Dr Jonathan Kerr

 Jonathan Kerr qualified in medicine from Queen’s University of Belfast (1987), and completed training as a medical microbiologist (1995).

He has worked as a microbiologist in Belfast, Manchester and London, taking up post as a Consultant Senior Lecturer in Microbiology at Royal Brompton Hospital / Imperial College in June 2001, and then Sir Joseph Hotung Clinical Senior Lecturer in Inflammation at St George’s University of London in 2005.

His interest in Chronic Fatigue Syndrome (CFS) began during a study of the consequences of parvovirus B19 infection, when he showed that a percentage of infected cases developed CFS which persisted for several years.

He is now the principal investigator in a programme of research in CFS. This involves development of a diagnostic test using mass spectrometry, analysis of human and viral gene expression in the white blood cells, and clinical trials of immunomodulatory drugs.

Dr. Jonathan Kerr and colleagues at St. George’s University of London reported in the July 27, 2005 issue of the Journal of Clinical Pathology that a preliminary study of 25 CFS patients and 25 matched healthy controls revealed abnormalities in 35 of 9,522 genes analyzed using microarray technology. Polymerase chain reaction studies showed the same results for 16 of these genes.

The study, and its results, raises some important questions. The first of which pertains to the need for funding of microbiological CFS research. He is funded (>£1million) by the CFS Research Foundation  a charitable organization based in the U.K., and leads a group of 5 scientists at St George's.

His research on gene expression has resulted in several published papers – including evidence of 7 distinct sub types of ME/CFS. Dr. Kerr also runs a ME/CFS research program. He studied the consequences of parvovirus B19 infection in ME/CFS and showed that a percentage of infected cases developed ME/CFS which persisted for several years. He has reported 88 human genes whose dysregulation is associated with CFS, and which can be used to derive genomic CFS subtypes which have marked differences in clinical phenotype and severity.

The Foundation needs private support to continue their research efforts. They also openly post the results of their efforts on their website