particular RNA than did uninfected cells. Surprisingly, it was a piece of a transfer RNA. Transfer
RNAs, or tRNAs, are the assembly line workers
of protein building. tRNAs read instructions in a
messenger RNA and deliver the amino acids the
ribosome needs to make a protein.
Scientists knew that working tRNAs are essential employees. Fragments, when they were found,
were considered leftover bits of decommissioned
tRNAs. But the fragments that Bao and colleagues
discovered aren’t just worn out bits of tRNAs.
Each fragment, about 30 bases long, is precisely
cut from a tRNA when RSV infects cells. The fragments aid the virus’s infection in more than one
way. For instance, two fragments help the virus
make copies of itself in cells, Bao and colleagues
reported in 2017 in the Journal of General Virology.
tRNA fragments may also boost the body’s
susceptibility to a virus. Last year, Bao’s group
described in Scientific Reports how exposure to
some heavy metals, via air or water pollution, can
produce tRNA fragments that trigger inflammation, which may make people more susceptible to
respiratory infections such as RSV.
SACRIFICING INFECTED CELLS
Another type of RNA may help protect against
infection by certain viruses, including herpesvirus.
Virologist Britt Glaunsinger has long marveled at
the way viruses manipulate host cells by controlling RNAs in the cell. She became intrigued by
transposons, mobile stretches of DNA that can
jump from one location to another in the genome.
Transposons make up nearly half of all the DNA in
the human genome (SN: 5/27/17, p. 22).
“We tend to think of [transposons] as parasites
and things our own cells are constantly trying to
shut down,” says Glaunsinger, a Howard Hughes
Medical Institute investigator at the University
of California, Berkeley. That’s because some are
relics of ancient viruses. “While they may have
initially been bad, some of them may actually be
useful to us,” she says.
One class of transposons, called SINEs for
short interspersed nuclear elements, are peppered throughout the genome. People have more
than a million of one type of SINE known as Alu
elements. Mice have similar SINEs, called B2s.
When active, SINE transposons make RNA
copies of themselves. These SINE RNAs don’t
carry instructions for building proteins and alone
don’t enable the transposons to jump around the
genome. So researchers puzzled over their role.
Glaunsinger and colleagues discovered that some
SINE RNAs may protect against viral infections.
Normally, cells keep a tight lock on transposons,
preventing them from making any RNA. But in
Glaunsinger’s experiments, cells infected with
herpesvirus “were producing tons of these non-
coding RNAs in response to infection,” she says.
“That sort of captured our interest.”
Details of the process are still being worked
out, but Glaunsinger and others have discovered
that SINE RNA production triggers a cascade of
events that eventually kills infected human and
mouse cells. Once the RNA production gets going,
Glaunsinger says, “the cell is destined to die.”
Inflammation appears to be an important step in
the cell-killing chain reaction. It’s all for the greater
good: Killing the infected cell may protect the rest
of the organism from the infection’s spread.
Blow it up In cells
infected with herpesvirus, production of
RNAs copied from a
class of transposons
called SINEs may slate
the cells for death.
Killing infected cells
may head off the virus’s