You picked an interesting virus (and illness) to ask about. There are still a lot of studies being conducted and many of the answers aren't in.
A bit of background. Epstein-Barr virus (EBV - the virus that causes infectious mononucleosis) is a member of the herpesvirus family, very "successful" viruses in that most of the world's population are infected (90% of the world's population has been infected with EBV), and the viruses are known to remain in the host's body throughout their lifetimes (that is, the host doesn't usually die from the disease, instead living to pass it on to others). With Herpes Simplex, reactivation is in the form of cold sores. With varicella-zoster virus - the cause of chickenpox - reactivation takes the form of "shingles". So, to expect EBV of periodic reactivation isn't very far fetched.
In the US, ~50% of the population seroconverts (becomes infected as manifested by antibodies to the virus) before 5 years of age. This population has not been extensively studied for asymptomatic viral shedding. In the rest of the population, most cases of EBV infection are still subclinical, but some adolescents and young adults - about 25% of those newly infected - get the illness known as infectious mononucleosis (IM). This has been the group most studied group in terms of who is shedding virus and who isn't.
Once infected, humans carry the virus for life in a small number of white blood cells called "memory B lymphocytes". Immediately following infection, the cells shedding the most virus are pharyngeal epithelial cells (though this has been challenged), so virus is present in the saliva, but has also been found in other bodily fluids.
One study in France followed 30 patients for 6 months: 20 after diagnosis of IM, and 10 healthy EBV carriers (determined by the presence of IgG antibodies against EBV and the absence of IgM) as controls. Blood and saliva samples were collected at day 0 [D0]), D3, D7, D15, D30, D60, D90, and D180 on all subjects.
Infectivity of saliva was determined by lymphocyte transformation in cell cultures of fresh cord-blood lymphocytes.
All newly infected patients had sustained viral shedding in the saliva, and all still had infectious saliva at day 180, 16 patients maintaining a high EBV load during the 6 months of follow-up, and 4 showing a low level of virus, though viral load was significantly lower at D180 than at D90 in all patients. Of the controls (healthy people who had positive antibodies), 8 subjects had 2–4 episodes of detectable EBV in their saliva, with the remaining 2 having no EBV in their saliva during the follow-up period.
In the patient blood samples, EBV-infected B cells decreased significantly from day 0 to day 180, with 18 showing a viral rebound between D30 and D90. Among these 18, 4 patients had tonsillitis and lymphadenopathy (!) which indicates a recurrence. Only one of the control subjects showed no detectable EBV in their Memory B Cells during the entire follow-up period. This shows that patients with IM remain highly infectious during convalescence.
A Japanese study analyzed the prevalence of EBV in saliva and throat washings from healthy people. EBV DNA was detected in 43 of 48 throat washings from healthy adults aged 21 to 57 years of age, and in 35 of 93 salivas from healthy children 0 to 6 years old. Umbilical cord lymphocytes were transformed by some throat washings from EBV seropositive donors, indicating infectivity of the virus. Furthermore, EBV DNA was detected in throat washings from 2 healthy adults whose EBV antibody was not detected.
In a study of 22 healthy EBV-seropositive blood donors over a period of 15 months, serology suggested reactivation (significant changes in viral load plus a serological response) in eight donors. Another five individuals also exhibited significant changes in viral load but no serologic response. Of the 13 volunteers with significant increases in viral load, 6 had a period of viremia accompanying the rise in viral load, that is, they had a viral infection clinically.
What triggers reactivation in healthy subjects is not known precisely. The presumption is that it occurs when latently infected B cells respond to unrelated infections, because B-cell receptor stimulation triggers reactivation in B-cell lines.
So, whatever you have read, there is probably proof for it, as well as much else that wasn't read! It appears that healthy adults and children shed virus intermittently for an unknown number of years.
Image from On the dynamics of acute EBV infection and the pathogenesis of infectious mononucleosis, Hadinoto et al, Blood. 2008 Feb 1; 111(3): 1420–1427.
Progress and Problems in Understanding and Managing Primary Epstein-Barr Virus Infections
Long-Term Shedding of Infectious Epstein-Barr Virus after Infectious
Detection of Epstein-Barr virus in salivas and throat washings in healthy adults and children
Molecular Parameters for Precise Diagnosis of Asymptomatic Epstein-Barr Virus Reactivation in Healthy Carriers
On the dynamics of acute EBV infection and the pathogenesis of infectious mononucleosis