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apparently out of the blue, but also viruses which arealtered slightly but just enough to guarantee survival.Other things not understood about influenza are why anepidemic comes to an end when so many people remainstill open to infection, what happens to the virus in theintervals before its reappearance the next winter, andwhat happens to the old viruses when new variantsbegin to circulate. Do they indeed disappear for ever? Itwas thought they did until the H1N1 virus from theearly 1950s reappeared unexpectedly in 1977. The puz-zles are many, and so far no one has produced a satisfy-ing hypothesis to link all these odd features.Dr R. E. Hope-Simpson has been brooding over these

matters for many years and has lately published hisideas on how to explain many of these facets of in-fluenza epidemiology. He is in a better position thanmost to indulge in this game since over a long period hehad a stable population in his clinical care and he alsohad the support of a laboratory with a skilled virologist.His observations have been directed, firstly, to a com-parison of the sort of variant viruses found locally in hisarea with those detected nationally and, secondly, to fol-lowing the spread of influenza in the family setting. Heis not the only one to have noticed that influenza doesnot seem to spread nearly as effectively in the home ashad been supposed of a disease which in its pandemicform has no difficulty in getting round the world in amatter of months. From his findings he concludes thatdirect spread is not the way by which influenza is main-tained in the community and there must be anothermechanism.

Hope-Simpson’s hypothesis is that the key lies in

latency. Influenza A virus, having caused an influenzalillness, would rapidly become latent somewhere in theaffected human host and undetectable by current

methods. A subsequent stimulus, possibly related to sea-sonal variation in solar radiation, would then activatethis latent virus, and the host, while remaining symp-tom-free himself, would become highly infectious to hisnon-immune contacts. Thus in an epidemic, the victimswould consist largely of persons infected from symptom-less carriers, with the sick not infecting their non-immune contacts. The virus would always differ fromthe original infecting virus because the immune state ofthe host would have induced antigenic drift and thecharacter of this drifted variant would tend to be thesame, the same progenitor shedding the same assortmentof mutants from which the non-immune contacts selectthe fittest to survive and continue the species.

This hypothesis has some attractive features despitethe lack of direct evidence that influenza virus can belatent in man. One can only speculate about the way aseasonal factor might spark off reactivation. How wouldthe carrier host spread the virus? There would surelyhave to be some coughing and sneezing to help the viruson its way, yet he is presumed to be symptom-free; andthe lack of spread in the home may reflect the abun-dance of space per person, since in a boarding school ormilitary camp the virus spreads very efficiently. But ifwe are unable to accept latency as a valid concept, muchcareful surveillance will be necessary to demonstrate thealternative-that virus spread goes on all the time, at

1. Hope-Simpson RE. Epidemic mechanisms of type A influenza. Hyg 1979;83: 11-26.

such a low level between epidemics that it escapes detec-tion. The reappearance of the influenza H1N1 sub-typein 1977 and the careful monitoring of its behaviour overthe next few years may yield some of the evidence stillneeded to show how influenza really survives so effi-

ciently in the world.

AUTOIMMUNE SENSORINEURAL HEARING LOSS

McCabe’ has reported eighteen cases of a rare formof inner-ear disease seen in his Iowa clinic during thepast ten years. This clinical picture is variable but a

diagnostic pattern has emerged. The patient tends to bea man aged about twenty-five, who complains of grad-ually increasing loss of hearing, severe in one ear and atfirst only slight in the other. About a month after theonset a facial palsy may develop on the deafer side andpersist for two months or more while the hearing con-tinues to deteriorate in both ears. The disease is bilater-

al, though asymmetrical, and always involves the hear-ing, with localising signs pointing to the end-organs.Vestibular function is involved as well, but symmetri-cally, so that vertigo is not a feature of the disease;ataxia in the dark has been noted. Tissue destruction ofthe tympanic membrane, middle ear, and mastoid hasbeen observed in a few patients.

Extensive investigations and exhaustive laboratorytests have yielded largely negative results. The time-cQurse of the hearing loss is perhaps the best clue todiagnosis. The disease differs from other causes of pro-gressive sensorineural deafness in that it is eitherquicker or slower in its development. Thus the "sudden"deafness with which we are all much more familiaroccurs over minutes or hours whereas this condition

progresses over weeks or months. Unlike cochlearMeniere’s disease which is both sudden and fluctuating,this disease is insidious and progresses slowly withoutremission. Chronic progressive deafness of adolescenceand presenile presbyacusis are seen in younger and olderpeople, respectively; and in both the progress of thehearing loss is very much slower.

This disease warrants separate identification becauseit is one of -the few forms of sensorineural deafnesswhich respond to treatment. A vasculitis consistent withautoimmune disease was present in the one patient fromwhom tissue could be obtained for histological examina-tion. The presence of autoimmune disease in this smallseries is thus far from being established, yet McCabe’ssuspicion is warranted and supported by his experiencethat all patients responded to a long course of cortisoneand cyclophosphamide.

RECURRENCE OF RENAL STONES

THE decision to introduce long-term drug treatmentfor renal calcium stone disease is often taken reluc-

tantly. The benefit to be expected depends, in each case,on the likelihood of recurrence and its associated penal-ties (pain, surgery, and so on). The only evidence wehave on which to base such a forecast, apart from the

1. McCabe BF. Autoimmune sensorineural hearing loss. Ann Otol Rhinol Lar-yngol 1979; 88: 585-90.