin during pregnancy, as some studies have shown that it may have teratogenic effects. If LCMV causes aseptic meningitis, encephalitis, or meningoencephalitis, hospitalization and supportive treatment may be required. In some cases, anti-inflammatory drugs can also be considered. Generally speaking, the mortality rate is less than 1%. A potential novel therapeutic approach, NMT inhibitors, has been shown to completely inhibit LCM infection in cell-based assays.
Reference
| Target | Cat. No. | Product Name | Size | Isotype | |
| LCMV | DEIAJX007 | Human Lymphocytic choriomeningitis virus Antibody ELISA Kit | 96T | Quantitative | Inquiry |
| DEIAJX008 | G. Pig Lymphocytic choriomeningitis virus Antibody ELISA Kit | 96T | Quantitative | Inquiry | |
| DEIAJX009 | Mouse Lymphocytic choriomeningitis virus IgG ELISA Kit | 96T | Qualitative | Inquiry | |
| DEIA7163 | Mouse Lymphocytic Choriomeningitis Virus (LCMV) ELISA Kit | 96T | Qualitative | Inquiry | |
| DEIA-JY2452 | Mouse Lymphocytic Choriomeningitis Virus (LCMV) Antibody ELISA Kit | 96T | Qualitative | Inquiry | |
| DEIA-JY2481 | Hamster Lymphocytic Choriomeningitis Virus (LCMV) Antibody ELISA Kit | 96T | Qualitative | Inquiry |
| Target | Cat. No. | Product Name | Host | |
| LCMV | DAG-WT5840 | Recombinant Lymphocytic choriomeningitis virus Nucleoprotein [His] | E. coli | Inquiry |
| DAG-WT5841 | Recombinant Lymphocytic choriomeningitis virus Glycoprotein G2 [His] | E. coli | Inquiry | |
| DAG-WT5842 | Recombinant Lymphocytic choriomeningitis virus Glycoprotein G2 [His-SUMO] | E. coli | Inquiry | |
| DAG-WT5843 | Recombinant Lymphocytic choriomeningitis virus Glycoprotein G1 [His] | E. coli | Inquiry |
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