Longitudinal study of genital infection by herpes simplex virus type 1 in western Scotland over 15 years

EDITOR--Scoular et al describe the rising incidence of herpes simplex
virus type 1 (HSV-1) as the cause of genital infections for the years 1986
to 2000, with predominance in the young and female sex, together with
differences in recurrence rates, subclinical shedding and mode of
infection as compared to HSV-2.[1] The article lacks serological
confirmation. Genital strains (HSV-2) were first isolated by egg embryo
inoculation experiments performed by myself, demonstrating large pock
size by growth in incubators used for gonococcal cultures in the Venereal
Diseases Department of St Mary's Hospital, Paddington, in 1962.[2]
Subsequently these were found to exhibit serological differences, as a
result of further research,[3] finally culminating in isolation from the
cervix of a genital strain (HSV-2), mimicking carcinoma cell changes for
the first time.[4] The venereal transmission of genital strains (HSV-2)
was then described for the first time.[5] With the rise in incidence of
AIDS and HIV infections over the same time span, 1986 to 2000, coupled
with the increased use of condoms and other preventive measures, venereal
transmission has been blocked in favour of HSV-1 auto-inoculation with
recurrences.

The majority of patients, or 72% as described by Scoular et al,[1] were
from the venereal disease clinic; likewise a series of 100 patients
investigated by Hutfield et al were also from the venereal diseases
department and had an average age of 27.4 years (range 18 to 54).[3] The
number testing positive to complement fixing antibodies or HSV-1 was 49%,
or the same as quoted by Scoular et al.[1] The number testing positive to
neutralizing antibodies prepared from a genital strain (HSV-2) was 81%,
whereas Scoular et al quote 51% for HSV-2,[1] or a drop of 30%. In effect
the number testing positive to HSV-1, or 49%, has remained the same over a
period of 33 years-ie, 1967-2000¾whereas the number testing positive to
HSV-2 has dropped by 30% over the same period. Also in their investigation
Hutfield et al found the incidence of subclinical recurrences in female
genital tracts to be less than 1%,[3] or in line with Scoular et al. In a
survey of 140 cases of herpes genitalis 39.3% were prone to recurrences,
and not due to orogenital transmission. Since 10 male cases are seem to
every female case, then the majority of cases are recurrent attacks
associated with the trauma of intercourse.

Finally, the reasons for the high female infection rate can be found in
the world's largest clinical description to be written on herpes
genitalis, which cites menstruation, vulvo vaginitis caused by sexually
transmitted disease, cystitis, trauma of intercourse in relation to
virginity, stress and psychosomatic disorders and the neuralgic herpes of
Mauriac, which act as trigger mechanisms.[2] [5] My publication and
research can, therefore supply the answer to queries raised by Scoular et
al, since my assays, isolations and titres are now used in medical
laboratories worldwide and described in the centennial edition of the
Merck manual.

David C Hutfield M.D. (Hons.) Lond.

Consultant Physician in Venereology to the European Union R.C.P.

Emeritus Consultant in Venereology, Manchester Royal Infirmary.

Honorary Lecturer in Venereology, University of Manchester.

1. Scoular A, Norrie J, Gillespie, G, Noreen M, Carman WF.
Longitudinal study of genital infection by Herpes simplex virus type 1
in Western Scotland over 15 years.
BMJ 2002 324, 1366-7 (8 June).

2. Hutfield, D.C. Herpes genitalis M.D. thesis (1962) University of
London.

3. Hutfield, D.C., Wasley, G.D., Gray, E. Immunological and
epidemiological
investigations of genital strains of the herpes simplex virus. Brit J.
Vener Dis (1967) 43. 48-52.

4. Hutfield, D.C. Herpes simplex cervicitis (1968) BMJ 1.560.

5. Hutfield, D.C. Herpes genitalis as a venereal disease. Brit J Hosp
Med (1970) 881.4.