THE ENIGMA OF SLOW VIRUSES
By Peter Duesberg
The Lancet 18 Sept. 1993
P.P. Liberski, 'The Enigma of Slow Viruses; Facts and Artefacts', Archives
of Virology 6, Springer-Verlag 1993, DM 250. ISBN 3-2118224278.
Virology and the law have much in common: a few basic rules like the
Ten Commandments and Koch's postulates, and many practitioners who can
obscure the basic rules with specialised interpretations. A highly specialsed
attorney may secure acquittal of a drug dealer caught in the act, despite
the Ten Commandments, and a scientist can blame phantom viruses for rare
genetic diseases, despite the rules of virology. The later case is the
subject of this book written for the 70th anniversary of Carlton Gajdusek.
Gajdusek won the 1977 Nobel Prize in medicine for the hypothesis that
human neurodegenerative diseases such as kuru, Creutzfeldt-Jakob disease,
Alzheimer's disease, and scrapie in sheep are caused by "unconventional"
slow viruses that "may induce disease months or even decades after
infection" (Science 1977; 197: 943-60). This hypothesis has
attracked attention because it suggests that kuru is naturally transmitted
by cannibalism practised by the Fore tribe in New Guinea; Gajdusek showed
that the disease can be experimentally transmitted to chimpanzees by inoculating
their brains with homogenates of the brains of patients with kuru who died.
But Gajdusek and his followers have not shed much light on this viral
hypothesis over the past 20 years. Despite numerous efforts neither the
kuru virus nor any other slow virus has been isolated. Therefore, the claim
for an infectious origin of these neurological diseases is open to several
questions. Why was intracerebral inoculation, instead of feeding, chosen
as a model for transmission by cannibalism? Were toxins excluded? - clearly
brain homogenates of death kuru patients must be toxic. Is human kuru indistinguisable
from diseases observed in monkeys intracerebrally inoculated with brain
homogenates? Moreover, Gajdusek's claim about cannibalism has been questioned
because the original photographic documentation that claimed to depict
a human was in fact a pig (Science 1986; 232:1497). Challenged to
provide further evidence, Gajdusek cited arrests for cannibalism of New
Guineans by Australian authorities (Science 1986; 233:926).
Despite his admiration for Gajdusek and his fascination with slow viruses,
Liberski retains an element of scepticism as the title of his book suggests.
It is probably for this reason that he dedicates a lot of space to an hypothesis
that offers a "self-replicating" protein (a prion) as a
solution to the undetectable enigmatic viruses. The paradox of a self-replicating
protein seemed to be solved when the prion proved to be a cellular protein.
But that created a new enigma - a pathogenic cellular protein. Prion researchers
quickly proposed that the mutated prions were to be blamed for neurological
disease, until some patients proved to have normal prions and some normal
people proved to have mutated prions.
According to this book, conventional and slow viral diseases are about
as compatible as night and day. For example, in conventional viral diseases,
all viruses conatin nucleic acid and can be seen under the electron microscope.
Conventional viral diseases elicit a febrile response, whereas slow viral
diseases do not. Conventional viral diseases, like viruses, spread horizontally,
but neurodegenerative diseases such as kuru are "familial", "tribal",
or genetically detremined, just like conventional genetic diseases. For
conventional viral diseases, the latent period between infection and disease
is determined by the generation time of viruses (8-48 h) and the number
of cells that need to be infected for pathogenicity. For slow viral diseases,
the latent period is determined by "incubation period genes"
of the host.
In the author's words, the purpose of his book was to summarise "almost
all existing data on scrapie and related infections, asking... whether
[they] fit one complete pattern. Having written this review, the author
is convinced... that such a task is not possible..." However, if one
changes one's point of view just a little, a surprisingly complete pattern
emerges - the neurodegenerative diseases are conventional genetic diseases
and the slow viruses are phantoms of virology. But can we afford an alternative
hypothesis in view of the number of papers (more than 1000) on slow viruses
that Liberski's book cites? Certainly not until the scientific monarchy
of the slow virologists is broken - a process that may be slower than the
alleged neuropathogenesis by slow viruses. *