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.
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 enterovirus persistence in muscle is due to a defect in control of viral RNA synthesis.
Cunningham
L
L
Department of Biochemistry, Charing Cross and Westminster Medical School, London, U.K.
Bowles
N E
NE
Lane
R J
RJ
Dubowitz
V
V
Archard
L C
LC
D000818:Animals; D002460:Cell Line; D003673:Defective Viruses / Q000235:genetics / Q000378:metabolism; D029822:Enterovirus B, Human / Q000235:genetics / Q000378:metabolism*; D015673:Fatigue Syndrome, Chronic / Q000382:microbiology*; D005814:Genes, Viral; D006801:Humans; D009132:Muscles / Q000382:microbiology*; D015347:RNA Probes; D012367:RNA, Viral / Q000032:analysis / Q000096:biosynthesis*; D013698:Templates, Genetic
D015347:RNA Probes; D012367:RNA, Viral