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