The human nervous system can be infected by many different types of viruses. Once a virus gains access to the nervous system, there are several potential outcomes, including acute replication, persistence, and latency. During all three scenarios, local and peripherally derived immune cells will mount a defense response and attempt to eradicate the pathogen and, in some cases, this immune defense results in severe disease. The ideal scenario is for the host to eliminate the invading virus quickly without causing disease or death; however, some viruses can evade this stage and establish persistence or latency. Persistent viral infections are defined by continual viral replication, whereas latency is a ‘dormant’ state during which the production of infectious virions is minimized or ceases entirely but the pathogen is not eliminated. Persistent and latent viral infections that stay within the nervous system can cause a vast array of symptoms including chronic fatigue, muscle weakness or tightness, body pain, numbness or coldness when the periphery nervous system is infected, anxiety, depression when central nervous systems is infected, as well as loss of smell or taste.
There are many different types viruses that can cause infection of the human nervous system. Rabies((-)ssRNA) virus and the West Nile ((+)ssRNA) virus can infect the brain causing encephalitis. Poliovirus, a serotype of the species Enterovirus C is the causative agent of polio. Herpes simplex virus (HSV), usually type 2 (HSV-2) and enterovirus such as echovirus and coxsackievirus which tend to reside in the digestive tract can infect the layers of the tissue that covers the brain and spinal cord, causing meningitis.
Many prominent childhood- and adult-onset neurological and psychiatric diseases are hypothesized to be due to infections by viruses such as the herpes virus and Cytomegalovirus (CMV) that occurred at a much younger age. CMV causes chickenpox, herpes simplex, and mononucleosis and it is a common virus for people of all ages. Once infected, your body retains the virus for life. A healthy person's immune system usually keeps the virus from causing illness. However, in an unhealthy person, it can cause many neurological diseases which include Alzheimer’s disease, Parkinson’s disease, multiple sclerosis, temporal lobe epilepsy, schizophrenia, bipolar disorder, and autism.
Many arenaviruses, such as lymphocytic choriomeningitis virus (LCMV), which is a rodent-borne virus, do not kill host cells but instead cause a persistent infection if the host immune system cannot clear the virus. LCMV which can cause neurological diseases is transmitted when exposed to fresh urine, droppings, saliva, or nesting materials from infected rodents such as mice which are the natural host and principal reservoir of LCMV. A much more severe disease ensues when the infection occurs prenatally. LCMV can infect the fetal brain and retina, where it leads to substantial injury and permanent dysfunction.
Central nervous system (CNS) complications of Epstein-Barr virus (EBV) infection occur in 1 to 18% of patients with infectious mononucleosis and include encephalitis, meningitis, cerebellitis, polyradiculomyelitis, transverse myelitis, cranial and peripheral neuropathies, and psychiatric abnormalities.6 EBV may also exist in a latent state within the nervous system and reactivation of a latent virus can invade the CNS and cause myelopathic syndromes such as multiple sclerosis.7
Chronic Fatigue
Although it is hard to pin down the exact cause of chronic fatigue syndrome (CFS), researchers have long believed that many cases are caused by an active viral infection or by an infection that permanently alters the immune system before leaving the body. This is because the bodies of patients who suffer from CFS show signs of an activated immune system. A 2010 study linked enterovirus and EBV as two of the most common infectious triggers of CFS.4
Human herpes viruses including EBV, which infects over 90% of the world population, has also been linked to CFS. Although B and T cells are supposed to help keep the virus at bay when it is reactivated, studies have found that both cell types were unable to remember EBV.2,6 This means that when reactivated, the virus would be able to thrive, reproduce, and cause symptoms such as chronic fatigue. Of the 400 participants in the study, 76% of them had impaired cellular memory in their immune system.2
Enterovirus, which live and reproduce in the intestinal tract, has also been linked to CFS. It is now understood that enterovirus B serotypes such as coxsackievirus B and echovirus are capable of mutating during the acute infection into an aberrant viral form called non-cytolytic enterovirus that can cause persistent low-level infections. These persistent non-cytolytic enterovirus infections deriving from mutated enterovirus B serotypes are found in CFS. There have also been over 30 studies on enterovirus infections in CFS and most of the studies have found enterovirus present in CFS patients’ muscle, stomach, brain tissues, and blood cells.
Depression and Anxiety
Viral latency in the nervous system which can later be activated has been shown to cause cognitive and behavioral disturbances. Human herpesvirus when active has been shown to provide molecular evidence of causing major depression disorder.
Human herpesvirus type 6 (HHV6) is the virus that causes Roseola infantus, also called exanthema subitum, which is a common infectious disease in infants. Roseola is generally mild infection with symptoms including several days of high fever, followed by a rash which may appear as many small pink spots. Almost all people are infected during their infancy, and after that, they carry the latent virus in their bodies. Normally, the virus remains dormant, but when the body is fatigued, HHV6 is awakened and is present in saliva to escape from the weakening host.3 Some of the virus reaches and infects the olfactory bulb, the center in the brain connected to the sense of smell, by flowing up from the mouth to the nose.3 A research team determined that if reinfection occurs, a certain protein, SITH1, are produced in the olfactory bulb.3 By their production, excessive calcium flows into brain cells and kill them. The result of this leads to the development of depression.
If the patient is experiencing anxiety and depression symptoms not related to a viral infection, please see the Stress, Depression, and Anxiety Protocol for a wellness recommendation.
Olfactory Issues
Although major symptoms are primarily generated from the respiratory system, neurological symptoms are also being reported in some confirmed cases of COVID-19. The potential for significant neurological deficits recently became a concern following the report of a COVID-19 patient who demonstrated loss of involuntary control of breathing due to presumed involvement of the inspiratory area in the brainstem, as well as reports of SARS-CoV-2 infected patients developing ataxia, loss of smell, and convulsions.8
SARS-CoV-2, the coronavirus that causes COVID-19, binds to a protein called ACE2 that’s found on the surface of potential host cells. ACE2 is abundant on cells found in the nose and mouth. Researchers have found ACE2 on cells that surround and support nerve cells that detect scents.1 It’s possible that infection of these surrounding cells could lead to levels of inflammation or damage that impact the ability to smell and therefore taste.1 This inflammation can persist even after the patient tests negative for COVID-19 leading to prolonged symptoms of loss of taste and smell.
Several routes have been proposed for coronaviruses gaining access to the CNS. In a study done on mice, SARS-CoV seems to enter the brain via the olfactory bulb post intranasal inoculation before disseminating transneuronally to distal connected neurons.8
If the patient is experiencing other symptoms such as fever, shortness of breath, coughing, or other COVID-19 related symptoms, please refer to the COVID-19 Protocol for a wellness recommendation.
