Skip to main content

Table 3 Possible viral contributions towards ME/CFS

From: Chronic viral infections in myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS)

Viruses Contribution in ME/CFS
Human herpesviruses Persist after primary infection in latent phase and can reactivate causing lytic virus replication
Infected cells are recognized by immune system resulting in chronic inflammation that causes ME/CFS symptoms
Disturb first class major histocompatibility complex (MHC) molecules presenting virus antigen
Alter NK, T and B cell function
Modify expression of cellular transcripts
Trigger immune dysregulation
Alter cytokine production resulting in appearance of ME/CFS typical symptoms
Contribute in affecting signalling pathways to proper immune response
Activate humoral immune response by herpesviruses-encoded dUTPases
Infect neurons and immune cells to impair CNS capillaries and micro-arteries, leading to brain damage
Produce a pro-inflammatory environment and autoimmune activity
Damage tissue, leads to inflammation and may activate auto-reactive T and B cells, thereby contributing to autoimmunity
Local virus-associated inflammation of nervous structures results in altered CNS and PNS signalling
Alter ATP homeostasis, increase ROS, change mitochondrial metabolism and modulate mitochondrial DNA content
Enteroviruses Infect various tissue (blood, gastric, muscle, brain) and stool
Persistence of viral RNA could contribute to muscle dysfunction
Induce tissue damage
Dysregulate host microRNAs
Induce greater oxidative stress, inflammation, and pro-inflammatory M1 macrophage activity
Induced inflammation can result in bystander activation of auto-reactive cells
Coxsackie B4 virus infects beta cells leading to NK cell induced non-destructive inflammation
Severe acute enterovirus 71 infection diminishes number of NK and T cells and induces ROS accumulation
Parvovirus B19 After primary infection and acute phase can establish persistent infection and lead to the manifestation of ME/CFS
Interacts directly with cells leading to a more aggressive fibroblast function and degradation of cartilage matrix
Active infection is linked to an increased frequency of joint pain
VP1 protein affects arachidonic acid metabolism promoting inflammatory reactions
NS1 protein stimulates pro-inflammatory cytokines production causing local inflammation
Activates NK cells
Causes neuroinflammation
Contributes to greater expression of the human CFS-associated genes NHLH1 and GABPA
May induce autoimmunity
Retroviruses No contribution
Ross-River virus Infect macrophages using antibody-dependent enhancement mechanism
Suppresses transcription and translation of antiviral genes
Generate neurocognitive manifestations affected by functional polymorphisms in cytokine genes
Cause joint pain, persistent tiredness, lethargy, myalgia, lymphadenopathy, headache and depression