Lymphocytic Choriomeningitis Virus - Pathogenesis, Symptoms, Treatment, and Prevention.

Introduction:

The common human pathogen Lymphocytic Choriomeningitis Virus (LCMV) infects many people. Neurologists frequently are not familiar with it, even though it can result in serious neurological issues like meningitis (inflammation of the layers in the brain and the spinal cord), encephalitis (brain inflammation), and neurological birth abnormalities. The Arenaviridae family of viruses includes LCMV. The single-stranded RNA (ribonucleic acid) viruses known as arenaviruses got their name from the Latin word arenosus, which means sandy, because of the tiny granularities inside the virion when seen under an electron microscope. Postnatal people often contract LCMV either by inhaling aerosolized virus or contacting contaminated fomites. Organ transplantation is another way that postnatal individuals can contract the virus. When a woman contracts a primary LCMV infection while pregnant, congenital LCMV infection results. The virus spreads transplacentally to the fetus during maternal viremia. The fetus could contract the virus during labor and delivery. There is no evidence of horizontal LCMV transmission from person to person (except when infected tissues are transplanted).

What Is the Pathogenesis of LCMV Infection?

The pathogenesis of LCMV infections is

• Acquired LCMV Infection - The combination of LCMV infection and the host immune system's reaction to the infection results in both acquired and congenital LCMV diseases. When contracting an infection, the virus normally enters the body as an aerosol. It is then deposited in the lung, where viral replication occurs. Early in the course of the disease, this parenchymal lung infection frequently presents with interstitial lung infiltrates and lung edema. The virus then enters the bloodstream and spreads to more organs, where it replicates itself once more. The last sites where LCMV may replicate to high titers and produce the pathology and symptoms of meningitis that give the virus its name are the meninges, choroid plexus, and ventricular ependymal linings. The host immunological response to acquired LCMV infection is both beneficial and harmful. The immune response serves the vitally crucial purpose of eradicating the virus and guarding against re-infection, making it protective. Yet, the immune response is harmful since tissue inflammation causes illness symptoms.

• Congenital LCMV Infection - The fetus usually contracts the virus transplacentally in congenital LCMV infections. Occasionally, the fetus may contract the virus during the intrapartum period through contact with maternal vaginal fluids or blood when the mother is virulent. The virus shows a great preference for the brain in the human fetus after it has entered, where infection causes its most prevalent and harmful pathologic effects. Microcephaly (a condition where the baby’s head is small), periventricular calcifications a condition where hard deposits are formed in the brain), hydrocephalus (a condition where there is uncommon cerebrospinal fluid accumulation in the brain), cerebellar hypoplasia (a neurologic condition where the cerebellum is underdeveloped or is smaller than its normal size), localized cerebral damage (brain damage), and gyral dysplasia (malformation in the arrangement of layers covering the brain and strange appearance of neurons) are just a few of the pathologic changes that neuroimaging studies have shown LCMV can cause in the developing brain.

What Are the Signs and Symptoms of LCMV Infection?

The patient's developmental stage at the time of infection completely determines the clinical signs and symptoms of LCMV infection. The clinical symptoms, in particular, vary depending on whether the infection happens during postnatal life or the prenatal period. When an infected person does become unwell, it often happens 8 to 13 days after the initial virus infection as part of a biphasic febrile illness (an illness that has two phases). This first stage, which can last up to a week, often starts with any or all of the symptoms listed below:

• Muscle aches.

• Headaches.

• Nausea.

• Vomiting.

• Lethargy.

• Fever.

• Lack of appetite.

• Sore throat.

• Cough.

• Joint discomfort.

• Chest pain.

• Testicular pain.

• Parotid (salivary gland) pain.

A disease may enter a second phase after a few days of recovery.

• Meningitis symptoms include fever, headache, and stiff neck.

• Meningoencephalitis (the meninges and brain are both inflamed).

• Encephalitis symptoms include sleepiness, disorientation, sensory problems, and motor abnormalities, including paralysis (inflammation of both the brain and meninges).

• Acute hydrocephalus (excess fluid on the brain), which frequently necessitates surgical shunting to lower elevated intracranial pressure, has also been linked to LCMV.

• Myelitis, or spinal cord inflammation, is a rare but serious consequence of infection and manifests as symptoms including muscle weakness, paralysis, or changes in body sensation.

• Myocarditis, or the inflammation of the heart muscles.

How Is LCMV Transmitted?

LCMV infections can develop following contact with fresh urine, rodent feces, saliva, or nesting materials. Moreover, these substances may cause transmission if they are directly inserted into open wounds, the nose, the eyes, or the mouth, or possibly through the bite of an infected rodent. Except for vertical transmission from an infected woman to the fetus and, rarely, through organ transplantation, there have been no reports of person-to-person transfer.

How Is LCMV Diagnosed?

The laboratory findings used to diagnose LCMV are:

• Low white blood cell counts (leukopenia).

• Low platelet counts (thrombocytopenia) are the most prevalent test abnormalities during the disease's early stages.

• Serum liver enzyme levels may also be slightly elevated.

• The cerebrospinal fluid (CSF) typically shows an increase in protein levels, a rise in white blood cell count, or a drop in glucose levels following the start of neurological disease during the second phase.

• IgM (immunoglobulin M) and IgG (immunoglobulin G) antibodies are typically found in the serum and CSF and are used to make a laboratory diagnosis.

• Viruses can be found in the CSF during the acute stage of disease using PCR (polymerase chain reaction) or virus isolation.

How Is LCMV Treated?

Depending on the severity, aseptic meningitis, encephalitis, or meningoencephalitis necessitates hospitalization and supportive care. In certain situations, anti-inflammatory medications like corticosteroids may be taken into consideration. Unfortunately, there is no proven evidence to support the routine use of Ribavirin, a medication used to treat some other viral illnesses, for treating LCM in humans, despite research showing that it is effective against LCMV in vitro.

How Can LCMV Be Prevented?

No vaccine exists to protect against LCMV infection. Nonetheless, measures can be taken to significantly lower the chance of contracting LCMV. Without a woman developing a primary LCMV infection while pregnant, congenital LCMV infection will not happen. Women can lower their chance of catching the virus by limiting their exposure to the excretions and secretions of mice, which are the main source of LCMV for humans. The best way to do this is to get rid of the mice that live there. Also, pregnant women should stay away from pet rodents, particularly mice and hamsters. Those who work in laboratories with rats run a higher risk of contracting LCMV. To protect themselves from potential aerosolized or secreted LCMV, pregnant women working in animal care facilities or laboratories at research institutes should put on gloves, gowns, and face masks.

Receiving LCMV after receiving a solid organ transplant puts the recipient's life in danger. Organ recipients are clearly and significantly at risk of contracting a deadly infection from an organ donor with LCMV. Healthcare professionals, transplant facilities, and organizations that purchase organs should be aware of the dangers; LCMV poses and should take LCMV into account in any potential donor who exhibits symptoms of aseptic meningitis but has no known infectious agent. It is important to carefully assess the advantages and disadvantages of providing and receiving organs from donors who may have LCMV infection.

Conclusion:

Children with congenital LCMV infection typically have a bad prognosis. Both domestically and internationally, rodent hosts are widely distributed geographically. However, the capacity of scientists to determine incidence rates and frequency of disease among humans has been hampered by uncommon detection and diagnosis, as well as historical underreporting of LCM. The epidemiology of LCM and LCMV infections can be better understood to identify risk factors for infection and create efficient prevention measures. In addition, by improving disease recognition and reporting, physicians will be better able to characterize the natural history and underlying immunopathological mechanisms of disease, encouraging further research and development of new therapeutics.