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Prolonged illness after infectious mononucleosisis associated with altered immunity but not increased viral load
Cameron B, Bharadwaj M, Burrows J, Fazou C, Wakefield D, Hickie I, FFfench R, Khanna R, Lloyd A
Prolonged illness after infectious mononucleosisis associated with altered immunity but not increased viral load.
Journal of Infectious Diseases 193:664-671, 2006.
Summary
This is another of the post-infectious fatigue studies conducted in collaboration with the group from the University of New South Wales. This manuscript involves 8 persons who did not improve following acute EBV-positive infectious mononucleosis and 31 matched controls who suffered acute infectious mononucleosis but had completely recovered within 6-months. The objective was to determine whether control of the virus EBV or dynamics of the immune response predicted development of CFS. Thus, development of CFS following infectious mononucleosis in previously health adults cannot be readily explained by differences in amount of virus or by alterations in immune response to the virus.
Abstract
Background. Primary Epstein-Barr virus (EBV) infection causes a spectrum of characteristics that range from asymptomatic seroconversion to severe infectious mononucleosis (IM), sometimes with prolonged symptoms and disability. We examined the relationships between clinical course, number of viral copies, and immunological parameters in a prospective cohort of subjects with recent IM.
Methods. Eight case patients with at least 6 months of disabling symptoms and 31 matched control subjects who had recovered promptly were included. Symptom scores were recorded at regular intervals over the course of 12 months. Cellular EBV load, EBV-specific antibody responses, lymphocyte subsets, and EBV-specific interferon (IFN)– g induction were measured.
Results. In case patients with prolonged illness, the severity of acute-phase symptoms was greater, the development of anti–EBV nuclear antigen–1 immunoglobulin G was more rapid, and the time to development of the peak IFN- g response to the majority of latent-cycle EBV peptides was generally slower than those in control subjects. However, in both groups, neither viral nor immune parameters correlated with the severity or duration of symptoms.
Conclusions. The resolution of symptomatic IM is not determined by control of viremia, nor is it easily explained by altered host responses to EBV infection. The detailed determinants of delayed recovery remain to be elucidated.
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