My model of CFS is that is the result of a stable dysfunction in microbiome after an illness or other event (which can include inoculations, stress, etc). The short answer is that the microbiome change caused by the illness stayed, and with it, many of the symptoms of the illness. This implies that many symptoms are the result of the microbiome changes and NOT directly connected to the infection.
I thought a quick review of the literature on PIDS would be informative. A good summary from 1988, is a smart place to start.
“Many post-infectious syndromes have been recognized in the last 50 years [from 1938!], some following viral infections and others closely related to bacterial disease. The occurrence of prolonged fatigue following an apparent viral illness of varying severity is also well documented. The lack of a recognizable precipitating cause and the tendency for epidemic fatigue to occur among hospital staff led many to believe that the illness may be psychogenic in origin.” It cites mononucleosis (Epstein-Barr virus) and enterovirus“
A related article entitled Post-Infectious Fatigue was published in 1987, which writes
“In most cases the illness is attributed to a chronic Epstein-Barr virus infection. Symptoms include weakness and fatigue in the absence of physical findings or significant laboratory abnormalities. These patients are frequently depressed and have considerable disability resulting in prolonged loss of time from work. The illness may be persistent or can be relapsing, but often lingers for two years or more. There is no effective therapy.”
Jumping ahead to 1998, we find “Post-infection fatigue syndrome following Q fever“,
“In summary, we conclude that a syndrome characterized by undue fatigue, breathlessness on exertion, excessive sweating and blurring of vision occurs after infection by Coxiella burnetii, and that these symptoms persist for many years. The mechanism for this effect remains elusive, but possibilities such as sub-clinical cardiomyopathy or autonomic dysfunction need to be tested using this unique cohort of patients.”
Post-infectious irritable bowel syndrome (PI-IBS) may develop in 4 – 31 % of affected patients following bacterial gastroenteritis (GE), symptoms persist after successful treatment in some for months as shown below taken from this 2005 article. Note that at 1 year, there are some still showing symptoms.
- irritable bowel syndrome (39.4%) by Rome III criteria – Relative risk to matched population 3.4 times as likely
- chronic fatigue (30.8%) in the exposed group – Relative risk to matched population 2.9 times as likely
As time went on from 3 years to 6 years:
- the prevalence of irritable bowel syndrome decreased by 6.7%
the prevalence of chronic fatigue decreased by 15.3%
“Development of IBS in a subset of patients with acute gastroenteritis is uncontested. This is expected to open a paradigm shift in understanding the pathogenesis of IBS.” 
The mechanism for Post-Infection Fatigue has traditionally been not understood by the medical establishment. There is growing evidence that it is a slow (or never) return from a shifted microbiome caused by a disease, vaccination, antibiotic, stress, etc (and I mean and so forth — the list goes on and on) that may be the cause.
“A growing body of work provides evidence supporting a role for pathogen-mediated modifications in the resident intestinal microbiota, epithelial barrier integrity, effector cell functions, and innate and adaptive immune features, all proposed physiological manifestations that can underlie GI abnormalities in IBS.” 
Or as this title states, Redefining the gut as the motor of critical illness.