News & Comment
TRENDS in Microbiology Vol.9 No.2 February 2001
61
cite examples of cellular proteins
assembling into icosahedra. There is much
to recommend this idea: capsids
(icosahedral or helical) are the most
characteristically viral structures known
and are essential for the viral lifestyle.
Hendrix et al. focus on tailed doublestranded (ds) DNA bacteriophages, in
which icosahedral capsids are the rule. In
making capsid formation the primary
event, they imply a separate origin for
helical viruses.
Most viral capsids are not complete
delivery systems, but for some simpler
viruses, such as picornaviruses, they
are. Hendrix et al.4 discuss a possible
role for primitive viral capsids as
vehicles for the lateral transfer of host
genes. The importance of this is
debatable. Pre-cells might have
transferred DNA rather easily, through
cell fusion or transformation, with
subsequent selection acting more to
create barriers than to circumvent
them6. At any rate, such a role is not a
cornerstone of their hypothesis. They
correctly state that encapsidation of
DNA provides a selfish advantage to the
encapsidation genes, which would at
least sometimes be transferred.
Another major feature of their
scheme is the ongoing acquisition of
small DNA segments (‘morons’) that can
add to viral genomes, as extensively
documented in their previous work.
Extrapolating this process into the past,
viral evolution probably included many
such additions, as well as fusions of
larger modules. Such serial acquisitions
could well also be crucial to cellular
evolution7. The databases for the extent
of gene transfer into viral and host
genomes are not totally independent:
more than one-third of the genes in
Escherichia coli that were classified as
alien by codon usage patterns8 lie within
defective prophages9.
We can hope for a lively round of
discussion by students of a wider range of
viruses, some of which has already
commenced5.
References
1 Luria, S.E. et al. (eds) (1978) General Virology
(3rd edn), John Wiley & Sons
2 Campbell, A. and Botstein, D. (1983) Evolution of
the lambdoid phages. In Lambda II (Hendrix, R.
et al., eds), pp. 365–380, Cold Spring Harbor
Laboratory Press
3 Campbell, A. (1977) Defective bacteriophages
and incomplete prophages. In Comprehensive
Virology 8 (Fraenkel-Conrat, H. and
Wagner, R.R., eds), pp. 259–328, Plenum Press
4 Hendrix, R.W. et al. (2000) The origins and
ongoing evolution of viruses. Trends Microbiol.
8, 504–508
5 Balter, M. (2000) Evolution on life’s fringes.
Science 289, 1866–1867
6 Campbell, A.M. (2000) Lateral gene transfer in
prokaryotes. Theoret. Pop. Biol. 57, 71–77
7 Lawrence, J.G. (1999) Gene transfer, speciation
and the evolution of bacterial genomes. Curr.
Opin. Microbiol. 2, 519–523
8 Karlin, S. et al. (1998) Codon usages in different
gene classes of the Escherichia coli genome. Mol.
Microbiol. 29, 1341–1355
9 Campbell, A. et al. Eubacterial genomes.
In Mobile DNA II (Craig, N.L. et al., eds),
ASM Press
Letters
The origins and
evolution of viruses
Early in the 20th century, three
hypotheses were advanced for the origin
of viruses: (1) viruses are degenerate
intracellular parasites; (2) viruses are
relics of precellular life; and (3) viruses
are cellular genes that escaped. Research
in the latter half of the 20th century
revolutionized our knowledge of the
physical nature of viruses, but
comparable progress in understanding
viral origins is conspicuously lacking. It
has long been appreciated that viruses
need not be a monophyletic group.
Beyond that, the three classical
hypotheses can be restated today, with
only minor refinements.
(1) The degenerate parasite hypothesis
currently has few supporters, ostensibly
because the absence of intermediate forms
and the extent of the implied degeneration
render such speculation non-productive;
ironically, the decline in favor of this
hypothesis coincided with general
acceptance of an endosymbiont origin for
organelles, which presents some of the
same problems.
(2) From the outset, the precellular life
hypothesis faced the dilemma that
viruses require cellular hosts and
therefore could not have preceded them;
a currently viable, related hypothesis is
that some RNA viruses originated in the
RNA world.
(3) Most virologists today probably
view at least the larger DNA viruses as
escaped cellular genes. Molecular
genetics has gradually replaced the
primitive concept of individual genes
going out on their own with scenarios
where blocks of genes (possibly from
diverse cellular sources) comprise
functional modules that merged with one
another, giving the typical virus a
chimeric ancestry1,2. Simplistic searches
for primordial cellular modules have
generally been confounded by the
presence of degraded relics of viral DNA
(defective proviruses) in most
chromosomes3.
At the dawn of the 21st century, it is
gratifying that this subject is receiving
renewed attention4,5. Hendrix et al.4
postulate that the initiating event was the
occurrence of the icosahedral capsid, and
Allan Campbell
Dept of Biological Sciences,
Stanford University,
Stanford, CA 94305, USA.
e-mail:
allan.campbell@forsythe.stanford.edu
Why does
Helicobacter pylori
actually have Lewis
antigens?
Humans are adapted to a life in a
microbial world, and host–microbial
interactions span a spectrum from
dependence, via tolerance, to
parasitism. A primal driving force for all
living organisms is the perpetuation of
the species. Microorganisms are
masters of this trade, far superior to
their human hosts in adapting to
changes in their environment and in
acquiring traits that confer increased
fitness. The co-evolution of man and
microorganisms – as long as the
existence of mankind – has provided
ample opportunities for refining
genotypes and phenotypes to maximize
multiplication and spread of
microorganisms using humans and
other mammals as hosts1. Perhaps it is
not surprising that, in many cases, this
evolution has led to common features in
genetic composition and phenotype
between man and microorganism. Still,
the finding that a microbial species
expresses genes and gene products
previously considered exclusive to
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