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Rapid Responses: Rapid Responses published:
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Which herpes virus is to blame?
- Marian J. Nicholson (13 January 2006)
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Other B viruses
- Oliver R Dearlove (15 January 2006)
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Cerebral palsy and perinatal exposure to neurotropic viruses
- Stephanie S Thomas, Ken Mutton, Paul Klapper (24 February 2006)
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Marian J. Nicholson, director Herpes Viruses Association, 41 North Road, London N7 9DP
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Editor, Unfortunately, Catherine Gibson et al have chosen their own classification for herpesviruses (into groups ‘A’ and ‘B’) and have allocated viruses to these group in a different pattern to the accepted classification of ‘alpha’, ‘beta’ and ‘gamma’.(1) This has confused the media because cytomegalovirus (CMV), the virus shown to be most frequently implicated in causing cerebral palsy, is a beta virus, not an ‘A’ virus as in the Australian study. Patients with genital herpes (an alpha virus) have been needlessly alarmed by sloppy reporting of study, which was made almost inevitable by the bizarre Australian reclassification. The abstract is written in a way that allows even dedicated medical correspondents to become confused so that chickenpox (an alpha herpes virus allocated to their ‘B’ group) is also being blamed for causing cerebral palsy. As chickenpox is so common a large number of people will be needless alarmed. Since 6th January, we have receive headlines from around the world showing the muddle this report has created. Marian Nicholson
(1) http://www.ihmf.org/general/HerpesVir.asp Competing interests: None declared |
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Oliver R Dearlove, Consultant Anaesthetist Manchester
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A confused doctor writes; I was one of the readers confused by the media releases on this piece of research. The news reports tantalisingly told us that herpes group B viruses were implicated in cerebral palsy. There is yet another B Virus which is not associated with this piece of research, and that is the monkey B virus (1). If a reader googles Herpes B then papers on this animal virus will show up. It is a dermatropic virus causing a cold sore like eruption in monkeys (macaque, old world monkeys). It cross reacts with oral herpes virus antisera (2), and is neurotropic in man causing an unpleasant encephalomyelitis. Work was commissioned on this in the seventies as B virus shows latency (3) and there were fears that vaccines made from monkey kidney cells could be infected. This is clearly not the virus in this paper but at least I picked up the BMJ this week with far more surprise and enthusiasm than normal. It may be worth a clarification. Oliver Dearlove Refs 1. Holmes GP et al Guidelines and prevention of B virus infection in exposed persons Clin Inf Dis 1995 20 421-439 2. Vizoso AD letter; Simian viruses Lancet 1975 1037 3. Vizoso AD Latency of Herpes Simiae B virus in rabbits Br J Exp Path 1975 489-494 Competing interests: None declared |
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Stephanie S Thomas, Specialist Registrar in Virology Department of Virology, Manchester Royal Infirmary, Oxford Road, Manchester M13 9WL., Ken Mutton, Paul Klapper
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We read with interest the recent report of a high rate of congenital virus infection in cerebral palsy (1). High rates of human cytomegalovirus were reported in newborns (26.7% in controls, 27.7% in cerebral palsy). However, active surveillance for congenital CMV in Australia suggests a far lower rate of 0.6%(2). A recent Italian study (3) using dry blood spots also showed little congenital CMV (0.18%), suggesting the wide gap between the data of Barbi et al and Gibson et al was not due to enhanced case ascertainment. For HSV the rate observed by Gibson et al (1) (4.3% in controls and 3.1% in cerebral palsy), is very different to previous data. Baldwin and Whitley (4) suggest a rate of intrauterine HSV infection of 1/300,000 live births/year. Previous Guthrie card testing shows that infants who suffer perinatally acquired HSV infections may not have DNAaemia at the time of sampling (circa. 3 days post-natally)(5). Thus, even if the data presented by Gibson et al.(1) includes intrauterine and postnatal HSV infections, rates are discrepant from previous studies. The methodological description prevents the reader from evaluating possible confounders of Guthrie card analysis. Contamination of samples when excising blood spots from the card may occur(5) and there is the possibility of cross-contamination of negative cards by adjacent positives(5). Without such information evaluation is difficult. While systematic study of blood spots may be expected to yield higher numbers than just observation of symptomatic cases, the data presented does not concur with previous studies using similar analytical techniques. Gibson et al.(1) fail to comment upon the differences in observed versus expected rates. Missing methodology and a lack of percentage data in the cerebral palsy group make the study difficult to evaluate. The data as presented do not suggest a strong causal link. References 1.Gibson CS, Maclennan AH, Goldwater PN, Haan EA, Priest K, Dekker GA. Neurotropic viruses and cerebral palsy: population based case-control study. BMJ 2006;332:76-9 2.Munro SC, Trincado D, Hall B, Rawlinson W. Symptomatic infant characteristics of congenital cytomegalovirus disease in Australia. J. Paediatr.Child Health.2005;41:449-452 3.Barbi M, Binda A, Caproppo S, Calvario A, Germinario C Bozzi A et al. Multicity Italian Study of Congenital Cytomegalovirus Infection. Pediatr. Infect Dis J. 2006;25:156-159 4.Baldwin S, Whitley R. Teratogen Update: Intrauterine Herpes Simplex Virus Infection. Teratology 1989;39:1-10 5.Lewensohn-Fuchs I, Osterwall P, Forsgren M, Malm G. Detection of herpes simplex virus DNA in dried blood spots making a retrospective diagnosis possible. J. Clin. Virology. 2003;26:39-48 Competing interests: None declared |
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