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J Gen Virol 71 (1990), 1399-1402; DOI 10.1099/0022-1317-71-6-1399
© 1990 Society for General Microbiology

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Persistence of enteroviral RNA in chronic fatigue syndrome is associated with the abnormal production of equal amounts of positive and negative strands of enteroviral RNA

Louise Cunningham1, N. E. Bowles1,{dagger}, R. J. M. Lane2, V. Dubowitz3 and L. C. Archard1

1 Department of Biochemistry, Charing Cross and Westminster Medical School, St Dunstan's Road, London W6 8RF
2 Regional Neurosciences Centre, Charing Cross Hospital (Fulham), Fulham Palace Road, London W6 8RF
and3 Department of Paediatrics, Royal Postgraduate Medical School, Hammersmith Hospital, Du Cane Road, London W12 0HS, U.K.

A subgenomic restriction fragment from cDNA prepared from Coxsackie B2 virus (CVB2) RNA was subcloned into a riboprobe vector allowing the production of enteroviral group-specific RNA probes complementary to either the positive (genomic) or negative (template) strand of enteroviral RNA. These riboprobes were used to follow productive infection of cultured cells by CVB2; as expected, positive strand RNA was synthesized in approximately 100-fold excess over negative strand. RNA was extracted from muscle biopsy samples from patients with chronic fatigue syndrome and probed for the presence of enteroviral RNA. In cases where enteroviral RNA was detected the amounts of positive and negative strands of enteroviral RNA were approximately equal, in contrast to the situation in lytic infection of cultured cells. This suggests that entrovirus pesistence in muscle is due to a defect in control of viral RNA synthesis.

{dagger} Present address: Département de Biologie Moléculaire, Université de Genève, Sciences II, 30 Quai Ernest Ansermet, CH-1211 Genève 4, Switzerland.

Received 6 November 1989; accepted 13 February 1990.


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