Why does mono cause fatigue

That decades-long emphasis on cognitive behavioral therapy meant that promising areas of research were underfunded, Chu said, including immunological, neurological, infection-related and metabolic research. The CDC says that between , and 2. The research team is continuing to evaluate the patients, six years after the initial group joined the study. Deficiencies in certain proteins known as cytokines may suggested "predisposing irregularities in immune response," the researchers reported.

They plan to analyze these cytokine networks in participants' blood. Kissing the Epstein-Barr virus goodbye? Updated June 24, Epstein-Barr: Scientists decode secrets of a very common virus that can cause cancer. Published December 15, Centers for Disease Control and Prevention. Reviewed March 19, Infectious mononucleosis in university students in the United Kingdom: evaluation of the clinical features and consequences of the disease. Clin Infect Dis. Your Privacy Rights. To change or withdraw your consent choices for VerywellHealth.

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Sign Up. Was this page helpful? Thanks for your feedback! A diagnosis of mononucleosis is usually based on reported symptoms. However, diagnosis can be confirmed with specific blood tests and other lab tests, including:. White blood cell count, which is not diagnostic, but the presence of certain types of white blood cells lymphocytes may support the diagnosis. Heterophile antibody test or monospot test, which, if positive, indicates infectious mononucleosis.

Avoid kissing or sharing dishes, food utensils, or personal items with anyone who has the infection. Symptoms may include fever, swollen lymph glands in the neck, armpits, and groin, constant fatigue, sore throat, enlarged spleen, and jaundice, a yellow discoloration of the skin.

Health Home Conditions and Diseases. What causes infectious mononucleosis? What are the symptoms of infectious mononucleosis?

Of particular interest, the first reported cohort study showed that neither premorbid mood disorder nor recent stressful life events predicted post-IM CFS, once comorbid mood disorder had been controlled for [ 12 ]. By contrast, these same factors did predict depressive illness after IM, reinforcing the contrast with mood disorders.

Predictiors of prolonged fatigue 6 months after onset were early positivity for heterophil antibody and evidence of physical deconditioning 4 months earlier. There were no significant associations with any other immune response to EBV [ 11 , 12 ]. No other cohort has shown convincing associations with the immune response to EBV [ 5 , 13 ]. Lloyd and colleagues in Australia have collaborated with Reeves and colleagues at the Centers for Disease Control and Prevention, and this has led to a cohort study of not 1 but 3 high-risk infections: IM, Q fever, and Ross River virus infection.

The population was based around Dubbo, a rural area in Australia. This work has already shown that the risk of CFS is about the same in all 3 cohorts, with some 1 in 10 going on to develop CFS [ 5 ]. The to-date limited evidence base for significant predictors and associations is unlikely to be related to the apparent heterogeneity of CFS, because at most there are only 2 apparent phenotypic illnesses of prolonged fatigue after IM [ 8 , 9 ]. It is more likely related to looking for the wrong risk factor over the wrong time scale.

These problems may be overcome by the method used by Cameron et al. Cameron and colleagues used a nested case-control study from the Dubbo cohort of EBV-infected people to examine gene expression over time, seeking associations and predictions in those patients with prolonged fatigue. The study was innovative and may provide a means of understanding the pathophysiology of complex syndromes such as postinfectious fatigue syndrome. The authors found 35 genes that were abnormally expressed over time in those with prolonged disabling fatigue.

More genes were found to be associated with fatigue and separately with musculoskeletal pain. The genes identified had no obviously coherent pattern of functions, but some genes were related to signal transduction pathways, metal ion binding, and ion channel activity. No consistent target tissue was identified. Although cluster analysis was reasonably accurate in differentiating case from control subjects soon after infectious onset, no differentiation was possible 6 months after onset.

The strengths of the study include its longitudinal cohort design and repeated measures. Although none of the identified genes had previously been found in gene expression studies of CFS, this may be because of the heterogeneity of CFS [ 15 ]. The authors acknowledge this but point out that there was a pattern in the genes found in that they are important in immune response and neuronal function. The weaknesses of the study include the small number of subjects with type I errors likely , the lack of matching by sex, and the lack of validation by real-time polymerase chain reaction analysis of messenger RNA.

We cannot be sure that gene expression in lymphocytes reflects gene expression in other tissues, such as the brain.