Viral Genomes Come in a Variety of Forms and Can Be
Either RNA or DNA
As discussed earlier, the DNA double helix has the advantages of stability and easy repair. If one
polynucleotide chain is accidentally damaged, its complementary chain permits the damage to be
readily corrected. This concern with repair, however, need not bother small viral chromosomes
that contain only several thousandnucleotides. The chance of accidental damage is very small
compared with the risk to a cell genome containing millions of nucleotides.
The genetic information of a virus can, therefore, be carried in a variety of unusual forms,
including RNA instead of DNA. A viral chromosome may be a single-stranded RNA chain, a
double-stranded RNA helix, a circular single-stranded DNA chain, or a linearsingle-stranded
DNA chain. Moreover, although some viral chromosomes are simple linear DNA double helices,
circular DNA double helices and more complex linear DNA double helices are also common.
Several viruses have protein molecules covalently attached to the 5' ends of their DNA strands,
for example, and the DNA double helices from the very large poxviruses have their opposite
strands at eachend covalently joined through phosphodiester linkages (Figure 6-75).
RNA viruses have particularly specialized requirements for replication, since to reproduce their
genomes they must copy RNA molecules, which means polymerizing nucleoside triphosphates
on an RNA template. Cells normally do not have enzymes to carry out this reaction, so even the
smallest RNA viruses must encode their ownRNA-dependent polymerase enzymes in order to
Both RNA Viruses and DNA Viruses Replicate Through the
Formation of Complementary Strands
Like DNA replication, the replication of the genomes of RNA viruses occurs through the formation
of complementary strands. For most RNA viruses this process is catalyzed by specific RNAdependent
RNA polymerase enzymes (replicases). These enzymes areencoded by the viral
RNA chromosome and are often incorporated into the progeny virus particles, so that upon entry
of the virus into a cell, they can immediately begin replicating the viral RNA. Replicases are
always packaged into the capsid of the so-called negative-strand RNA viruses, such as influenza
or vesicular stomatitis virus. Negative-strand viruses are so called because theinfecting single
strand does not code for protein; instead its complementary strand carries the coding sequences.
Thus the infecting strand remains impotent without a preformed replicase. In contrast, the viral
RNA of positive-strand RNA viruses, such as poliovirus, can serve as mRNA and produce a
replicase once it enters the cell; therefore the naked genome itself is infectious.
The synthesis ofviral RNA always begins at the 3' end of the RNA template, starting with the
synthesis of the 5' end of the new viral RNA molecule and progressing in the 5'-to-3' direction
until the 5' end of the template is reached. There are no error-correcting mechanisms for viral
RNA synthesis, and error rates are similar to those in DNA transcription (about 1 error in 104
nucleotides synthesized). This isnot a serious deficiency as long as the RNA chromosome is
relatively short; for this reason the genomes of all RNA viruses are small relative to those of the
large DNA viruses.
All DNA viruses begin their replication at a replication origin, where special initiator proteins bind
and then attract the replication enzymes of the host cell (see Figure 8-34). There are many
different replicationpathways, however. The complexity of these diverse replication schemes
reflects, in part, the problem of replicating the ends of a simple linear DNA molecule, given a DNA
polymerase enzyme that cannot begin synthesis without a primer (see pp. 253-254). DNA viruses
have solved this problem in a variety of ways: some have circular DNA genomes and thus no
ends; others have linear DNA genomes that...
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